The modulation of dopamine DA₁ receptors of cultured rat renal arterial smooth muscle cells by phorbol ester, glucocorticoid and sodium chloride was studied. The extent of [³H]Sch-23390 binding to phorbol ester-treated cell was increased without any change in the dissociation constant (K_d). At a concentration of 10nmol/l, the synthetic glucocorticoid dexamethasone increased maximum receptor binding (B_max) but had no effect on the K_d. 100mmol/l sodium chloride did not change B_max, but increased the K_d for DA₁ receptor. The production of cAMP in response to DA₁ receptor stimulation was enhanced without any change of the adenylate cyclase activity. The glucocorticoid effect on DA₁ of arterial smooth muscle cells became apparent after hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10μg/ml) and by the glucocorticoid receptor antagonist RU- 38486, indicating that the effect required protein synthesis through glucocorticoid receptors. Treatment of cells with 1μmol/l dexamethasone for 24h increased basal and DA₁-stimulated adenylate cyclase activity. Basal adenylate cyclase was decreased by sodium chloride in a dose-dependent manner. These results suggest differential control of DA₁ receptors on vascular smooth muscle cells by protein kinase C, glucocorticoid or sodium chloride. (Hypertens Res 1995; 18 Suppl. I: S29-S33)