Vascular aldosterone. Biosynthesis and a link to angiotensin II-induced hypertrophy of vascular smooth muscle cells.

摘要: Mineralocorticoids have been suggested to act on blood vessels, leading increased vasoreactivity and peripheral resistance. However, the site of their production has so far believed be only adrenal cortex. Here, we show direct evidence that vascular cells per se are aldosteronogenic, possessing own system responds steroid. Using polymerase chain reaction after reverse transcription, CYP11B2 mRNA encoding key enzyme for biosynthesis aldosterone was detected in both endothelial smooth muscle cultivated from human pulmonary artery. The receptor (type 1 mineralocorticoid receptor) gene also found expressed and, a lesser extent, cells. expression stimulated by angiotensin II, effector peptide renin-angiotensin system. Furthermore, II-induced increase [3H]leucine incorporation significantly enhanced but inhibited ZK 91587, type antagonist. This may indicate participates hypertrophy present study therefore provides starting point novel understanding molecular basis remodeling hypertension.