Activation mechanisms of human renal artery: effects of KCl, norepinephrine and nitrendipine upon tension development and 45Ca influx.

The activation of human vascular smooth muscle by KCl-induced depolarization or norepinephrine and the inhibition produced by nitrendipine were studied in the isolated human renal artery. The contractile response of arterial rings to 80 mM KCl was abolished when extracellular Ca2+ was removed, and was inhibited by nitrendipine (IC50 = 10(-8) M). In contrast, a residual, transient contractile response to norepinephrine remained when extracellular Ca2+ was removed and the norepinephrine-induced contractions obtained in the presence of extracellular Ca2+ were not blocked by nitrendipine. KCl caused a stimulation of 45Ca influx which was completely prevented by 10(-6) M nitrendipine. Norepinephrine also caused a stimulation of 45Ca influx; however, the norepinephrine-induced 45Ca influx was not prevented by 10(-6) M nitrendipine. These findings are consistent with the concept that depolarization-induced activation of the human renal artery is primarily dependent upon a stimulation of Ca2+ influx; whereas activation by norepinephrine involves the release of intracellular Ca2+ in addition to the activation of a separate, receptor-operated Ca2+ influx pathway.