The Optimal Circulation: Cells’ Contribution to Arterial Pressure

Rafik D. Grygoryan
Cybernetics Center of National Academy of Sciences of Ukraine, Kiev, Ukraine

Series: Cell Biology Research Progress
BISAC: SCI017000

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Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick

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Prevailing physiological concepts (PPC) of blood circulation consider the cardiovascular system (CVS) an autonomous system that has its own goal and mechanisms for achieving it. Physiologists agree that complex neural and humoral controllers of a mean arterial pressure (MAP) indirectly alter the blood flow for satisfying cellular needs. However, PPCs are incapable of explaining the causes of long-term shifts of a MAP’s rest level. In particular, this affects the current understanding and cure technologies of arterial hypertension (AH). Considering AH as a disease, physicians seek a cure that effectively decreases the elevated pressure. This gives rise to the palliative cure softening of AH symptoms without an understanding of AH’s primary causes. But this strategy, working until the patient intakes antihypertensive drugs, often leads to AH’s further development, and in extreme cases, current antihypertensive drugs are helpless. These limitations of PPC are forced to seek a circulation’s extended physiological theory (EPT), explaining the mechanisms of both normal and altered MAP’s.

In the EPT presented in the book, CVS is considered a constituent part of a more complex functional super-system (FSS) that appears in a multi-cellular animal organism during the co-evolution of specialized cells. The general goal of FSS is to provide optimal physiochemical and energy states of the cell cytoplasm. To achieve this goal under a stochastic total and local variations of cells’ activity, FSS should control: i) The cardiac output; ii) the regional and local blood flows; and iii) the chemical composition of both arterial and venous blood. Under chronic energy shortage, FSS should also provide an adequate increasing of ATP-synthesis in mitochondria of stagnated cells. So, under the ineffectiveness of current mitochondria, FSS must enrich the arterial blood by chemicals providing the biogenesis of mitochondria. However, neither the energy providers nor the providers of blood chemistry are properly involved in PPC of the blood circulation.

The EPT for the first time integrates the hemodynamic and metabolic aspects of cell life at the organism scale. It is proved that the CVS activity is inversely associated with the activity of mechanisms controlling the rates of both pulmonary ventilation and erythropoiesis. Under significant and chronic energy deficiency, the cells activate additional FSS mechanisms, materially supporting the biogenesis of mitochondria. The activity of FSS mechanisms forming the chemical composition of arterial and venous blood is in reciprocal relationships with the function of CVS. So, the EPT associates the function of CVS with energy and metabolic problems in cells.

The EPT concerns both traditional and additional determinants of the MAP level. It is proved that stochastic combinations of these determinants force the MAP level to “float”. In particular, both the mitochondrial insufficiency and the chemical contamination of cytoplasm are capable of causing AH. The normal arterial pressure is always individual. Before correcting the altered arterial pressure, a complex medical examination for ascertaining the mitochondrial function, the status of the FSS mechanisms is recommended. The diagnosis of AH should be reoriented for detecting cellular abnormalities. The therapy of AH should be targeted at finding strategies for optimizing the entire FSS function. (Imprint: Nova Biomedical)

Preface

Acknowledgements

List of Abbreviations

Introduction

Chapter 1. Challenges for Survival in Unfavorable Conditions

Chapter 2. Interpretations of the Normal Value of Arterial Pressure

Chapter 3. Primary and Secondary Determinants of Arterial Pressure

Chapter 4. Opportunities and Limitations of Traditional Regulators of the Cardiovascular System

Chapter 5. A Fight of an Aerobic Cell for Energy

Chapter 6. Organism-Scale Enhancers of Stagnated Cells

Chapter 7. A Concept of Physiological Super-Systems

Chapter 8. Disturbers of Mean Arterial Pressure

Chapter 9. How Do the Stagnated Cells Increase Arterial Pressure?

Chapter 10. Circulation in an Evolving Organism

Conclusion

References

Endorsements

Index

[1] Andersen, M; Rasmussen, H. (2012). AMPK: a regulator of ion channels. Communicative & Integrative Biology.5, 35,4804–4884.
[2] Angell James, JE; de Burgh, Daly M. (1971). Effects of graded pulsatile pressure on the reflex vasomotor responses, elicited by changes of mean pressure in the perfused carotid sinus–aortic. J. Physiol. 214, 1. 51–64.
[3] Armour,JA.(1994). Peripheral, autonomic, neuronal interactions in cardiac regulation. In:Neurocardiology, eds Armour, JA; Ardell, JL.(Oxford Univ Press, New York),219–244.
[4] Bader, M; Ganten, D. (2008). Update on tissue renin-angiotensin systems. J. Mol. Med. (Berl).86, 6, 615–621.
[5] Bader, M; (2013). ACE2, angiotensin-(1–7), and Mas: the other side of the coin. Pflugers Archiv: European journal of physiology. 465,1,79–85.
[6] Baker, KM; Chernin, MI; Schreiber, T; et al. (2004). Evidence of a novel intracrine mechanism in angiotensin II-induced cardiac hypertrophy. Regul. Pept. 120, 5–13.
[7] Barrett, CJ; Malpas, SC. (2005).Problems, possibilities, and pitfalls in studying the arterial baroreflexes' influence over long-term control of blood pressure. Am. J. Physiol. Regul. Integr. Comp. Physiol. 288,R837–R845.
[8] Beall, CM. (2006). Andean, Tibetan and Ethiopian Patterns of Adaptation to High–Altitude Hypoxia. Integ. Comp. Biol. 46. 18–24.
[9] Beard, DA; Mescam, M. (2012). Mechanisms of pressure-diuresis and pressure-natriuresis in Dahl salt-resistant and Dahl salt-sensitive rats. BMC Physiology.12,6–11.
[10] Belchenko, LA. (2001). Adaptation of humans and animals to hypoxia of different origins. SOJ, 7, 33-39 (Russian).
[11] Bergeron, R; Ren, JM; Cadman, KS; et al. (2001). Chronic activation of AMP kinase results in NRF-1 activation and mitochondrial biogenesis. Am. J. Physiol. Endocrinol. Metab. 281, 6, E1340–1346.
[12] Bianciardi, P; Fantacci, M; Caretti, A; et al.(2006). Chronic, in vivo hypoxia in various organs: hypoxia-inducible factor-1alpha and apoptosis. Biochem. Biophys. Res. Commun. 342, 875–880.
[13] Bishop, VS; Malliani, A; Thoren, P. (1983). Cardiac mechanoreceptors. In: Handbook of Physiology. The Cardiovascular System. Peripheral Circulation and Organ Blood Flow. Bethesda, MD: Am. Physiol. Soc,3, Pt. 2, 15, 497–555.
[14] Blanco MM; Gonzalez, CR; Saha, AK; et al.(2009). Hypothalamic AMP-activated protein kinase as a mediator of whole-body energy balance. Obes. Facts.2, 2,126–35.
[15] Bolignano,D; Rastelli,S; Agarwal,R. (2013).Pulmonary hypertension in CKD.Am J Kidney Dis,61,612–622.
[16] Bonner, JT. (1998). The origins of multi-cellularity. Integrative Biology: Issues, News, and Reviews. 1, 1, 27–36.
[17] Boscan, P; Pickering, AE; Paton, JF. (2002). The nucleus of the solitary tract: an integrating station for nociceptive and cardiorespiratory afferents. Exp Physiol.87, 2,259-266.
[18] Bossy-Wetze, E; Lipton, SA.(2003). Nitric oxide signaling regulates mitochondrial number and function. Cell Death and Differentiation. 10, 757–760.
[19] Brown, G; Cooper, C. (1994). Nanomolar concentrations of nitric oxide reversibly inhibit synaptosomal respiration by competing with oxygen at cytochrome oxidase. FEBS. Lett

