Chronic mineralocorticoid excess and cardiovascular remodeling.
Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.
Weber
K T
KT
Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, USA.
Sun
Y
Y
Campbell
S E
SE
Slight
S H
SH
Ganjam
V K
VK
Griffing
G T
GT
Swinfard
R W
RW
Diaz-Arias
A A
AA
D042842:11-beta-Hydroxysteroid Dehydrogenases; D000236:Adenoma / Q000473:pathology; D000310:Adrenal Gland Neoplasms / Q000473:pathology; D000311:Adrenal Glands / Q000201:enzymology*; D000312:Adrenal Hyperplasia, Congenital; D000328:Adult; D000450:Aldosterone / Q000097:blood* / Q000627:therapeutic use; D000818:Animals; D003900:Desoxycorticosterone / Q000097:blood*; D004719:Endomyocardial Fibrosis / Q000097:blood* / Q000201:enzymology; D005260:Female; D006801:Humans; D006913:Hydroxysteroid Dehydrogenases / Q000037:antagonists & inhibitors; D006929:Hyperaldosteronism / Q000188:drug therapy; D008901:Mineralocorticoids / Q000097:blood*; D051381:Rats; D013997:Time Factors
D008901:Mineralocorticoids; D003900:Desoxycorticosterone; D000450:Aldosterone; D006913:Hydroxysteroid Dehydrogenases; D042842:11-beta-Hydroxysteroid Dehydrogenases