ISSN 2415-3060 (print), ISSN 2522-4972 (online)
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JMBS 2019, 4(2): 168–172
https://doi.org/10.26693/jmbs04.02.168
Clinical Medicine

Features of the Activity of Separate Components of the Renin-Angiotensin-Aldosterone System in Arterial Hypertension and Concomitant Obesity

Psaryova V. G.
Abstract

Renin-angiotensin-aldosterone system plays a key role in the blood pressure regulation. The study of the activity of such components of the renin-angiotensin-aldosterone system as renin and aldosterone, as well as their ratio in hypertensive patients, depending on the presence and absence of obesity, is an acute problem that requires further study. The purpose of the study was to evaluate the content of aldosterone, renin and their ratio in arterial hypertension and concomitant obesity. Material and methods. The study included 188 patients with arterial hypertension. The first group consisted of 107 patients with obesity of I-II degrees, the second group had 40 patients with overweight, the third group included 41 patients with normal body weight. The control group consisted of 25 practically healthy individuals. The concentrations of aldosterone and renin in serum were determined. At the renin levels <0.65 ng/ml/h, low-renin hypertension was established, and the renin levels ≥ 0.65 ng/ml/h, high-renin hypertension was established. Results and discussion. The patients with concomitant obesity had a significantly lower incidence of low-renin hypertension compared to hypertensive patients with normal body weight and overweight. Hypertensive patients with different body mass had significantly higher aldosterone and renin levels compared to the control group (in the absence of differences in aldosterone-renin ratio). At the same time hypertensive patients with different body mass were not significantly different as to the indicated parameters. Patients with low-renin and high-renin arterial hypertension did not differ significantly in age, sex, and anthropometric indices; however, low-renin hypertensive patients had a significantly lower aldosterone serum and a significantly higher aldosterone-renin ratio in comparison with high-renin hypertensive patients. Conclusions. In hypertensive patients, obesity is associated with a lower incidence of low-renin hypertension compared to patients with normal body weight and overweight. We found no differences in anthropometric indices in low-renin and high-renin arterial hypertension, in the presence of differences in levels of renin, aldosterone and aldosterone-renin ratio

Keywords: arterial hypertension, obesity, renin-angiotensin-aldosterone system, low-renin hypertension