. 356,295–298.
[20] Bruehl, S; Ok, YC. (2004). Interactions between the cardiovascular and pain regulatory systems: an updated review of mechanisms and possible alterations in chronic pain. Neuroscience & Biobehavioral Reviews. 28, 4, 395–414.
[21] Bruick, RK; McKnight, SL. (2001). A conserved family of prolyl hydroxylases that modify HIF. Science. 294,1337–1340.
[22] Brunelle, JK; Bell, EL; Quesada, NM; et al. (2005). Oxygen sensing requires mitochondrial ROS but not oxidative phosphorylation. Cell Metab. 1,409–414.
[23] Burns, KD. (2000). Angiotensin II and its receptors in the diabetic kidney. Am. J. Kidney Dis. 36, 3, 446–467.
[24] Bursi, F; McNallan, SM; Redfield, MM; et al. (2012).Pulmonary pressures and death in heart failure: a community study. J Am Coll Cardiol,59,222-231.
[25] Burykh, EA. (2009). Compensatory and adaptive rearrangement in the human respiratory system under acute hypoxic conditions. Human Physiology. 35,332-342.
[26] Cannon, WB. (1929). Organization for physiological homeostasis. Physiol. Rev. 9,399–431.
[27] Casteilla, L; Rigoulet, M; Panicaud, L. (2001). Mitochondrial ROS metabolism: modulation by uncoupling proteins. Life. 52,3-5,181–188.
[28] Caro, CG; Pedley, TJ; Schroter, RC; Seed, WA. (2012). The mechanics of the circulation. Cambridge University Press; 2 edition.
[29] Clanton, TL. (2007). Hypoxia-induced, reactive oxygen species formation in skeletal muscle. Journal of Applied Physiology.102, 6,2379–2388.
[30] Chang, DTW; Reynolds, IJ. (2006). Mitochondrial trafficking and morphology in healthy and injured neurons. Progress in Neurobiology. 80,241–268.
[31] Chapleau, MW; Li, Z; Meyrelles, SS; et al. (2001). Mechanisms determining sensitivity of baroreceptor afferents in health and disease. Ann N Y Acad Sci. 940.1-19.
[32] Chapleau, MW; Lu, Y; Abboud, FM. (2007). Mechanosensitive ion channels in blood pressure-sensing baroreceptor neurons. Curr Top Membr. 59,541-567.
[33] Chitravanshi, VC; Sapru, HN.(1995). Chemoreceptor-sensitive neurons in commissural subnucleus of nucleus tractus solitarius of the rat. Am. J. Physiol. 268,R851–R858.
[34] Chobanian, AV. (2009). The hypertension paradox: more uncontrolled disease despite improved therapy. N. Engl. J. Med. 361, 878–887.
[35] Chong, AY; Blann, AD; Lip, BY. (2003). Assessment of endothelial damage and dysfunction: observations in relation to heart failure. QJM. 96, 4,253–267.
[36] Coote, JH. (2006). Landmarks in understanding the central nervous control of the cardiovascular system. Exp. Physiol. 92, 3–18.
[37] Corton, JM; Gillespie, JG; Hardie, DG.(1994). Role of the AMP-activated protein kinase in the cellular stress response. Current Biol. 4.315324.
[38] Cossins, A; Berenbrink, M. (2008). Myoglobin’s new clothes. Nature. 454,416-417.
[39] Cowley, AW, Jr. (1992). Long–term control of arterial blood pressure. Physiol. Rev. 72,231– 300.
[40] Cowley, AW, Jr. (2003). Genomics and homeostasis. Am J Physiol.284,611–617.
[41] Cowley, AW, Jr. (2008). Renal, medullary, oxidative stress, pressure-natriuresis, and hypertension. Hypertension. 52,777–786.
[42] Crescenzo, R; Bianco, F; Mazzoli, A; et al. (2015). Skeletal muscle mitochondrial energetic efficiency and aging. Int. J. Mol. Sci. 16, 5,10674–10685.
[43] Dahout-Gonzalez, C; Nury, H; Truzuguet, V; et al. (2006). Molecular, functional, and pathological aspects of the mitochondrial ADP/ATP carrier. Physiology (Bethesda). 21,4, 242–249.
[44] Dampney, RA; Coleman, MJ; Fontes, MA. (2002). Central mechanisms underlying short– and long–term regulation of the cardiovascular system. Clin. Exp. Pharmacol. Physiol. 29,261–268.
[45] Davern, PJ. (2014). A role for the lateral parabrachial nucleus in cardiovascular function and fluid homeostasis. Front Physiol. 5, 436–443.
[46] Debold, EP; Patlak, JB, Schmitt, JP. (2007). Hypertrophic and dilated cardiomyopathy mutations differentially affect the molecular force generation of mouse, alpha-cardiac myosin in the laser trap assay. Am J Physiol Heart Circ Physiol. 293,284–291.
[47] Dellefave, L., McNally, EM. (2010).The genetics of dilated cardiomyopathy.Curr. Opin. Cardiol.25,198–204.
[48] De Mello, WC; Frohlich, ED. (2011). On the local, cardiac, renin angiotensin system. Basic and clinical implications. Peptides.32,1774–1779.
[49] Deuchars, J; Li, YW; Kasparov, S; Paton, JF. (2000). Morphological and electrophysiological properties of neurons in the dorsal vagal complex of the rat, activated by arterial baroreceptors. J. Comp. Neurol. 7, 417,233–249.
[50] Dhaun, N; Goddart, J; Webb, D. (2006). The endothelin system and its antagonism in chronic kidney disease. J. Am. Soc.Nephrol. 17, 4,943-955.
[51] Dhingra, H; Roongsritong, C; Kurtzman, NA. (2002). Brain natriuretic peptide: role in cardiovascular and volume homeostasis. Semin. Nephrol. 22,423-437.
[52] Distler, JH; Hirth, A; Kurowska-Stolarska, M; et al. (2003). Angiogenic and angiostatic factors in the molecular control of angiogenesis. Q. J. Nucl. Med. 47,149-161.
[53] Doward, PK. (1987). Does the brain “remember” absolute blood pressure? News in Physiol. Sciences. 2,10–13.
[54] Duling, B; Berne, R. (1970). Longitudinal gradient in periarteriolar pO2. Circ. Res. 27,669-678.
[55] Eckberg, DL. (1979). Baroreceptor-cardiac reflex physiology. Acta Physiol. Polon. 30,9-17.
[56] Ekelund, L; Gothlin, J. (1976). Compensatory renal enlargement in older patients. AJR Am J. Roentgenol. 127, 5,713–718.
