Renal artery smooth muscle is refractory to contraction by angiotensin II

The vasomotor responses of vascular smooth muscle from different vascular smooth muscle beds have not been well characterized. The purpose of this study was to compare the contractile responses of vascular smooth muscle from two vascular beds, the peripheral vascular bed (carotid artery) and the visceral vascular bed (renal artery) to vasoactive agonists. Fresh bovine carotid and renal artery smooth muscle contractile responses to serotonin, endothelin, angiotensin, and dopamine were determined in a muscle bath. Serotonin and dopamine cause rapidly developing sustained contractions in carotid and renal artery smooth muscle. The magnitude of the contractile response to serotonin is significantly greater in carotid artery and the magnitude of the response to dopamine is similar between carotid and renal artery. Endothelin induces a slowly developing sustained contraction of greater magnitude in renal artery. Angiotensin II causes transient contractile responses in carotid artery but renal artery smooth muscle is uniquely refractory to angiotensin stimulation. This lack of response to angiotensin II may be protective in the role of the kidney in regulating blood pressure through the renin-angiotensin system. Differences in receptor expression or affinity or in postreceptor cellular signaling events may account for these differential responses to endogenous vasoactive agonists.