Abstract

Administration of nitroprusside (NP) subsequent to induction of contraction in canine renal arterial strips with norepinephrine (NE) yielded a dose-dependent relaxation and with 80 mM potassium (KCl) yielded only a small degree of relaxation. The effect elicited with 0.1 mM NP was significantly greater for responses obtained with NE (68%) than for those with KCl (12%). However, responses of muscles pretreated for 5 min with NP to NE to KCl were reduced by 23 and 31%, respectively. The relaxant effect of NP persisted after incubation with D-600 and/or 30 min of a 0-Ca plus 0.05 mM EDTA solution (low EDTA). Neither D-600 nor NP altered 45Ca uptake in the absence of stimulatory agents. Efflux of 45Ca (into low EDTA solution) was decreased by NP in a maintained manner but was unaffected by D-600. The NE-induced decrease in 45Ca efflux (but not that with KCl) was blocked by NP. However, changes in 45Ca efflux elicited with KCl or NE were not affected by D-600. In contrast to D-600 (which is known to inhibit increased Ca++ entry associated with some stimulatory conditions), NP acts in a manner that is relatively independent of uptake of extracellular Ca++. Thus, these two vasodilators appear to affect Ca++ utilization by different mechanisms and, presumably, in an additive manner.