Involvement of Potassium Channels in the Acetylcholine-Induced Dilatations of the Rat Renal Vasculature
We examined the mechanism of acetylcholine (ACh)-induced dilatations in rat isolated kidneys. Wistar rats of both sexes were anesthetized with ether and kidneys were isolated and perfused via renal artery. Optimal perfusion pressure was found to be 50–75 mmHg and optimal flow rate was 6–8 ml/min. In control experiments Ach caused concentration-dependent dilatations and the maximum dilatation was 65.38 ± 4.05% of maximum phenylephrine constriction. Atropine (10−6M), hexametonium (10−4M), indomethacin (10−5M), and 4-aminopyridine (10−3M) attenuated the ACh-induced dilatations significantly (p<0.05, n=6, ANOVA). Tetraethylammonium (10−3), ouabain (10−6), and quinacrine (3*10−6M) did not change the dilatations. On the other hand, methylene blue (10−5M), tetrodotoxin (10−6M) and capsaicin (10−6M) caused significant inhibition of ACh-induced dilatations (p<0.01, n=6, ANOVA). These results suggest that ACh-induced dilatations may occur vial the factors released from endothelium and presynaptic nerves and act through soluble guanylate cyclase and both ATP-sensitive and calcium-dependent potassium channels.