Мембранная теория патогенеза артериальной гипертензии: что мы знаем об этом полвека спустя?
https://doi.org/10.20538/1682-0363-2019-2-234-247
Аннотация
В обзоре кратко изложена история открытия в середине 1970-х гг. нарушений ионного транспорта через плазматические мембраны клеток при первичной артериальной гипертензии. Анализируется полувековая история исследований молекулярной природы ионных транспортеров, лежащих в основе этих нарушений, и опосредованных ими механизмов, приводящих к развитию гипертонической болезни и осложнений, обусловленных долгосрочным повышением артериального давления.
При поддержке: Работа была поддержана грантами Канадского института исследований в области здравоохранения (MOP-81392), Обществ по изучению сердца и почек Канады, Федераль- ной целевой программой 2009–2013 гг. «Научно-исследовательские кадры инновационной России», Российским фондом фундаментальных исследований (09-0073/04; 15-04-08832; 18-04-00063) и Российским научным фондом (14-15-00006 и 16-15-10026).
Об авторе
С. Н. Орлов
Московский государственный университет (МГУ) им. М.В. Ломоносова; Национальный исследовательский Томский государственный университет (НИ ТПУ); Сибирский государственный медицинский университет (СибГМУ)
Россия
Россия
Орлов Сергей Николаевич, д-р биол наук, профессор
119991, г. Москва, ул. Ленинские Горы, 1
634050, г. Томск, пр. Ленина, 36
634050, г. Томск, Московский тракт, 2
Список литературы
1. Орлов С.Н., Данилов В.С., Малков А.Ю., Ребров В.Г. Свободнорадикальное окисление липидов биологических мембран. V. Флуоресценция жирных кислот и фосфолипидов. Биофизика. 1975; 20 (2): 228–232.
2. Jones A.W. Altered ion transport in vascular smooth muscle from spontaneously hypertensive rats. Influence of Aldosterone, Norepinephrine and Angiotensin. 1973; 33:563–572.
3. Folkow B., Grimby G., Thulesius O. Adaptive structural changes of the vascular walls in hypertension and their relation to the control of the peripheral resistance. Acta Physiol. Scand. 1958; 44 (3–4): 255–272.
4. Постнов Ю.В., Орлов С.Н., Шевченко А.С. Изменение проницаемости мембраны эритроцитов у крыс со спонтанной гипертензией. Кардиология. 1975; 15 (1): 88–92.
5. Postnov Yu.V., Orlov S.N., Gulak P.V., Shevchenko A.S. Altered permeability of the erythrocyte membrane for sodium and potassium in spontaneously hypertensive rats. Pflugers Archiv. 1976; 365 (2–3): 257–263.
6. Ben-Ishay D., Aviram A., Viskoper R. Increased erythrocytes sodium efflux in genetic hypertensive rat of the Hebrew University strain. Experientia. 1975; 31 (6): 660–662.
7. Friedman S.M., Nakashima M., McIndoe R.A., Friedman C.L. Increased erythrocyte permeability to Li and Na in the spontaneously hypertensive rats. Experientia. 1976; 32(4): 476–478.
8. Friedman S.M., Nakashima M., McIndoe R.A. Glass electrode measurement of net Na+ and K+ fluxes in erythrocytes of the spontaneously hypertensive rats. Can. J. Physiol. Pharamacol. 1977; 55 (6): 1302–1310.
9. Postnov Yu.V., Orlov S.N., Shevchenko A.S., Adler A.M. Altered sodium permeability, calcium binding and NaK-ATPase activity in the red blood cell membrane in essential hypertension. Pflugers Archiv. 1977; 371 (3):263–269.
10. Orlov S.N., Riazhski G.G., Kravtsov G.M., Postnov Yu.V. Relation between abnormalities of erythrocyte membrane permeability for monovalent ions and intracellular distribution of calcium in primary hypertension. Kardiologiya. 1984; 24 (3): 87–95.
11. Postnov Yu.V., Orlov S.N. Cell membrane alteration as source of primary hypertension. J. Hypertens. 1984; 2 (1): 1–6.
12. Postnov Yu.V., Orlov S.N. Ion transport across plasma membrane in primary hypertension. Physiol. Rev. 1985; 65 (4): 904–945.
13. Orlov S.N., Adragna N., Adarichev V.A., Hamet P. Genetic and biochemical determinants of abnormal monovalent ion transport in primary hypertension. Am. J. Physiol. 1999; 276 (3): C511–C536. DOI: 10.1152/ajpcell.1999.276.3.C511.
