INVERSION OF THE CONCEPT ABOUT BIOLOGICAL ROLE OF RENIN → ANGIOTENSIN-II → ALDOSTERONE SYSTEM AND FUNCTION OF ARTERIAL BLOOD PRESSURE AS A METABOLISM REGULATOR

The phylogenetic theory of general pathology postulates an inversion of the concept about the role of arterial blood pressure (AP) in physiology and pathology. Activation of the synthesis of the renin → angiotensin-II (AG-II) system components by nephron and increase in aldosterone secretion are not aimed at elevating AP., but at maintaining the volume of extracellular medium, part of the Third Word Ocean where all cells still live as millions of years ago. Phylogenetically early internal organs cannot regulate the effects of phylogenetically late AP., a physical factor of metabolism. AP is not increased by kidneys, but by the vasomotor center that attempts to reanimate nephronal function, the biological function of endoecology and biological reaction of excretion by increasing AP in proximal and, subsequently, hydrodynamic pressure in the distal region of arterial bed. In addition to the major role in the realization of the biological function of locomotion, AP is a physical factor involved in compensation of impaired functions of homeostasis, trophology, endoecology and adaptation. Levels of metabolism regulation have developed during phylogenesis. Biochemical reactions are specifically regulated at the autocrine level. In paracrine-regulated cell communities of distal arterial bed, metabolism is regulated by millions of local peristaltic pumps by compensating the biological reactions of endothelium-dependent vasodilation, microcirculation, effects of humoral messengers and hormones. In vivo metabolism is regulated nonspecifically from the vasomotor center level by a physical factor (AP) by sympathetic activation of the heart; AP in proximal and distal regions of arterial bed overcomes peripheral resistance and «squeezes through» the arterioles where microcirculation is impaired. AG-II acts as a vasoconstrictor only in the distal arterial bed. In essential (metabolic) arterial hypertension, paracrine cell communities of nephrons and kidneys are involved in realization of pathologic compensation in the second turn and often “suffer being innocent” , similar to other “target” organs”, such as brain, lungs and heart.

филогенез, межклеточная среда, ангиотензин-II, альдостерон, микроциркуляция, артериальное давление, phylogenesis, extracellular medium, angiotensin-II, aldosterone, microcirculation, arterial pressure

1. Титов В.Н. Филогенетическая теория общей патологии. Патогенез медицинских пандемий. Артериальная гипертония. М. ИНФРА-М. 2014. 212 с.

2. Титов В.Н. Через полтора века после гуморальной теории К. Рокитанского и целлюлярной теории Р. Вирхова -филогенетическая теория патологии. Нефрология. 2012; 16(4): 11 - 27.

3. Titov V.N. Statins-induced inhibition of cholesterol synthesis in liver and very low density lipoproteins. Statins, fatty acids and insulin resistance. Pathogenesis. 2013. 11(1): 18 - 26.

4. Ощепкова Е.В., Дмитриев В.А., Титов В.Н. и др. Показатели неспецифичного воспаления у больных гипертонической болезнью. Тер. архив. 2007. 12; 18 - 25.

5. Gu Q., Burt V.L., Dillon C.F., Yoon S. Trends in antihypertensive medication use and blood pressure control among United States adults with hypertension: the National Health And Nutrition Examination Survey, 2001 to 2010. Circulation. 2012; 126: 2105 - 2114.

6. Hanninen M., Niiranen T.J., Puukka P.J., Jula F.V. Metabolic risk factors and masked hypertension in the general population: the Finn-Home study. J. Human Hypertens. 2014; 28: 421 - 426.

7. Громова О.А. Магнезиальная терапия в поликлинической практике. Consilium Мedicum. 2006; 4(1): 26 - 35.

8. Кондаков А.В., Кобылянский А.Г., Тищенков В.Г., Титов В.Н. Функциональный тест клинической диагностической лаборатории: определение дефицита магния в тесте с нагрузкой. Клин. лаб. диагностика. 2012; 6: 16 - 20.

9. Abramochkin D.V., Vornanen M. Inhibition of the cardiac ATPdependent potassium current by KB-R7943. Comp. Biochem. Physiol. A Mol. Integr. Physiol. 2014; 175: 38 - 45.

10. Grgic I., Kaistha B.P., Hoyer J., Kohler R. Endothelial Cat-activated K+ channels in normal and impaired EDHF-dilator responses--relevance to cardiovascular pathologies and drug discovery. Br. J. Pharmacol. 2009; 157: 509 - 526.

11. Lindner G., Exadaktylos A.K. Disorders of serum sodium in emergency patients : salt in the soup of emergency medicine. Anaesthesist. 2013; 62(4): 296 - 303.

12. Zhuo J.L., Ferrao F.M., Zheng Y., Li X.C. New frontiers in the intrarenal renin-angiotensin system: a critical review of classical and new paradigms. Front. Endocrinol. 2013; 4: 166 - 175.

13. Титов В.Н. Биологические функции (экзотрофия, воспаление, трансцитоз) и патогенез артериальной гипертонии. М. - Тверь: ООО «Издательство Триада». 2009. 440 с.

14. Bassi E., Park M., Azevedo L. Therapeutic strategies for highdose vasopressor-dependent shock. Crit. Care. Res. Pract. 2013; 2013: 654708.

15. Шхвацебая И.К., Чихладзе Н. Первичный альдостеронизм. М. Медицина. 1984. 136 с.

16. Song A.L., Zeng Z.P., Tong A.L. et al. Differences of blood plasma renin activity, angiotensin II and aldosterone levels in essential or secondary hypertension. Zhonghua. Nei. Ke. Za. Zhi. 2012; 51(4): 294 - 298.

