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

Experiments were performed to evaluate the hypothesis that opening of Ca²⁺-activated K⁺ channels (BK_Ca channels) 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 BK_Ca channel opener NS-1619 evoked concentration-dependent afferent arteriolar dilation. BK_Ca 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 BK_Ca channel agonist was able to curtail afferent (but not efferent) arteriolar constrictor responses to ANG II, BK_Ca channel blockade did not allow exaggerated agonist-induced arteriolar constriction. These observations suggest that the BK_Ca channels evident in afferent arteriolar smooth muscle do not provide a prominent physiological brake on agonist-induced constriction under our experimental conditions.