14. Orlov S.N. Hypertension. In: Bernhardt I., Ellory J.C. (Eds). Red cell membrane transport in health and disease. Berlin, Springer, 2003; 587–602.
15. Постнов Ю.В., Орлов С.Н. Первичная гипертензия как патология клеточных мембран. М.: Медицина, 1987: 192. [Postnov Yu.V., Orlov S.N. Primary hypertension as the pathology of cell membranes. Moscow: Medicine Publ., 1987: 192 (in Russ.)].
16. Postnov Yu.V., Orlov S.N. Alteration of cell membrane in primary hypertension. In: Jenest J., Kuchel O., Hamet P., Cantin M. (Eds). Hypertension. Physiolpathology and treatment. New York: McGraw-Hill, 1983; 95–108.
17. Orlov S.N., Mongin A.A. Salt sensing mechanisms in blood pressure regulation and hypertension. Am. J. Physiol. Heart Circ. Physiol. 2007; 293 (4): H2039–H2053.
18. Schermann J., Briggs J.P. Tubuloglomerular feedback: mechanistic insights from gene-manipulated mice. Kidney Int. 2008; 74 (4): 418–426. DOI: 10.1038/ki.2008.145.
19. Noda M., Hiyama T.Y. Sodium sensing in the brain. Pfluger Arch. – Eur. J. Physiol. 2015; 467 (3): 465–474. DOI: 10.1007/s00424-014-1662-4.
20. Zicha J. Red cell ion transport abnormalities in experimental hypertension. Fundam. Clin. Pharmacol. 1993; 7(3–4): 129–141.
21. Zidek V., Vetter H., Zumkley H. Intracellular cation activities and concentrations in spontaneously hypertensive and normotensive rats. Clin. Sci. 1981; 61 (Suppl. l.): 41–43.
22. Orlov S.N., Pokudin N.I., Kotelevtsev Yu.V., Postnov Yu.V. Characteristics of the structural-functional organization of erythrocyte membrane in three strains of spontaneously hypertensive rats. Kardiologiya. 1988; 28 (1): 57–63.
23. Yokomatsu M., Fujito K., Numahata H., Koide H. Erythrocyte sodium ion transport system in DOC-salt, goldblatt and spontaneously hypertensive rats. Scand. J. Clin. Lab. Invest. 1992; 52 (6): 497–506.
24. Pravenec M., Klir P., Kren V., Zicha J., Kunes J. An analysis of spontaneous hypertension in spontaneously hypertensive rats by means of new recombinant inbred strains. J. Hypertens. 1989; 722 (7): 217–221.
25. Orlov S.N., Petrunyaka V.V., Kotelevtsev Yu.V., Postnov Yu.V., Kunes J., Zicha J. Cation transport and adenosine triphosphatase activity in rat erythrocytes: a comparison of spontaneously hypertensive rats with normotensive Brown Norway strain. J. Hypertens. 1991; 9 (10): 977–982.
26. Salvati P., Ferrario R.G., Parenti P., Bianchi G. Renal function of isolated perfused kidneys from hypertensive (MHS) and normotensive (MNS) rats of the Milan strain: role of calcium. J. Hypertens. 1987; 5 (1): 31–38.
27. Bianchi G., Ferrari P., Trizio P. et al. Red blood cell abnormalities and spontaneous hypertension in rats. A genetically determined link. Hypertension. 1985; 7 (3 Pt. 1): 319–325.
28. Rapp J.P., Dene H. Development and characterizatics of inbred strains of Dahl salt-sensitive and salt-resistant rats. Hypertension. 1985; 7 (3 Pt. 1): 340–349.
29. Zicha J., Duhm J. Kinetics of Na+ and K+ transport in red blood cells of Dahl rats. Effect of age and salt. Hypertension. 1990; 15 (6 Pt 1): 612–627.
30. McCormick C.P., Hennessy J.F., Rauch A.L., Buckalew V.M. Erythrocyte sodium concentration and 86Rb in weanling Dahl rats. Am. J. Hypertens. 1989; 2 (8): 604–609.
31. Akera T., Ng Y.-C., Shien I.-S., Bero E., Brody T.M., Braselton W.E. Effects of K+ on the interaction between cardiac glycosides and Na,K-ATPase. Eur. J. Pharmacol. 1985; 111 (2): 147–157.
