Autonomic regulation of delayed rectifier K+ current in mammalian heart involves G proteins

摘要: The role of adrenergic and cholinergic stimulation in regulating the delayed outward K+ current (IK) was examined by using isolated guinea pig ventricular myocytes. Isoproterenol (ISO) stimulated IK a reversible manner. Similar effects were seen directly stimulating adenylate cyclase with forskolin (FSK). responses to ISO FSK reversed concurrent application acetylcholine (ACh), but ACh alone did not affect IK. When nonhydrolyzable analogue guanosine 5'-triphosphate introduced intracellularly, presence extracellular ISO, irreversibly stimulated. In cells pretreated pertussis toxin response blocked. These results suggest that autonomic regulation is similar Ca2+ involves guanine nucleotide-binding proteins. This has important implications respect control action potential duration pacemaker activity heart.