[57] Emerling, BM; Weinberg, F; Snyder, C; et al. (2009). Hypoxic activation of AMPK is dependent on mitochondrial ROS, but independent of an increase in AMP/ATP ratio. Free Radic. Biol. Med. 46, 10,1386–1391.
[58] Fadel, PJ; Ogoh, S; Keller, DM; Raven, PB. (2003). Recent insights into carotid baroreflex function in humans using the variable pressure neck chamber. Exp Physiol. 88, 6, 671-680.
[59] Farag, E; Maheshwari, K; Morgan, J; et al. (2015). An update of the role of renin angiotensin in cardiovascular homeostasis. Anesth. Analg. 120, 2,275–292.
[60] Fauvel, JP; Cerutti, C; Quelin, P; et al. (2000). Mental stress–induced increase in blood pressure is not related to baroreflex sensitivity in middle–aged healthy men. Hypertension. 35, 887–891.
[61] Ferguson, DW; Abboud, FM; Mark, AL. (1985). Relative contribution of aortic and carotid baroreflex to heart rate control in man during steady-state, and dynamics increases in arterial pressure. J. Clin. Invest. 76, 2265-2274.
[62] Ferrari, AU. (2002). Modifications of the cardiovascular system with aging. Am. J. Geriatr. Cardiol. 11,1,30–33.
[63] Finkel, T; Hwang, PM. (2009). The Krebs cycle meets the cell cycle: Mitochondria and the G1–S transition. Proc Natl Acad Sci USA.106, 29,11825-11826.
[64] Fioramonti, X; Marsollier, N; Song, Z; et al. (2010).Ventromedial, hypothalamic, nitric oxide production is necessary for hypoglycemia detection and counter regulation.Diabetes.59,519–528.
[65] Flogel, U; Merx, M; Godecke, A. (2001). Myoglobin: a scavenger of bioactive NO. PNAS. 98, 2,735–740.
[66] Flogel, U; Fago, A; Rassaf, T. (2010). Keeping the heart in balance: the functional interactions of myoglobin with nitrogenoxides.J. Exp. Biol.213,2726–2733.
[67] Gauer, OH. (1978). Regulation of blood volume. In: The arterial system. Dynamics, control theory, and regulation. Berlin, Heidenberg, New York, Springer – Verlag.153-161.
[68] Gnaiger, E; Mendez, G; Hand, S. (2000). High phosphorylation efficiency and depression of uncoupled respiration in mitochondria under hypoxia. PNAS.97, 20,11080–11085.
[69] Gnaiger, E. (2001). Bioenergetics at low oxygen: dependence of respiration, and phosphorylation on oxygen and adenosine diphosphate supply. Respir Physiol. 128,277–297.
[70] Grigoryan, RD. (1990). Mathematical Principles of the Analysis of Quantum Regularities in Multicomponent Formations of Biological Nature, Doklady of the Academy of Sciences of the USSR. Biophysics, 314,6.745-748.
[71] Grigoryan, RD. (1992). Fundamentals of mathematical theory and simulation studies of baroreflex regulation of hemodynamics. Diss. Doct. Biol. Sciences, Kiev. (Russian).
[72] Grigoryan, RD. (1990). Anisotropy and nonlinearity (General regularities of multicomponent formations’ state changing).Cybernetics Center, Kiev.(Russian).
[73] Grigoryan, RD; Aksenova, TV. (2008). Modeling of organism's adaptive reaction to environmental changes. Cybernetics and Systems Analysis. 44,107–115.
[74] Groebe, K. (1988). Coupling of hemodynamics to diffusional oxygen mass transport. Adv. Exp. Med. Biol. 222,3-14.
[75] Grygoryan, RD; Lissov, PN. (2004). A software simulator of the human cardiovascular system on the basis of its mathematical model. Problems of programming. 4,100-111. (Russian).
[76] Grygoryan, RD. (2004). Self-organization of homeostasis and adaptation: Academperiodica, Kiev (Russian).
[77] Grygoryan, RD; Lyabakh, EG. (2008). A formalized analysis of the adaptive response of a cell to energy deficit. Reports of National Academy of Sciences of Ukraine. 11,145-151 (Russian).
[78] Grygoryan, RD. (2016). The paradigm of “floating” arterial pressure. Palmarium Academic Publishing, Düsseldorf (Russian).
[79] Grygoryan, RD; Lissov, PN; Aksenova, TV; Moroz, AG. (2009). The specialized software-modeling complex “PhysiolResp.”Problems of programming, 2,140-150 (Russian).
[80] Grygoryan, RD; Lyabach, EG. (2015). The arterial pressure: a comprehension: Academperiodica, Kiev (Russian).
[81] Grygoryan, RD. (2009). Biodynamics and models of energy stress. Academperiodica, Kiev (Russian).
[82] Grygoryan, RD. (2011).Energy concept of arterial pressure. Reports of National Academy of Sciences of Ukraine. 7,148-155 (Russian).
[83] Grygoryan, RD. (2013). Individual physiological norm: the concept and problems. Reports of National Academy of Sciences of Ukraine. 8,156-162 (Russian).
[84] Grygoryan, RD; Lissov, PN. (2006). Internal originators of functions and fluctuations in multi–cellular organisms. In: Bioelectromagnetics (Current concepts). Springer. – Netherlands, 423–430.
[85] Grygoryan, RD, Hargens, AR. (2008). A virtual, multi–cellular organism with homeostatic and adaptive properties. Adaptation Biology and Medicine: Health Potentials. Ed. L. Lukyanova, N. Takeda, P.K. Singal. – New Delhi: Narosa Publishing House, 5,261 –282.
[86] Grygoryan, RD. (2012). The Energy basis of reversible adaptation. Nova Science, NY.
[87] Grygoryan, RD, Lyabakh, KG. (2012).The Cornerstones of Individual Adaptation to Environmental Changes. In: Daniels J.A. (Ed.). Advances in Environmental Research. 20, Nova Science Publishers, NY, 39 – 66.
[88] Grygoryan, RD. (2014). Formal analysis of mechanisms increasing arterial pressure. Cybernetics and computer engineering. Issue.177,68–78.
[89] Grygoryan, RD, Aksenova, ТV, Degoda AG. (2016). Modeling of mechanisms and hemodynamic effects of heart hypertrophy. Cybernetics and computer engineering. 184. 72–83 (Russian).
[90] Grygoryan, RD, Aksenova, ТV, Degoda AG. (2017).A computer simulator of mechanisms providing energy balance in human cells. Cybernetics and computer engineering. 192. 76–87 (Russian).