32. Zicha J., Dobesova Z., Vokurkova M., Kunes J. Abnormal Na,K-pump activity cosegregates with blood pressure in Dahl SS/Jr x SR/jr F2 hybrids fed a high-salt diet since weaning (Abstract). Hypertension. 1999; 34: 708.
33. Orlov S.N., Akimova O.A., Hamet P. Cardiotonic steroids: novel mechanisms of Na+i-mediated and -independent signaling involved in the regulation of gene expression, proliferation and cell death. Curr. Hypertens. Rev. 2005; 1: 243–257.
34. Leenen F.H.H. The central role of the brain aldosterone-«ouabain» pathway in salt-sensitive hypertension. Biochim. Biophys. Acta. 2010; 1802 (12): 1132–1139. DOI: 10.1016/j.bbadis.2010.03.004.
35. Bagrov A.Y., Shapiro J.I., Fedorova O.V. Endogenous cardiotonic steroids: physiology, pharmacology, and novel therapeutic targets. Pharmacol. Rev. 2009; 61 (1): 9–38. DOI: 10.1124/pr.108.000711.
36. Blaustein M.P., Zhang J., Chen L., Hamilton B.P. How does salt retention raise blood pressure? Am. J. Physiol. Regul. Integr. Comp. Physiol. 2006; 290 (3): R514–R523.
37. Canessa M.L., Adragna N., Solomon H.S, Connoly T.M., Tosteson D.C. Increased sodium-lithium countertransport in red cells of patients with essential hypertension. New Engl. J. Med. 1980; 302 (14): 772–776.
38. Elmariah S., Gunn R.B. Kinetic evidence that the NaPO 4 cotransporter is the molecular mechanism for Na/Li exchange in human red blood cells. Am. J. Physiol. Cell Physiol. 2003; 285 (2): C446–C456.
39. Кольцова С.В., Акимова О.А, Котелевцев С.В., Хамет П., Орлов С.Н. Увеличенный Na+/Li+ противотранспорт в эритроцитах больных гипертонической болезнью не опосредован активацией Na+,Pi котранспорта. Артериальная гипертензия. 2010; 16 (4): 385–389.
40. Koltsova S.V., Trushina Yu.A., Akimova O.A., Hamet P., Orlov S.N. Molecular origin of Na+/Li+ exchanger: evidence against the involvement of major cloned erythrocyte transporters. Pathophysiology. 2011; 18 (3): 207–213. DOI: 10.1016/j.pathophys.2010.12.001.
41. Orlov S.N., Pokudin N.I., Ryazhskii G.G., Kotelevtsev Yu.V. Valinomycin induces Na+/H+ exchange in rat erythrocytes: peculiarities of the effect of protein kinase A and C. Biol. Membr. 1987; 4: 1036–1046.
42. Orlov S.N., Pokudin N.I., Kotelevtsev Yu.V., Gulak P.V. Volume-dependent regulation of ion transport and membrane phosphorylation in human and rat erythrocytes. J. Membrane Biol. 1989; 107: 105–117.
43. Wooden J.M., Finney G.L., Rynes E. et al. Comparative proteomics reveals deficiency of SLC9A1 (sodium/hydrogen exchanger NHE1) in b-adducin null red cells. Br. J. Haematol. 2011; 154: 492–501. DOI: 10.1111/j.1365-2141.2011.08612. x.
44. Geering K. Na,K-ATPase. Curr. Opin. Nephrol. Hypert. 1997; 6 (5): 434–439.
45. Orlov S.N., Postnov I.Yu., Pokudin N.I., Kukharenko V.Yu., Postnov Yu.V. Na+/H+ exchange and other ion transport systems in erythrocytes of essential hypertensives and spontaneously hypertensive rats. J. Hypertens. 1989; 7 (10): 781–788.
46. Pontremoli R., Spalvins A., Menachery A., Torielli L., Canessa M. Red cell sodium-proton exchange is increased in Dahl salt-sensitive hypertensive rats. Kidney Int. 1992; 42 (6): 1335–1362.
47. Orlov S.N., Kuznetsov S.R, Pokudin N.I., Tremblay J., Hamet P. Can we use erythrocytes for the study of the activity of ubiquitous Na+/H+ exchanger (NHE-1) in essential hypertension? Am. J. Hypertens. 1998; 11 (7): 774–783.
