Role of Ca2+-Activated K+ Channels on Adrenergic Responses of Human Saphenous Vein

Background: We studied the participation of K+ channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca2+ channels on modulation of adrenergic responses by K+ channels blockade. Methods: Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. Results: Iberiotoxin (10−7 mol/L), an inhibitor of large conductance Ca2+-activated K+ channels, and charybdotoxin (10−7 mol/L), an inhibitor of both large and intermediate conductance Ca2+-activated K+ channels, enhanced the contractions elicited by electrical field stimulation and produced a leftward shift of the concentration–response curve to norepinephrine. In contrast, the inhibitor of small conductance Ca2+-activated K+ channels apamin (10−6 mol/L) did not modify the contractile response to electrical field stimulation or norepinephrine. In the presence of the dihydropyridine Ca2+-channel blocker nifedipine (10−6 mol/L), iberiotoxin and charybdotoxin failed to enhance the contractile responses to electrical field stimulation and norepinephrine. Conclusions: The results suggest that large conductance Ca2+-activated K+ channels are activated by stimulation with norepinephrine to counteract the adrenergic-induced contractions of human saphenous vein. Thus, inhibition of these channels increases significantly the contraction, an effect that appears to be mediated by an increase in Ca2+ entry through L-type voltage-dependent Ca2+ channels. Am J Hypertens 2007;20:78–82 © 2007 American Journal of Hypertension, Ltd.