Full text: PDF (Ukr) 196K

References
  1. Mulatero P, Verhovez A, Morello F, Veglio F. Diagnosis and treatment of low-renin hypertension. Clin Endocrinol. 2007; 67(3): 324–34. https://www.ncbi.nlm.nih.gov/pubmed/17573898. https://doi.org/10.1111/j.1365-2265.2007.02898.x
  2. Sagnella GA. Why is plasma renin activity lower in populations of african origin? J Hum Hypertens. 2001; 15(1): 17–25. https://www.ncbi.nlm.nih.gov/pubmed/11223998. https://doi.org/10.1038/sj.jhh.1001127
  3. Jose A, Crout JR, Kaplan NM. Suppressed plasma renin activity in essential hypertension. Roles of plasma volume, blood pressure, and sympathetic nervous systemy. Ann Intern Med. 1970; 72(1): 9–16. https://www.ncbi.nlm.nih.gov/pubmed/4312105. https://doi.org/10.7326/0003-4819-72-1-9
  4. Channick BJ, Adlin EV, Marks AD. Suppressed plasma renin activity in hypertension. Arch Intern Med. 1969; 123(2): 131–40. https://www.ncbi.nlm.nih.gov/pubmed/4303266. https://doi.org/10.1001/archinte.1969.00300120019003
  5. Conn JW. Evolution of primary aldosteronism as a highly specific clinical entity. J Am Med Assoc. 1960; 172: 1650–3. https://www.ncbi.nlm.nih.gov/pubmed/13811532. https://doi.org/10.1001/jama.1960.63020150008016
  6. Fisher ND, Hurwitz S, Ferri C, Jeunemaitre X, Hollenberg NK, Williams GH. Altered adrenal sensitivity to angiotensin II in low-renin essential hypertension. Hypertension. 1999; 34(3): 388–94. https://www.ncbi.nlm.nih.gov/pubmed/10489382. https://doi.org/10.1161/01.HYP.34.3.388
  7. Adlin EV, Marks AD, Channick BJ. The salivary sodium/potassium ratio in hypertension: Relation to race and plasma renin activity. Clin Exp Hypertens. 1982; 4(9-10): 1869–80. https://www.ncbi.nlm.nih.gov/pubmed/6754154
  8. Woods JW, Liddle GW, Michelakis AM, Brill AB. Effect of an adrenal inhibitor in hypertensive patients with suppressed renin. Arch Intern Med. 1969; 123(4): 366–70. https://www.ncbi.nlm.nih.gov/pubmed/5778117. https://doi.org/10.1001/archinte.1969.00300140012004
  9. Adlin EV, Marks AD, Channick BJ. Spironolactone and hydrochlorothiazide in essential hypertension. Blood pressure response and plasma renin activity. Arch Intern Med. 1972; 130(6): 855–8. https://www.ncbi.nlm.nih.gov/pubmed/5082465. https://doi.org/10.1001/archinte.1972.03650060047008
  10. Pizoń T, Rajzer M, Wojciechowska W, Wach-Pizoń M, Drożdż T, Wróbel K, et al. The relationship between plasma renin activity and serum lipid profiles in patients with primary arterial hypertension. Journal of the Renin-Angiotensin-Aldosterone System. 2018 Oct-Dec; 19(4): 1470320318810022. https://www.ncbi.nlm.nih.gov/pubmed/30404585. https://www.ncbi.nlm.nih.gov/pmc/articles/6240969. https://doi.org/10.1177/1470320318810022
  11. Mazzolai L, Hayoz D. The renin-angiotensin system and atherosclerosis. Curr Hypertens Rep. 2006; 8(1): 47–53. https://www.ncbi.nlm.nih.gov/pubmed/16600159. https://doi.org/10.1007/s11906-006-0040-9
  12. Fisher ND, Hurwitz S, Jeunemaitre X, Hopkins PN, Hollenberg NK, Williams GH. Familial aggregation of low-renin hypertension. Hypertension. 2002; 39: 914–8. https://doi.org/10.1161/01.HYP.0000013784.18175.51
  13. Kawarazaki W, Fujita T. Aberrant Rac1-mineralocorticoid receptor pathways in salt-sensitive hypertension. Clin Exp Pharmacol Physiol. 2013; 40(12): 929–36. https://www.ncbi.nlm.nih.gov/pubmed/24111570. https://doi.org/10.1111/1440-1681.12177
  14. Friso S, Carvajal CA, Fardella CE, Olivieri O. Epigenetics and arterial hypertension: The challenge of emerging evidence. Transl Res. 2015; 165(1): 154–65. https://www.ncbi.nlm.nih.gov/pubmed/25035152. https://doi.org/10.1016/j.trsl.2014.06.007
  15. Adlin EV, Braitman LE, Vasan RS. Bimodal aldosterone distribution in low-renin hypertension. Am J Hypertens. 2013; 26(9): 1076–85. https://www.ncbi.nlm.nih.gov/pubmed/23757402. https://www.ncbi.nlm.nih.gov/pmc/articles/3741228. https://doi.org/10.1093/ajh/hpt091
  16. Baudrand R, Vaidya A. The Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor. Int J Mol Sci. 2018; 19(2): 1–15. https://www.ncbi.nlm.nih.gov/pubmed/29439489. https://www.ncbi.nlm.nih.gov/pmc/articles/5855768. https://doi.org/10.3390/ijms19020546
  17. Funder JW, Reincke M. Aldosterone: A cardiovascular risk factor? Biochim Biophys Acta. 2010; 1802(12): 1188–92. https://www.ncbi.nlm.nih.gov/pubmed/20713154. https://doi.org/10.1016/j.bbadis.2010.08.005
  18. Pizoń T, Rajzer M, Kameczura T. The role of renin-angiotensin-aldosterone system in etiology and pathogenesis of arterial hypertension and its systemic complications – what remains from Laragh and Alderman idea? Arterial Hypertension. 2011; 15: 371–82.
  19. Ramalingam L, Menikdiwela K, LeMieux M, Dufour JM, Kaur G, Kalupahana N, et al. The renin angiotensin system, oxidative stress and mitochondrial function in obesity and insulin resistance. Biochim Biophys Acta Mol Basis Dis. 2017; 1863(5): 1106–14. https://www.ncbi.nlm.nih.gov/pubmed/27497523. https://doi.org/10.1016/j.bbadis.2016.07.019