48. Niu J., Vaiskunaite R., Suzuki N. et al. Interaction of heterotrimeric G13 protein with an A-kinase-anchoring protein 110 (AKAP110) mediates cAMP-independent PKA activation. Curr. Biol. 2001; 11 (21): 1688–1690.
49. Orlov S.N., Adarichev V.A., Devlin A.M. et al. Increased Na+/H+ exchanger isoform 1 activity in spontaneously hypertensive rats: lack of mutations within coding region of NHE1. Biochim. Biophys. Acta. 2000; 1500 (2): 169–180.
50. Hediger M.A., Romero M.F., Peng J.-B., Rolfs A., Takanaga H., Bruford E.A. The ABCs of solute carriers: physiological, pathophysiological and therapeutic implications of human membrane transport protein. Pfluger. Arch. – Eur. J. Physiol. 2004; 447 (5): 465–468.
51. Gamba G. Molecular physiology and pathophysiology of electroneutral cation-chloride cotransporters. Physiol. Rev. 2005; 85 (2): 423–493.
52. Markadieu N., Delpire E. Physiology and pathophysiology of SLC12A1/2 transporters. Pfluger. Arch. – Eur. J. Physiol. 2014; 466 (1): 91–105. DOI: 10.1007/s00424-013-1370-5.
53. Garay R.P., Alda O. What can we learn from erythrocyte Na-K-Cl cotransporter NKCC1 in human hypertension. Pathophysiology. 2007; 14 (3–4): 167–170.
54. Orlov S.N., Tremblay J., Hamet P. NKCC1 and hypertension: a novel therapeutic target involved in regulation of vascular tone and renal function. Curr. Opin. Nephrol. Hypert. 2010; 19 (2): 163–168. DOI: 10.1097/MNH.0b013e3283360a46.
55. Orlov S.N., Koltsova S.V., Tremblay J., Baskakov M.B., Hamet P. NKCC1 and hypertension: role in the regulation of vascular smooth muscle contractions and myogenic tone. Ann. Med. 2012; 44: S111–S118. DOI:10.3109/07853890.2011.653395.
56. Kotelevtsev Yu.V., Orlov S.N., Pokudin N.I., Agnaev V.M., Postnov Yu.V. Genetic analysis of inheritance of Na+,K+ cotransport, calcium level in erythrocytes and blood pressure in F2 hybrids of spontaneously hypertensive and normotensive rats. Bull. Exp. Biol. Med. 1987; 103: 456–458.
57. Flagella M., Clarke L.L., Miller M.L. et al. Mice lacking the basolateral Na-K-2Cl cotransporter have impaired epithelial chloride secretion and are profoundly deaf. J. Biol. Chem. 1999; 274 (38): 26946–26955.
58. Meyer J.W., Flagella M., Sutliff R.L. et al. Decreased blood pressure and vascular smooth muscle tone in mice lacking basolateral Na+-K+-2Cl– cotransporter. Am. J. Physiol. 2002; 283 (5): H1846–H1855.
59. Wall S.M., Knepper M.A., Hassel K.A. et al. Hypotension in NKCC1 null mice: role of the kidney. Am. J. Physiol. Renal. Physiol. 2006; 290 (2): F409–F416.
60. Kim S.M., Eisner C., Faulhaber-Walter R. et al. Salt sensitivity of blood pressure in NKCC1-deficient mice. Am. J. Physiol. Renal. Physiol. 2008; 295 (4): F1230–F1238. DOI: 10.1152/ajprenal.90392.2008.
61. Garg P., Martin C., Elms S.C. et al. Effect of the Na-K-2Cl cotransporter NKCC1 on systematic blood pressure and smooth muscle tone. Am. J. Physiol. Heart Circ. Physiol. 2007; 292 (5): H2100–H2105.
62. Lominadze D., Joshua I.G., Schuschke D.A. Blood flow shear rates in arterioles of spontaneously hypertensive rats at early and established stages of hypertension. Clin. Exp. Hypertens. 2011; 23: 317–328.
63. Hussein G., Goto H., Oda S. et al. Antihypertensive potential and mechanism of action of astaxanthin: II Vascular reactivity and hemotheology in spontaneously hypertensive rats. Biol. Pharm. Bull. 2015; 28: 967–971.
64. Plotnikov M.B., Aliev O.I., Shamanaev A.Y. et al. Effects of pentoxifylline on hemodynamic, hemorheological, and microcirculatory parameters in young SHRs during arterial hypertension development. Clin. Exp. Hypertens. 2017; 39: 570–578.
