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C-type natriuretic peptide (CNP) hyperpolarizes and relaxes the smooth muscle of blood vessels. We investigated whether G-protein-gated inwardly-rectifying K + channels (GIRK) and large-conductance calcium-activated K + channels (BK Ca channels) were involved in CNP-evoked vasodilatation in human arteries. Isometric tension in human gastroepiploic arteries was measured using a wire myograph. Ion channel currents were recorded by the whole-cell patch-clamp technique. The concentration-dependent vasodilation induced by CNP was reduced significantly after inhibition of GIRK channels (by tertiapin-Q) or of BK Ca channel (by paxilline). Immunochemical experiments showed that GIRK3 and GIRK4 subunits were expressed in human arteries. CNP also strongly increased the current density of GIRK and BK Ca channels in human arterial smooth muscles. This suggested that the GIRK channel was functionally expressed in smooth muscle and vasodilation action was produced by CNP partly by opening the GIRK and BK Ca channels in the human artery.

international heart journal

G-Protein-gated Inwardly-Rectifying K&lt;sup&gt;+&lt;/sup&gt; Channels and Large-conductance Calcium-Activated K&lt;sup&gt;+&lt;/sup&gt; Channels Are Involved in C-Type Natriuretic Peptide-Mediated Vasodilation in Human Arteries