Dopamine stimulates cAMP production in canine afferent arterioles via DA1 receptors.

Dopamine increases renal blood flow and dilates isolated afferent and efferent arterioles preconstricted with norepinephrine via dopamine 1 (DA1) receptors. DA1-receptor stimulation also results in dopamine-induced elevation of adenosine 3'5'-cyclic monophosphate (cAMP) in dog and rat renal arteries. The present study was undertaken to determine the effects of dopamine on cAMP accumulation in isolated canine superficial cortical afferent arterioles. The effect of Sch 23390, a specific DA1-receptor antagonist, on dopamine-stimulated cAMP accumulation was also examined. Forskolin (10(-5) M), a potent stimulator of adenylate cyclase, produced a greater than 11-fold increase in cAMP production compared with control. Dopamine produced a dose-dependent increase in cAMP accumulation in afferent arterioles at concentrations of 10(-4) M and 10(-6) M, Sch 23390 (2 x 10(-4) M) abolished dopamine (10(-4) M)-stimulated cAMP accumulation in afferent arterioles. The dopamine-induced increase in arteriolar cAMP accumulation was unaffected by propranolol (10(-4) M). Our results suggest that dopamine increases cAMP production in afferent arterioles via the DA1 receptor. Increased cAMP production may be responsible for dopamine-induced vasodilation in the afferent arteriole.