65. Orlov S.N., Gulak P.V., Litvinov I.S., Postnov Yu.V. Evidence of altered structure of the erythrocyte membrane in spontaneously hypertensive rats. Clin. Sci. 1982; 63: 43–45.
66. Gulak P.V., Orlov S.N., Pokudin N.I. et al. Microcalorimetry and electrophoresis of the erythrocyte membrane of spontaneously hypertensive rats. J. Hypertens. 1984; 2 (1): 81–84.
67. Orlov S.N., Koltsova S.V., Kapilevich L.V., Gusakova S.V., Dulin N.O. NKCC1 and NKCC2: The pathogenetic role of cation-chloride cotransporters in hypertension. Genes & Diseases. 2015; 2 (2): 186–196.
68. Chipperfield A.R., Harper A.A. Chloride in smooth muscle. Prog. Biophys. Mol. Biol. 2001; 74 (3–5): 175–221.
69. Davis J.P.L., Chipperfield A.R., Harper A.A. Accumulation of intracellular chloride by (Na-K-Cl) cotransport in rat arterial smooth muscle is enhanced in deoxycorticosterone acetate (DOCA) / salt hypertension. J. Mol. Cell Cardiol. 1993; 25 (3): 233–237.
70. Anfinogenova Y.J., Baskakov M.B., Kovalev I.V., Kilin A.A., Dulin N.O., Orlov S.N. Cell-volume-dependent vascular smooth muscle contraction: role of Na+-K+-2Cl–cotransport, intracellular Cl– and L-type Ca2+ channels. Pflugers. Arch. – Eur. J. Physiol. 2004; 449 (1): 42–55.
71. Barthelmebs M., Stephan D., Fontaine C., Grima M., Imbs J.L. Vascular effects of loop diuretics: an in vivo and in vitro study in the rat. Naunyn-Schmiedebergs Arch. Pharmacol. 1994; 349 (2): 209–216.
72. Lavallee S.L., Iwamoto L.M., Claybaugh J.R., Dressel M.V., Sato A.K., Nakamura K.T. Furosemide-induced airway relaxation in guinea pigs: relation to Na-K-2Cl cotransporet function. Am. J. Physiol. 1997; 273: L211–L216.
73. Tian R., Aalkjaer C., Andreasen F. Mechanisms behind the relaxing effect of furosemide on the isolated rabbit ear artery. Pharmacol. Toxicol. 1990; 67 (5): 406–410.
74. Kovalev I.V., Baskakov M.B., Anfinogenova Y.J. et al. Effect of Na+-K+-2Cl– cotransport inhibitor bumetanide on electrical and contractile activity of smooth muscle cells in guinea pig ureter. Bull. Exp. Biol. Med. 2003; 136 (8): 145–149.
75. Kovalev I.V., Baskakov M.B., Medvedev M.A. et al. Na+-K+-2Cl– cotransport and chloride permeability of the cell membrane in mezaton and histamine regulation of electrical and contractile activity in smooth muscle cells from the guinea pig ureter. Russian Physiol. J. 2008; 93 (3): 306–317.
76. Stanke F., Devillier P., Breant D. et al. Furosemide inhibits angiotensin II-induced contraction on human vascular smooth muscle. Br. J. Clin. Pharmacol. 1998; 46 (6):571–575.
77. Stanke-Labesque F., Craciwski J.L., Bedouch P. et al. Furosemide inhibits thrombaxane A2-induced contraction in isolated human internal artery and saphenous vein. J. Cardiovasc Pharmacol. 2000; 35: 531–537.
78. Wang X., Breaks J., Loutzenhiser K., Loutzenhiser R. Effects of inhibition of the Na+-K+-2Cl– cotransporter on myogenic and angiotensin II responses of the rat afferent arteriole. Am. J. Physiol. Renal. Physiol. 2007; 292:F999–F1006.
79. Mozhayeva M.G., Bagrov Y.Y. The inhibitory effects of furosemide on Ca2+ influx pathways associated with oxytocin-induced contractions of rat myometrium. Gen. Physiol. Biophys. 1995; 14 (5): 427–436.
80. Mozhayeva M.G., Bagrov Y.Y., Ostretsova I.B., Gillespie J.I. The effect of furosemide on oxytocin-induced contractions of the rat myometrium. Exp. Physiol. 1994; 79 (5): 661–667.
