Kv channels contribute to nitric oxide- and atrial natriuretic peptide-induced relaxation of a rat conduit artery.

The role of K(+) channels in nitric oxide (NO)-induced vasorelaxation has been largely investigated in resistance vessels where iberiotoxin-sensitive MaxiK channels play a predominant role. However, the nature of the K(+) channel(s) involved in the relaxation triggered by NO-releasing compounds [nitroglycerin, NTG; NOR 3 [(+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide]] or atrial natriuretic peptide (ANP) in the conduit vessel aorta has remained elusive. We now demonstrate that, in rat aorta, the relaxation due to these vasorelaxants is not affected by the MaxiK channel blocker iberiotoxin (10(-7)-10(-6) M) as was the control vascular bed used (mesenteric artery).

Comparison of the inhibitory effects of docosahexaenoic acid (DHA) on U46619- and phenylephrine-induced contractions in guinea-pig aorta.

Inhibitory effects of docosahexaenoic acid (DHA) on the muscle contractions induced by U46619, a thromboxane A2 (TXA2) mimetic, and phenylephrine were compared in guinea-pig aorta. In de-endothelialized guinea-pig aortic ring preparations, DHA at 10 microM strongly inhibited a sustained contraction produced by U46619 (3-100 nM) whereas it did not exhibit an appreciable effect on phenylephrine (3-10 microM)-induced contraction. The present findings indicate that DHA inhibits more selectively TXA2 receptor (TP receptor)-mediated vascular contraction than alpha-adrenoceptor-mediated response.

Functional contribution of voltage-dependent and Ca2+ activated K+ (BK(Ca)) channels to the relaxation of guinea-pig aorta in response to natriuretic peptides.

We examined the relaxant effects of natriuretic peptide family on the isolated guinea-pig aorta to determine the receptor subtype which primarily mediates this vascular relaxation, with particular attention to the apparent contribution of voltage-dependent and Ca2+-activated KS (BK(Ca)) channels to the response. Three endogenous natriuretic peptide ligands (natriuretic peptide, ANP; brain natriuretic peptide, BNP; C-type natriuretic peptide, CNP) produced a concentration-dependent relaxation in de-endothelialized guinea-pig aorta pre-contracted by noradrenaline (NA), with a potency order of ANP > or = BNP >> CNP. Although the relaxations elicited by these three natriuretic peptide ligands were significantly diminished by iberiotoxin (IbTx, 10(-7) M), a selective BK(Ca) channel blocker, the inhibitory effect of IbTx was most pronounced for the CNP-induced relaxation; when estimated at 10(-7) M of each peptide, the apparent extent of BK(Ca) channel contribution to the total relaxant response was approximately 60% for CNP > approximately 20% for either ANP or BNP.