Mechanism for Aldosterone Potentiation of Angiotensin II–Stimulated Rat Arterial Smooth Muscle Cell Proliferation

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Abstract
After earlier studies in which secretion of aldosterone was demonstrated to be important in rat arterial smooth muscle cell (RASMC) proliferation in vitro, the presence of both 11β-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) gene transcription were shown in these cells by real-time reverse transcription–polymerase chain reaction (RT-PCR). In proliferation studies, tritiated thymidine incorporation into RASMC and RASMC cell number were both significantly increased by angiotensin II (Ang II) (10 −7 mol/L) compared with controls ( P −6 mol/L and 10 −5 mol/L, P −10 mol/L and 10 −8 mol/L ( P 1 ) receptor mRNA in RASMC treated by aldosterone (10 −8 mol/L) compared with untreated controls, and this was correlated with a small but significant increase in AT 1 receptor protein ( P 1 receptor.