81. Akar F., Skinner E., Klein J.D., Jena M., Paul R.J., O’Neill W.C. Vasoconstrictors and nitrovasodilators reciprocally regulate the Na+-K+-2Cl– cotransporter in rat aorta. Am. J. Physiol. 1999; 276 (6): C1383–C1390. DOI: 10.1152/ajpcell.1999.276.6.C1383.
82. Palacios J., Espinoza F., Munita C., Cifuentes F., Michea L. Na+-K+-2Cl–cotransporter is implicated in gender differences in the response of the rat aorta to phenylephrine. Br. J. Pharmacol. 2006; 148 (7): 964–972.
83. Koltsova S.V., Maximov G.V., Kotelevtsev S.V. et al. Myogenic tome in mouse mesenteric arteries: evidence for P2Y receptor-mediated, Na+-K+-2Cl¯ cotransport-dependent signaling. Purinergic Signaling. 2009; 5 (3): 343–349. DOI: 10.1007/s11302-009-9160-4.
84. Koltsova S.V., Luneva O.G., Lavoie J.L. et al. HCO3-dependent impact of Na+-K+-2Cl– cotransport in vascular smooth muscle excitation-contraction coupling. Cell Physiol. Biochem. 2009; 23 (4–6): 407–414. DOI:10.1159/000218187.
85. Орлов С.Н., Кольцова С.В., Капилевич Л.В., Дулин Н.О., Гусакова С.В. Котранспортеры катионов и хлора: регуляция, физиологическое значение и роль в патогенезе артериальной гипертензии. Успехи биологической химии. 2014; 54: 267–298.
86. Korpi E.R., Luddens H. Furosemide interactions with brain GABAA receptors. Br. J. Pharmacol. 1997; 120: 741–748.
87. Lee H.-A., Baek I., Seok Y.M. et al. Promoter hypomethylation upregulates Na+-K+-2Cl– cotransporyter 1 in spontaneously hypertensive rats. Biochem. Biophys. Res. Commun. 2010; 396 (2): 252–257. DOI: 10.1016/j.bbrc.2010.04.074.
88. Cho H.-M., Lee H.-A., Kim H.Y., Han H.S., Kim I.K. Expression of Na+-K+-2Cl– cotransporter is epigenetically regulated during postnatal development of hypertension. Am. J. Hypertens. 2011; 24 (12): 1286–1293. DOI:10.1038/ajh.2011.136.
89. Orlov S.N., Resink T.J., Bernhardt J., Buhler F.R. Na+-K+ pump and Na+-K+ co-transport in cultured vascular smooth muscle cells from spontaneously hypertensive rats: baseline activity and regulation. J. Hypertens. 1992; 10 (8): 733–740.
90. Jiang G., Cobbs S., Klein J.D., O’Neill W.C. Aldosterone regulates the Na-K-Cl cotransporter in vascular smooth muscle. Hypertension. 2003; 41 (5): 1131–1135.
91. Orlov S.N., Li J.-M., Tremblay J., Hamet P. Genes of intracellular calcium metabolism and blood pressure control in primary hypertension. Seminar in Nephrology. 1995; 15 (6): 569–592.
92. Hamet P., Orlov S.N., Tremblay J. Intracellular signalling mechanisms in hypertension. In: Laragh J.H., Brenner B.M. (Eds). Hypertension: pathophysiology, diagnosis, and treatment. New York, Raven Press, 1995: 575–608.
93. Kahle K.T., Rinehart J., Giebisch G., Gamba G., Hebert S.C., Lifton R.P. A novel protein kinase signaling pathway essential for blood pressure regulation in humans. Trends Endocrin. Metab. 2008; 19 (3): 91–95. DOI: 10.1016/j.tem.2008.01.00.1
94. Susa K., Kita S., Iwamoto T. et al. Effect of heterozygous deletion of WNK1 on the WNK-OSR1/SPAK-NCC/NKCC1/NKCC2 signal cascade in the kidney and blood vessels. Clin. Exp. Nephrol. 2012; 16 (4): 530–538.
95. Rafigi F.H., Zuber A.M., Glover M. et al. Role of the WNK-activated SPAK kinase in regulating blood pressure. EMBO Mol. Med. 2010; 2 (2): 63–75. DOI: 10.1002/emmm.200900058.