17. Алан Г.Б. Ву. Клиническое руководство Тица по лабораторным тестам. М. Лабора. 2013. 1280 с.

18. Moon J.Y. Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension. Electrolyte Blood Press. 2013; 11: 41 - 45.

19. Титов В.Н., Дмитриев В.А., Ощепкова Е.В. Мочевая кислота. Биология, биохимия и диагностическое значение в роли интегрального теста. Клин. лаб. диагностика. 2009; 1: 23 - 34.

20. Smink P.A., Bakker S.J., Laverman G.D. et al. An initial reduction in serum uric acid during angiotensin receptor blocker treatment is associated with cardiovascular protection: a post-hoc analysis of the RENAAL and IDNT trials. J. Hypertens. 2012; 30(5): 1022 - 1028.

21. Nakamura M., Sasai N., Hisatome I., Ichida K. Effects of irbesartan on serum uric acid levels in patients with hypertension and diabetes. Clin. Pharmacol. 2014; 6: 79 - 86.

22. Savoia C., Volpe M., Alonzo A. et al. Natriuretic peptides and cardiovascular damage in the metabolic syndrome: molecular mechanisms and clinical implications. Clin. Sci. 2009; 118(4): 231 - 240.

23. Sparks M.A., Crowley S.D., Gurley S.B. et al. Classical renin-angiotensin system in kidney physiology. Compr. Physiol. 2014; 4(3): 1201 - 1228.

24. Cowen L.E., Hodak S.P., Verbalis J.G. Age-associated abnormalities of water homeostasis. Endocrinol. Metab. Clin. North. Am. 2013; 42(2): 349 - 370.

25. Ring R.H. The central vasopressinergic system: examining the opportunities for psychiatric drug development. Curr. Tharm. Des. 2005; 11: 205 - 225.

26. Hauck C., Frishman W.H. Systemic hypertension: the roles of salt, vascular Na+/K+ ATPase and the endogenous glycosides, ouabain and marinobufagenin. Cardiol. Rev. 2012; 20(3): 130 - 138.

27. Иорданский Н.Н. Развитие жизни на земле. Изд-во Просвещение. 1981. М. 191 с.

28. Мелькумянц А.М., Капелько В.И. Руководство по кардиологии под ред. И.Е. Чазовой. Изд. дом «Практика». 2014.

29. Реутов В.П., Сорокина Е.Г., Швалев В.Н. Возможная роль диоксида азота, образующегося в местах бифуркации

30. сосудов, в процессах их повреждения при геморрагических инсультах и образовании атеросклеротических бляшек. Успехи физиол. наук. 2012; 43(4): 73 - 93.

31. Yugandhar V.G., Clark M.A. Angiotensin III: a physiological relevant peptide of the renin angiotensin system. Peptides. 2013; 46: 26 - 32.

32. Dmitriev L.F. Biological membranes are nanostructures that require internal heat and imaginary temperature as new, unique physiological parameters related to biological catalysts. Cell. Biochem. Biophys. 2011; 59(3): 133 - 146.

33. Reinders I., Virtanen J.K., Brouwer I.A., Tuomainen T.P. Association of serum n-3 polyunsaturated fatty acids with C-reactive protein in men. Eur. J. Clin. Nutr. 2012; 66: 736 -741.

34. Пшенникова М.Г. Роль генетических особенностей организма в устойчивости к повреждающим воздействиям и в защитных эффектах адаптации. Патол. физиол. и эксп. терапия. 2011; 4: 7 - 16.

35. Швалев В.Н., Реутов В.П., Рогоза А.Н. и др. Развитие современных представлений нейрогенной природе кардиологических заболеваний. Тихоокеанский мед. жунал. 2014; 1: 10 - 14.

36. Kohler R., Ruth P. Endothelial dysfunction and blood pressure alterations in K+-channel transgenic mice. Pflugers. Arch. 2010; 459(6): 969 - 976.

37. Титов В.Н., Ощепкова Е.В., Дмитриев В.А. С-реактивный белок, микроальбуминурия, эндогенное воспаление и артериальная гипертония. Москва. 2009. 375 с.

38. Hage F.G. C-reactive protein and hypertension. J. Hum. Hypertens. 2014; 28: 410 - 415.

39. Чазов Е.И. Дизрегуляция и гиперреактивность организма как факторы формирования болезни. Кардиол. вестник. 2006; 1(3): 5 - 9.

40. Gironacci M.M., Cerniello F.M., Longo Carbajosa N.A. et al. Protective axis of the renin-angiotensin system in the brain. Clin. Sci. 2014; 127(5): 295 - 306.

41. Dahlof B. Effect of angiotensin II blockade on cardiac hupertrophy and remodeling: a review. J. Hum. Hpertens. 1995; 5: S37 - S44.

42. Barst R.J. A review of pulmonary arterial hypertension: role of ambrisentan. Vasc. Health. Risk. Management. 2007; 3(1):11 - 22.

43. Гришин О.В. Адаптивный гипометаболизм у человека. Вестник РАМН. 2011; 8: 33 - 41.

44. Чазова И.Е., Ратова Л.Г. Гипертоническая болезнь. 4. Гипертоническая болезнь и вторичные артериальные гипертонии. М.: Медиа медика. 2011. 54 -98.

45. Pao A.C. Update on the Guytonian view of hypertension. Curr. Opin Nephrol. 2014; 23(4): 391 - 398.

46. Derhaschnig U., Testori C., Riedmueler E. et al. Decreased renal function in hypertensive emergencies. J. Human. Hupertens. 2014; 28: 427 - 431.