title: Physiological role of inward rectifier K(+) channels in vascular smooth muscle cells.
abstract: K(+) channels play indispensable roles in establishing the membrane potential and in regulating the contractile tone of arterial smooth muscle cells. There are four types of K(+) channels in arterial smooth muscle: voltage-dependent K(+) (K(V)), Ca(2+)-dependent K(+) (BK(Ca)), ATP-dependent K(+) (K(ATP)), and inward rectifier K(+) (Kir2) channels. Comparatively few physiological studies have focused on Kir2 channels because they are present only in certain small-diameter cerebral and submucosal arterioles and in coronary arterial smooth muscle. Here, we review the characteristics and regulation of Kir2 channels in vascular arterial smooth muscle. Current knowledge of the predominant Kir2 channel subtype is Kir2.1, not Kir2.2 and 2.3. Electrophysiological measurements to determine the current-voltage relationship in arterial smooth muscle revealed inward rectification with a single-channel conductance of 21 pS. Kir2 channels were found to influence the resting tone of cerebral and coronary arteries based on the fact that barium (Ba(2+)) induces the constriction of these arteries at resting tone. Kir2 channels are also highly responsive to vasoconstrictors and vasodilators. For example, the vasoconstrictors endothelin-1 and angiotensin II inhibit Kir2 channel function by activating protein kinase C (PKC), and the vasodilator adenosine stimulates Kir2 channel function by increasing the level of cAMP, which subsequently activates protein kinase A (PKA). Certain pathological conditions such as left ventricular hypertrophy are associated with a decrease in Kir2 channel expression. Although our understanding of the physiological role and regulation of Kir2 channels is incomplete, it is believed that Kir2 channels contribute to the control of vascular tone in small-diameter vessels via various intracellular signalling pathways that regulate cell membrane potential.
authors.affiliation: National Research Laboratory for Mitochondrial Signalling, Department of Physiology and Biophysics, College of Medicine, Cardiovascular and Metabolic Disease Center, 613-735, South Korea.
authors.forename: Won Sun
authors.initials: WS
authors.lastname: Park
authors.forename: Jin
authors.initials: J
authors.lastname: Han
authors.forename: Yung E
authors.initials: YE
authors.lastname: Earm
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D001685:Biological Factors / Q000494:pharmacology; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024661:Potassium Channels, Inwardly Rectifying / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001685:Biological Factors; D026902:Potassium Channel Blockers; D024661:Potassium Channels, Inwardly Rectifying; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D009599:Nitroprusside