ATP-sensitive potassium channels do not mediate vasorelaxation by acetylcholine or iloprost.

The influence of glibenclamide (GBC), a blocker of ATP-sensitive K+ channels, on relaxation caused by cromakalim (CKL), acetylcholine (ACh) and iloprost (ILO) was assessed in aortic rings (AR) with (E+) or without endothelium (E-) and in the perfused arterial mesentery (MES) of the rat. In AR preconstricted with noradrenaline, CKL (0.03-10 microM) and ILO (5.5 nM-1.6 microM) caused graded vasodilations which were not modified by endothelium removal. ACh (0.01-3 microM) only relaxed E+AR preparations. GBC (3 microM) markedly reduced responses to CKL in E+AR and E-AR, but did not affect vasodilation induced by ILO in E+AR or E-AR and by ACh in E+AR. In MES preconstricted with methoxamine, bolus injections of CKL (10 or 30 nmol) or ACh (0.03-1 nmol) caused graded reductions of perfusion pressure. Only the responses to CKL were significantly inhibited by GBC (10 microM). We conclude that AR and MES contain functional ATP-sensitive K+ channels, which, however, do not play a significant role in the endothelium-dependent vasodilation triggered by ACh or in the endothelium-independent relaxation induced by ILO.