[91] Guyenet, PG. (2006). The sympathetic control of blood pressure. Nature Reviews Neuroscience. 7,335-346.
[92] Guyton, A. (1963). Circulatory Physiology: Cardiac Output and Its Regulation: Saunders. Co., Philadelphia and London.
[93] Guyton, AC; Coleman, TG. (1967). Long-term regulation of the circulation: interrelation with body fluid volumes. In: Physical Bases of Circulatory Transport: Regulation and Exchange, Ed. by E.B. Reeve and A.C. Guyton. Philadelphia, PA: Saunders.179-201.
[94] Guyton, AC. (1991).Blood pressure control — special role of the kidneys and bodily fluids. Science. 252,1813–1816.
[95] Guyton, AC; Coleman, TG; Granger, HJ. (1972). Circulation: overall regulation. Annu Rev Physiol. 34,13–46.
[96] Guyton, AC; Hall, JE. (2006). Textbook of Medical Physiology. (11th ed). Philadelphia: Elsevier Saunders.
[97] Haider, DG; Bucek, RA; Giurgea, AG; et al. (2005). PGE-1 analog alprostadic induces VFGF and eNOS expression in endothelial cells. Am. J. Physiol. Heart. Circ. Physiol. 289, 5,2066-2072.
[98] Hainsworth, R.(1991). Reflexes from the heart. Physiol. Rev. 71,617–658.
[99] Haisman, EB. (1964). Aortic baroreceptors. Medicine, Moscow (Russian).
[100] Hall, JE; Guyton, AC; Brands, MW.(1996). Pressure-volume regulation in hypertension. Kidney Int Suppl. 55,S35-S41.
[101] Hall, JE; Brands, MW; Henegar, JR.(1999). Angiotensin II and long-term arterial pressure regulation: the overriding dominance of the kidney. J Am Soc Nephrol. 10(Suppl 12),S258-S265.
[102] Hall, JE; Guyton, AC; Coleman, TG; et al. (1986).Regulation of arterial pressure: role of pressure natriuresis and dieresis. Fed Proc. 45, 13,2897-2903.
[103] Hamm, LL; Hering-Smith, KS.(2010). Pivotal role of the kidney in hypertension. Am J Med Sci. 340,30–32.
[104] Hara, S; Hamada, J; Kobayashi, C; et al. (2001). Expression and characterization of hypoxia-inducible factors (HIF)-3alpha in human kidneys: suppression of HIF-mediated gene expression by HIF-3alpha.Biochem. Biophys. Res. Commun. 1287, 808-813.
[105] Hardie, DG; Hawley, SA. (2001). AMP–activated protein kinase: the energy charge hypothesis revisited. Bioessays. 23,1112–1119.
[106] Hardie, DG. (2008). AMPK: a key regulator of energy balance in the single cell and the whole organism. Int J Obes (Lond). 32, Suppl 4,7–12.
[107] Hardie, DG. (2011). Sensing of energy and nutrients by AMP-activated protein kinase. Am. J. Clin. Nutr.93, 4,891S–896S.
[108] Hardie, DG; Carling D; Gamblin, S. (2011). AMP-activated protein kinase: also regulated by ADP? Trends Biochem. Sci.36, 9,470-477.
[109] Hardie, DG; Ashford, ML. (2014). AMPK: regulating energy balance at the cellular and whole-body level. Physiology (Bethesda). 29, 2,99–107.
[110] Hardie, DG; Ross, FA; Hawley, SA. (2012). AMPK: a nutrient and energy sensor that maintains energy homeostasis. Nat. Rev. Mol. Cell Biol.13, 4,251–262.
[111] Harris, JK; Kelley, ST; Pace NR. (2004) New perspective on an uncultured bacterial phylogenetic division. Appl. Environ. Microbiol. 70,845-849.
[112] Harris, N. (2003). Arteriovenous pairing: a determinant of capillary exchange. News Physiol. Sci. 1883–1887.
[113] Hayashi, T; Hirshman, MF; Kurth, EJ; et al. (1998). Evidence for 5' AMP-activated protein kinase mediation on the effect of muscle contraction on glucose transport. Diabetes. 47, 8,1369–1373.
[114] Henin, N; Vincent, MF; Gruber, HE; et al. (1995). Inhibition of fatty acid and cholesterol synthesis by stimulation of AMP-activated protein kinase. FASEB. 9,7,541–546.
[115] Henry, RA; Lu, IL; Beightol, LA; Eckberg, DL. (1998). Interactions between CO2 chemoreflexes and arterial baroreflexes. Am. J. Physiol. Heart Circ. Physiol. 274, 2177–2187.
[116] Hfulica, I; Petrescu, G; Slatineanu, S; Bild, W. (1999). Present data concerning the renin-angiotensin system of extrarenal origin. Rom. J. Physiol. 36, 3-4,153–63.
[117] Hines, T; Toney, GM; Mifflin, SW. (1994).Responses of neurons in the nucleus tractus solitarius to stimulation of the heart and lung receptors in the rat. Circ. Res. 74,1188–1196.
[118] Holliday, R. (2006). Epigenetics: A Historical Overview. Epigenetics, 1,2,76-80.
[119] Hood, L; Friend, SH. (2011). Predictive, personalized, preventive, participatory (P4) cancer medicine. Nat Rev Clin Oncol.8,184-187.
[120] Hoppeler, H; Fluck, M. (2003). Plasticity of skeletal muscle mitochondria: structure and function. Med Sci. Sports Exerc.35,1,95-104.
[121] Huang, LE; Bunn, HF. (2003). Hypoxia–inducible factor–1 and its biological relevance. J. Biol Chem. 278,19575–19578.
[122] Hurst, D; Taylor, EB; Cline, TD; et al.(2005). AMP-activated protein kinase activity, and phosphorylation of AMP-activated protein kinase in contracting muscle of sedentary and endurance-trained rats. Am. J. Physiol. Endocrinol. Metab. 289, 4, E710–715.
[123] Imray, C; Wright, A; Subudhi, A; Roach, R. (2010). Acute mountain sickness: pathophysiology, prevention, and treatment. Prog. Cardiovasc. Dis.52, 6,467–484.
[124] Ivan, M; Kondo, K; Yang, HF; et al. (2001). HIF1α targeted for VHL mediated destruction by proline hydroxylation: Implications for O2 sensing. Science.292,464–468.
[125] Ivanov, KP. (2001). Fundamentals of the energy of the organism. Theoretical and practical aspects. SPb. Science (Russian).
[126] Jensen, F. (2009). The role of nitrite in nitric oxide homeostasis: a comparative perspective. Biochim Biophys Acta.1787, 7,841–848.