96. Bergaya S., Faure S., Baudrie V. et al. WNK1 regulates vasoconstriction and blood pressure response to a1-adrenergic stimulation in mice. Hypertension. 2011; 58 (3): 439–445. DOI: 10.1161/HYPERTENSIONAHA.111.172429.
97. Yang S.-S., Lo Y.-F., Wu C.-C. et al. SPAK-knockout mice manifest Gitelman syndrome and impaired vasoconstriction. J. Am. Soc. Nephrol. 2010; 21 (11): 1868–1877. DOI: 10.1681/ASN.2009121295.
98. Ye Z.-Y., Li D.-P., Byun H.S., Li L., Pan H.-L. NKCC1 upregulation disrupts chloride homeostasis in the hypothalamus and increases neuronal-sympathetic drive in hypertension. J. Neurosci. 2012; 32 (25): 8560–8568. DOI: 10.1523/JNEUROSCI.1346-12.2012.
99. Janardhan V., Qureshi A.I. Mechanisms of ischemic brain injury. Curr. Cardiol. Rep. 2004; 6 (2): 117–123.
100. O’Shaughnessy K.M., Karet F.E. Salt handling in hypertension. Annu. Rev. Nutr. 2006; 26: 343–365.
101. Koltsova S.V., Kotelevtsev S.V., Tremblay J., Hamet P., Orlov S.N. Excitation-contraction coupling in resistant mesenteric arteries: evidence for NKCC1-mediated pathway. Biochem. Biophys. Res. Commun. 2009; 379 (4): 1080–1083. DOI: 10.1016/j.bbrc.2009.01.018.
102. Folkow B. Cardiovascular «remodeling» in rat and human: time axis, extent, and in vivo relevance. Physiology. 2010; 25 (5): 264–265. DOI: 10.1152/physiol.00015.2010.
103. Loutzenhiser R., Griffin K., Williamson G., Bidani A. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the unerlying mechanisms. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2006; 290 (5): R1153–R1167.
104. Liu Y., Gutterman D.D. Vascular control in humans: focus on the coronary micocirculation. Basic Res. Cardiol. 2009; 104 (3): 211–227. DOI: 10.1007/s00395-009-0775-y.
105. Bidani A., Griffin K.A., Williamson G., Wang X., Loutzenhiser R. Protective importance of the myogenic response in the renal circulation. Hypertension. 2009; 54 (2): 393–398. DOI: 10.1161/HYPERTENSIONAHA.109.133777.
106. Orlov S.N. Decreased Na+,K+,Cl– cotransport and salt retention in blacks: a provocative hypothesis. J. Hypertens. 2005; 23 (10): 1929–1930.
107. Boone C.A. End-stage renal disease in African-Americans. Nephrol. Nurs. J. 2000; 27 (6): 597–600.
108. Kotchen T.A., Piering A.W., Cowley A.W. et al. Glomerular hyperfiltration in hypertensive African Americans. Hypertension. 2000; 35 (3): 822–826.
109. Orlov S.N., Gossard F., Pausova Z. et al. Decreased NKCC1 activity in erythrocytes from African-Americans with hypertension and dyslipidemia. Am. J. Hypertens 2010; 23 (3): 321–326. DOI: 10.1038/ajh.2009.249.
110. Hannaert P., Alvarez-Guerra M., Pirot D., Nazaret C., Garay R.P. Rat NKCC2/NKCC1 cotransport selectivity for loop diuretic drugs. Naunyn-Schmiedebergs Arch. Pharmacol. 2002; 365 (3): 193–199.
111. Delpire E., Lu J., England R., Dull C., Thorne T. Deafness and imbalance associated with inactivation of the secretory Na-K-2Cl co-transporter. Nature Genetics. 1999; 22 (2): 192–195.
112. Lang F., Vallon V., Knipper M., Wangemann P. Functional significance of channels and transporters expressed in the inner ear and kidney. Am. J. Physiol. Cell Physiol. 2007; 293 (4): C1187–C1208.
Рецензия
Для цитирования:
Орлов С.Н. Мембранная теория патогенеза артериальной гипертензии: что мы знаем об этом полвека спустя? Бюллетень сибирской медицины. 2019;18(2):234-247. https://doi.org/10.20538/1682-0363-2019-2-234-247
For citation:
Orlov S.N. Membrane theory of the pathogenesis of arterial hypertension: What do we know about this, half a century later? Bulletin of Siberian Medicine. 2019;18(2):234-247. https://doi.org/10.20538/1682-0363-2019-2-234-247
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