We have investigated the effect of mineralocorticoids on β-adrenergic receptors in cultured arterial smooth muscle cells. Mineralocorticoid (aldosterone) treatment resulted in a significant increase in β-adrenergic receptors measured by [3H]dihydroalprenolol (DHA) binding. This effect required at least 20 hours of incubation with aldosterone and was completely blocked by cycloheximide (10 μg/ml), indicating protein synthesis was required for this response. Aldosterone at the concentration range of 10-8-10-6M increased [3H]DHA binding, but was ineffective at 10-9 M. Scatchard analysis of [3H]DHA binding revealed that the observed significant increase in binding was due to an increased number of binding sites (P < 0.05), and that the affinity was unchanged. The aldosterone (1 × 10-8 M) effect was completely blocked by the combination of RU 38486 (10-6M) and spironolactone (10-7 M), but not by the glucocorticoid antagonist RU 38486 alone. While basal c-AMP levels were not changed by aldosterone (10-6 M) treatment, the isoproterenol (10-6 M) stimulated level of c-AMP was significantly higher in cells treated with aldosterone (P < 0.05). We conclude that aldosterone, acting through the mineralocorticoid receptor, has a direct effect on arterial smooth muscle cells mediated through modulation of β-adrenergic receptors of these cells.
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