[127] Jeong Sook Kim-Han, Jo Ann Antenor-Dorsey, and Karen L. O'Malley. (2011). The Parkinsonian Mimetic, MPP, Specifically Impairs Mitochondrial Transport in Dopamine Axons. J. Neurosci.31, 19,7212-7221.
[128] Jones, DP. (2006). Redefining oxidative stress. Antioxid. Rwedox Signal.8, 9-10,1865-1879.
[129] Jurgensen, SB; Treebak, JT; Viollet, BS. et al. (2007). Role of AMPKα2 in basal, training, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle. Endocrinology and metabolism.292, 1, E331–E339.
[130] Kanda, T; Itoh, H. (2012). The ACE2/Ang(1-7)/Mas receptor axis in cardiovascular and renal diseases. Nihon Rinsho.70, 9,1487–1491.
[131] Kanai, A; Peterson, J. (2004). Function and regulation of mitochondrially produced nitric oxide in cardiomyocytes. Am. J. Physiol. Heart Circ. Physiol.286,1,11–12.
[132] Kang, L; Dunn-Meynell, AA; Routh, VH; et al. (2006). Glucokinase is a critical regulator of ventromedial hypothalamic neuronal glucosensing.Diabetes.55,412–420.
[133] Kaufman, JM; Siegel, N; Lytton, B; Hayslett, JP. (1976). Compensatory renal adaptation after progressive renal ablation. Invest. Urol.13, 6,441–444.
[134] Kawar,B; Ellam,T; Jackson,C; Kiely,DG.(2013).Pulmonary hypertension in renal disease: Epidemiology, potential mechanisms, and implications.Am J Nephrol, 37,281–290.
[135] Kemp, BE; Mitchelhill, KI; Stapleton, D; et al. (1999). Dealing with energy demand: the AMP–activated protein kinase. Trends Biochem Sci.24,22–25.
[136] Kirchheim, HR. (1989). Cardiopulmonary–arterial baroreceptor interaction in the control of bloodpressure. News Physiol Sci.4,56–59.
[137] Kirchhiem, HR. (2003). Our fragmentary knowledge of the regulatory functions of ANG II “fragments”: are we beginning to see the light? American journal of physiology. Regulatory, integrative and comparative physiology.285,R937-938.
[138] Kohlstedt, K;Trouvain, C;Boettger, T; et al. (2013). AMP-activated protein kinase regulates endothelial cell angiotensin-converting enzyme expression via p53 and the post-transcriptional regulation of microRNA-143/145. Circ. Res.1121,150–1158.
[139] Korner, PI. (1981). The central nervous system and its operation in cardiovascular control. Clin. Exp. Hypertension.3,343-368.
[140] Kositsky, GI. (1975). Afferent systems of the heart: Medicine, Moscow (Russian).
[141] Kotchen, TA; Cowley, AW, Jr; Frohlich, ED. (2013). Salt in health and disease-A delicate balance. NEJM.368,1229–1237.
[142] Kotelnikov, VA. (2006) On the capacity of “ether” and wire in telecommunications. Uspekhi Fizicheskikh Nauk. 7, 762-770 (Russian).
[143] Kumar, R; Singh, VP; Baker, KM. (2007). The intracellular renin-angiotensin system: a new paradigm. Trends. Endocrinol. Metab. 18,208–214.
[144] Kumar, R; Boim, MA. (2009). Diversity of pathways for intracellular angiotensin II synthesis. Curr. Opin. Nephrol. Hypertens.18,33–39.
[145] Kumar, R; Thomas, CM; Yong, QC; et al. (2012).The intracrine renin-angiotensin system. Clin. Sci. (Lond).123,273–284.
[146] Lane, MD; Wolfgang, M; Cha, SH; Dai, Y. (2008). Regulation of food intake and energy expenditure by hypothalamic malonyl-CoA. Int. J. Obes. (Lond).32, Suppl 4,49–54.
[147] Lane, N. (2014). Bioenergetic Constraints on the Evolution of Complex Life. Cold Spring Harb Perspect Biol. doi: 10.1101/cshperspect.a015982.
[148] Lane, N. (2011). Energetics and genetics across the prokaryote–eukaryote divide. Biol Direct.6,35.
[149] Lane, N; Martin, W. (2012). The origin of membrane bioenergetics. Cell.151,1406–1416.
[150] Lanfranchi, P; Somers, KW. (2002). Arterial baroreflex function and cardiovascular variability: interactions and implications. AJP Regul. Integr. Comp. Physiol.283,815–826.
[151] Lavrentyev, EN; Estes, AM; Malik, KU. (2007). Mechanism of high glucose induced angiotensin II production in rat vascular smooth muscle cells. Circ.Res. 101,455–464.
[152] Lawrence, HY.(2008). AMP-Activated protein kinase conducts the ischemic stress response orchestra. Circulation.117,832–840.
[153] Lee, M; Hwang, JT; Lee, HJ; et al. (2003). AMP-activated protein kinase activity is critical for hypoxia-inducible factor-1 transcriptional activity, and its target gene expression under hypoxic conditions in DU145 cells. J. Biol. Chem.278, 10,39653–61.
[154] Lee, W; Kim, M; Park, HS; (2006). AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPAR alpha and PGC-1. Biochem. Biophys. Res. Commun.340, 1,291–295.
[155] Lee, J; Kim, MS.(2007). The role of GSK3 in glucose homeostasis and the development of insulin resistance. Diabetes Res. Clin. Pract.77,S49–S57.
[156] Li, J; McCullough, LD. (2010). Effects of AMP-activated protein kinase in cerebral ischemia. Journal of Cerebral Blood Flow & Metabolism. 30, 3,480–492.
[157] Li, Y; Rempe, DA.(2010). During hypoxia, HUMMR joins the mitochondrial dance. Cell Cycle. 9, 1,50–57.
[158] Li, H, Weatherford, ET, Davis, DR. (2011). Renal, proximal tubule angiotensin AT1A receptors regulate blood pressure. Am. J. Physiol. Regul. Integr. Comp. Physiol.298,R1209–R1211.
[159] Liesa, M; Palacon, M; Zorzano, A. (2009). Mitochondrial Dynamics in Mammalian Health and Disease. Physiol. Rev. 89,799–845.
[160] Lohmeier, TE. (2003).Interactions between ANG II and baroreflexes in long-term regulation of renal sympathetic nerve activity. Circ Res.92,1282–1284.
[161] Lopez-Lazaro, M. (2006). HIF-1: hypoxia-inducible factor or dysoxia-inducible factor? FASEB J. 20,828–832.
[162] Lopez, M; Tovar, S; Vozquez, MJ; et al. (2007). Peripheral tissue brain interactions in the regulation of food intake. Proc. Nutr. Soc. 66, 1,131–55.
