BKCa channels in afferent arteriolar smooth muscle do not provide a prominent physiological brake on agonist-induced constriction under the studied experimental conditions.
Experiments were performed to evaluate the hypothesis that opening of Ca(2+)-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) microm, 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 microM 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.
Fallet et al. (2001) studied this question.