Figure 3.
Contribution of BKCa in NO-induced relaxation. (A) In rat aorta, acetylcholine-induced endothelium-dependent relaxation is blocked by the guanylate cyclase inhibitor ODQ and partially inhibited by IbTX, indicating that endogeneous NO induces cGMP-dependent relaxation and that the activation of BKCa contributes to the mechanism of this relaxation. (B) In rat aorta, a NO donor, DEA-NONOate, also produces cGMP-dependent relaxations, which involves the activation of BKCa. (C) In rat aorta, a NO-independent activator of soluble guanylate cyclase, BAY 58-2667, produces a slowly developing relaxation, which involves the activation of BKCa. (D) In freshly isolated smooth muscle cells from rabbit carotid artery SIN-1, a NO donor increases the amplitude of the BKCa current elicited by a step depolarization (whole cell configuration of the patch-clamp technique, left panel). The effect of SIN-1 is associated with an increase in the open probability of the channel (cell-attached configuration of the patch-clamp technique, right panel; modified from Quignard et al. (Eur J Pharmacol, 2000a). BKCa, calcium-activated potassium channels of large conductance; cGMP, cyclic-guanosine monophosphate; IbTX, iberiotoxin; NO, nitric oxide; sGC, soluble guanylate cyclase.