[163] Lopez, M; Lelliott, C; Vidal-Puig, A. (2011). Hypothalamic fatty acid metabolism: a housekeeping pathway that regulates food intake. Curr. Opin. Clin. Nutr. Metab.Care.14, №2.138–44.
[164] Lopez, M; Tovar, S; Vozquez, MJ; et al. (2012). AMP-Activated Protein Kinase (AMPK) and Energy-Sensing in the Brain. Exp. Neurobiol.21,250–260.
[165] Ma, X; Francois, M; Abboud, FM; Chapleau, MW.(2002). Analysis of afferent, central, and efferent components of the baroreceptor reflex in mice. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.283,5,R1033-R1040.
[166] Maeda, S, Iemitsu, M, Jesmin, S, Miyauchi, T. (2005). Acute exercise causes an enhancement of tissue renin-angiotensin system in the kidney in rats. Acta Physiol. Scand.185, 1,79–86.
[167] Mainwood, GW; Rakusan, K. (1982). A model for intracellular energy transport. Can. J. Physiol. Pharmacol. 60, 1,98–102.
[168] Malpas, SC. (2002). Neural influences on cardiovascular variability: possibilities and pitfalls. Am. J. Physiol. Heart Circ. Physiol. 282,6–20.
[169] Malpas, SC. (2010).Sympathetic Nervous System Overactivity and Its Role in the Development of Cardiovascular Disease. Physiological Reviews.90, 2,513-557.
[170] Mann, J; Ritz, E. (1988). The renin–angiotensin system in diabetic patients.Klein.Wochenschr.66, 18,883–893.
[171] Markhasin, VS; Katznelson, LB; Nikitina, LV; Protsenko, LYu. (1999). Biomechanics of a non-uniform myocardium. UrB RAS (Russian).
[172] Maynard, MA; Evans, A. J; Hosomi, T; et al. (2005). Human HIF-3α4 is a dominant-negative regulator of HIF-1 and is down-regulated in renal cell carcinoma. FASEB J. 19,1396-1406.
[173] McCrimmon, RJ; Song, Z; Cheng, H; et al. (2006). Corticotrophin-releasing factor receptors within the ventromedial hypothalamus regulate hypoglycemia-induced hormonal counter regulation. J Clin Invest.116,1723–1730.
[174] McCrimmon, R.(2008). The mechanisms that underlie glucose sensing during hypoglycemia in diabetes. Diabet Med.25,513–522.
[175] McKinley, MJ; Allen, AM; May, CN. (2001). Neural pathways from the lamina terminalis influencing cardiovascular and body fluid homeostasis. Clin. Exp. Pharmacol. Physiol.28,12,990-992.
[176] McConnaughey, MM; McConnaughey, JS; Ingenito, AJ. (1999). Practical considerations of the pharmacology of angiotensin receptor blockers. J. Clin. Pharmacol. 39,547–559.
[177] McGee, SL; van Denderen, BJ; Howlett, KF; et al.(2008).AMP-activated protein kinase regulates GLUT4 transcription by phosphorylating histone deacetylase. Diabetes. 57,860867.
[178] McCrimmon, RJ;Shaw, M;Fan, X;et al. (2008). Key role for AMP-activated protein kinase in the ventromedial hypothalamus in regulating counter regulatory hormone responses to acute hypoglycemia. Diabetes.57, 2,444-50.
[179] Meyerson, FZ. (1981). Adaptation, stress, and prevention. Nauka, Moscow (Russian).
[180] Meyerson, FZ. (1986). General mechanism of adaptation and the role of stress reactions in it: the main stages of the process. Physiology of Adaptation Processes. Nauka, Moscow, 77-124 (Russian).
[181] Mehta, PK; Griendling, KK.(2007). Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. American Journal of Physiology. Cell Physiology.292, 1,C82–C97.
[182] Merx, MW; Flogel, U; Stumpe, T.; et al.(2001). Myoglobin facilitates oxygen diffusion. FASEB J. 151,1077–1079.
[183] Michiels, C. (2004). Physiological and Pathological Responses to Hypoxia. Am J. Pathol.164,6, 1875–1882.
[184] Mifflin, SW.(1992). Arterial chemoreceptor input to nucleus tractus solitaries. Am. J. Physiol.263,R368–R375.
[185] Minokoshi, Y; Alquier, T; Furukawa, N; et al. (2004). AMP-kinase regulates food intake by responding to hormonal and nutrient signals in the hypothalamus. Nature. 428, (6982),569–74.
[186] Mironov, SL. (2009). Complexity of mitochondrial dynamics in neurons and its control by ADP produced during synaptic activity. Int. J. Biochem. Cell Biol. 41,10,2005–2014.
[187] Misra, Р; Chakrab, R. (2007). The role of AMP kinase in diabetes. Indian J. Med. Res. 125,389–398.
[188] Montan, i J-P; Van Vliet, B.N. (2009). Understanding the contribution of Guyton's large circulatory model in long-term control of arterial pressure. Exp. Physiol.94,382–388.
[189] Morgan, DO. (2007). The Cell Cycle: Principles of Control. London, New Science Press.
[190] Moybenko, AA; Pavlyuchenko, VB; Datsenko, VV; Maisky, VA. (2005).The Role of Nitric Oxide in the Mechanisms of the Formation of Reflex Vasomotor Reactions. Uspekhi fiziol. Sciences. 4, 3-14 (Russian).
[191] Moybenko, AA; Dosenko, VE; Parkhomenko, AN. (2008). Endogenous mechanisms of cardio protection as a basis for pathogenetic therapy of heart diseases. Naukova Dumka, Kiev (Russian).
[192] Mungai, PT; Waypa, GB; Jairaman, A; et al. (2011). Hypoxia triggers AMPK activation through reactive oxygen species-mediated activation of calcium release-activated calcium channels. Mol. Cell. Biol. 31, 17,3531–354.
[193] Nekrasova, OE; Kulik, AV; Minin, AA. (2007). Protein kinase C regulates the mobility of mitochondria. Biological membranes. 24, 2. 126-132 (Russian).
[194] Nguyen Dinh Cat, A; Touyz, RM. (2011). A new look at the renin-angiotensin system– focusing on the vascular system. Peptides. 32, 10,2141-50.
[195] Nicholls, DG; Budd, SL. (2000). Mitochondria and neuronal survival. Physiol. Rev. 80,315–360.
[196] Noordergraaf, AV; Groeneveldt, JA; Bogaard, HJ. (2016). Pulmonary Hypertension. European Respiratory Review. 25,4-11.


