Influence of Ca2+-activated K+ channels on rat renal arteriolar responses to depolarizing agonists

Abstract

Experiments were performed to evaluate the hypothesis that opening of Ca2+-activated K+ channels (BKCachannels) promotes juxtamedullary arteriolar dilation and curtails constrictor responses to depolarizing agonists. Under baseline conditions, afferent and efferent arteriolar lumen diameters averaged 23.4 ± 0.9 ( n = 36) and 22.8 ± 1.1 ( n= 13) μm, respectively. The synthetic BKCa channel opener NS-1619 evoked concentration-dependent afferent arteriolar dilation. BKCa channel blockade (1 mM tetraethylammonium; TEA) decreased afferent diameter by 15 ± 3% and prevented the dilator response to 30 μM NS-1619. ANG II (10 nM) decreased afferent arteriolar diameter by 44 ± 4%, a response that was reduced by 30% during NS-1619 treatment; however, TEA failed to alter afferent constrictor responses to either ANG II or arginine vasopressin. Neither NS-1619 nor TEA altered agonist-induced constriction of the efferent arteriole. Thus, although the BKCa channel agonist was able to curtail afferent (but not efferent) arteriolar constrictor responses to ANG II, BKCa channel blockade did not allow exaggerated agonist-induced arteriolar constriction. These observations suggest that the BKCa channels evident in afferent arteriolar smooth muscle do not provide a prominent physiological brake on agonist-induced constriction under our experimental conditions.