[197] Osborn, JW.(2005). Hypothesis: set-points and long-term control of arterial pressure. A theoretical argument for a long-term arterial pressure control system in the brain rather than the kidney. Clin. Exp. Pharmacol. Physiol.32,384–393.
[198] Ouchi, N; Shibata, R; Walsh, K. (2005). AMP-activated protein kinase signaling stimulates VEGF expression and angiogenesis in skeletal muscle. Circ. Res. 96,838–846.
[199] Pannabecker, TL. (2012). Structure and Function of the Thin Limbs of the Loop of Henle. John Wiley & Sons, Inc. American Physiological Society. Compr Physiol.2,2063-2086.
[200] Paton, JFR.(1998). Pattern of Cardiorespiratory Afferent Convergence to Solitary Tract Neurons, Driven by Pulmonary Vagal C-Fiber Stimulation in the Mouse. Journal of Neurophysiology.79,5,2365-2373.
[201] Paton, JF; Li, YW; Deuchars, J; Kasparov, S. (2000). Properties of solitary tract neurons receiving inputs from the sub-diaphragmatic vagus nerve. Neuroscience.95,1,141-53.
[202] Paton, JFR; Deuchars, J; Li, YW; Kasparov, S.(2001). Properties of solitary tract neurons responding to peripheral, arterial chemoreceptors. Neuroscience.105, 231–248.
[203] Paton, JFR.(1998).Convergence properties of solitary tract neurons driven synaptically by cardiac vagal afferents in the mouse. J. Physiol. 508,237–252.
[204] Person, RJ. (1989). Somatic and vagal afferent convergence on solitary tract neurons in cat: electrophysiological characteristics. Neuroscience. 30,283–295.
[205] Phillips, MI; Speakman, EA; Kimura, B. (1993). Levels of angiotensin and molecular biology of the tissue renin angiotensin systems. Regul. Pept. 43, 1–2,1–20.
[206] Podgoreanu, MV; Schwinn, DA. (2004). Genomics and the circulation. Br J Anaesth. 93,140–148.
[207] Raij, L. (2001).Workshop: hypertension and cardiovascular risk factors: role of the angiotensin II–nitric oxide interaction. Hypertension. 37,767–773.
[208] Ramamurthy, S; Ronnett, G. (2012). AMP-activated protein kinase (AMPK) and energy-sensing in the brain. Exp. Neurobiol. 21, 2,52–60.
[209] Rassaf, T; Flogel, U; Drexhage, C; et al. (2007). Nitrite reductase function of deoxymyoglobin: oxygen sensor and regulator of cardiac energetics and function. Circ .Res. 100, 12,1749–1754.
[210] Rhian, TM. (2012). New insights into mechanisms of hypertension. Current Opinion in Nephrology & Hypertension. 21,Issue 2,119-121.
[211] Riggs, A; Gorr, TA. (2006). Globin in every cell?PNAS. 103, 8,2469–2470.
[212] Ruckl, KS; Hirshman, MF;Brandauer, J; et al. (2007). Skeletal muscle adaptation to exercise training: AMP-activated protein kinase mediates muscle fiber type shift.Diabetes. 56, 8,2062–2069.
[213] Rosenthal, J. (1993). Role of renal and extrarenal renin-angiotensin system in the mechanism of arterial hypertension and its sequelae. Steroids.58, 12,566–72.
[214] Russell, AP. (2005). PGC-1alpha and exercise: important partners in combating insulin resistance. Curr. Diabetes Rev.1, 2.175–181.
[215] Sagach, VF; Bazilyuk, OV; Kotsyuruba, AV. (1998). Endothelial dysfunction as a consequence of changes in its enzymatic activity in arterial hypertension. Role of nitrogen monoxide in life processes. Polybig, Minsk, 144-146 (Russian).
[216] Sagach, VF; Shimanska, TV; Nadtochiy, SN. (2000). Studying the role of nitric oxide in oxygen consumption and changes in the value of the oxygen in the heart muscle. Physiol.,46, 2, 33-40 (in Ukrainian).
[217] Salabei, JK; Hill, BG. (2013).Mitochondrial Fission Induced by Platelet-Derived Growth Factor Regulates Vascular Smooth Muscle Cell Bioenergetics and Cell Proliferation. Redox Biology. 1,542-551.
[218] Schieke, SM; McCoy, JP; Finkel, T. (2008). Coordination of mitochondrial bioenergetics with G1-phase cell cycle progression. Cell Cycle.7,1782–1787.
[219] Schild, JH;Kunze, DL. (2012). Differential distribution of voltage-gated channels in myelinated and unmyelinated baroreceptor afferents.Autonomic Neuroscience. 172, 1-2,4-10.
[220] Shiva, S; Huang, Z;Grubina, R; Sun, J et al. (2007). Deoxymyoglobin is a nitrite reductase that generates nitric oxide and regulates mitochondrial respiration. Cir. Res. 100, 5,654–661.
[221] Schneeberger, M;Claret, M. (2012). Recent Insights into the Role of Hypothalamic AMPK signaling cascade upon metabolic control. Front Neurosci. eCollection.2012,185:6.
[222] Seagard, JL;van Brederode, JF;Dean C;et al. (1990). Firing characteristics of single-fiber carotid sinus baroreceptors. Circ Res.66, 6,1499-1509.
[223] Seagard, JL; Dean, C; Hopp, FA. (2000). Modulation of the carotid baroreceptor reflex by substance P in the nucleus tractus solitarius. J Auton Nerv Syst.78, 2-3,77-85.
[224] Seagard, JL; Dean, C; Hopp, FA. (2001).Properties of NTS neurons receiving input from barosensitive receptors.Ann N Y Acad Sci.940.–P.142-156.
[225] Semenza, GL; Wang, GL. (1992). A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol. Cell. Biol.12, 5447–5454.
[226] Semenza, GL. (2004). O2 regulated gene expression: transcriptional control of cardiorespiratory physiology by HIF1. J. Appl. Physiol. 96, 3,1173–1177.
[227] Semenza, GL. (2009). Involvement of oxygen-sensing pathways in physiologic and pathologic erythropoiesis. Blood J.114, 10,1-27.
[228] Sena, LA; Chandel, NS. (2012). Physiological roles of mitochondrial reactive oxygen species. Mol Cell.48, 2,158–167.
[229] Silva-Carvalho,L; Paton,JR; Rocha,I; et al.(1998). Convergence properties of solitary tract neurons responsive to cardiac receptor stimulation in the anesthetized cat.J. Neurophysiol. 79,2374–2382.
[230] Sise,ME; Courtwright,AM; Channick,RN.(2013). Pulmonary hypertension in patients with chronic and end-stage kidney disease.Kidney Int,84,682–692.
[231] Skov, J; Persson, F; Frokior, J; Christiansen, JS. (2014). Tissue renin-angiotensin systems: a unifying hypothesis of metabolic disease. Front Endocrinol (Lausanne). 28,5–23.
[232] Sukhodub, A;Jovanović, S;Du,Q; et al. (2007). AMP-activated protein kinase mediates preconditioning in cardiomyocytes by regulating activity and trafficking of sarcolemmal ATP-sensitive K(+) channels. J. Cell. Physiol.210, 1,224–236.
[233] Suwa, M; Egashira, T; Nakano, H; et al. (2006). Metformin increases the PGC-1alpha protein and oxidative enzyme activities possibly via AMPK phosphorylation in skeletal muscle in vivo. J. Appl. Physiol. 101, 6, 685–692.
[234] Szabo, S; Glavin, BG. (1990). Hans Selye and the concept of biologic stress: ulcer pathogenesis as a historical paradigm. Annals of the New York Academy of Sciences. 597,14–16.
[235] Tipoe, GL;Lau, TY;Nanji, AA;Fung, ML. (2006). Expression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemia. Cardiovasc. Hematol. Agents Med. Chem.4, 3,199–218.
[236] Toney, GM; Pedrino, GR; Fink, GD; Osborn, JW. (2010). Does enhanced respiratory-sympathetic coupling contribute to peripheral neural mechanisms of angiotensin II-salt hypertension? Exp Physiol.95, 5,587-594.
[237] Touyz, RM. (2004). Reactive oxygen species and angiotensin II signaling in vascular cells – implications in cardiovascular disease. Braz. J. Med. Biol. Res. 37, 8,1263–1273.
[238] Ungvari, Z. (2013). Role of mitochondrial oxidative stress in hypertension. Am. J. of Physiol.: Heart and Circulatory Physiology. 305. H1417–H1427.
[239] Vallon, V. (2003). Tubuloglomerular feedback and the control of glomerular filtration rate. News Physiol. Sci.18,169-174.
[240] Vanhoutte, PM. (1989). Endothelium and control of vascular function. State of the art lecture. Hypertension. 13, 6 (Pt 2),658–667.
[241] Varela, L; Vozquez, MJ; Cordido, F; et al.(2011). Ghrelin and lipid metabolism: key partners in energy balance. J. Mol. Endocrinol. 46, 2,R43–63.
[242] Viollet, B; Andreelli, F; Jorgensen, SB. (2003). The AMP-activated protein kinase α2 catalytic subunit controls whole-body insulin sensitivity.J. Clin. Invest. 111, 1,91–98.
[243] Wang, W; Xiao, Z-D; Li, X; et al. (2015). AMPK modulates Hippo pathway activity to regulate energy homeostasis. Nat. Cell Biol.17,490–499.
[244] Wenger, HR. (2002). Cellular adaptation to hypoxia: О2-sensing protein hydroxylases, hypoxia-inducible transcription factors, and O2-regulated gene expression. FASEB J. 16,1151–1162.
[245] West, JB. (2006). Human responses to extreme altitude. Integ. Comp. Biol.46,25–34.
[246] Weston, AD;Hood, L. (2004). Systems biology, proteomics, and the future of health care: toward predictive, and personalized medicine. J Proteome Res. 3,179-196.
[247] Wilson,FH; Disse-Nicodeme,S;Choate,KA.(2001). Human hypertension caused by mutations in WNK kinases.Science.293,1107–1112.
[248] Winder, WW. (2001). Energy-sensing and signaling by AMP-activated protein kinase in skeletal muscle.J. Appl. Physiol. 91, 31017–31028.
[249] Winder,WW;Hardie,DG.(1996). Inactivation of acetyl-CoA carboxylase and activation of AMP-activated protein kinase in muscle during exercise.Am. J. Physiol.270, 2,E299–304.
[250] Winder,WW;Holmes, BF; Rubink, DS; et al. (2000). Activation of AMP-activated protein kinase increases mitochondrial enzymes in skeletal muscle.J. Appl. Physiol.88,6, 22192226.
[251] Wittenberg, JB; Wittenberg, BA. (2006). Myoglobin function reassessed.J. Exp. Biol.206, 2011-2020.
[252] Wolf, G. (2003). Adiponectin: a regulator of energy homeostasis. Nutr Rev. 61,290–292.
[253] Yagil, Y; Yagil, C. (2003). Hypothesis ACE2 Modulates Blood Pressure in the Mammalian Organism. Hypertension. 41,871–873.
[254] Xing, W; Zhang, T–C; Cao, D; et al. (2006). Cardiomyocyte hypertrophy. Circ Res. 98,1089–1097.
[255] Zheng,D; MacLean,PS;Pohnert,SC et al. (2001). Regulation of muscle GLUT-4 transcription by AMP-activated protein kinase.J. Appl. Physiol.91, 3,107-113.

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