REGULATION OF 4 AMINOPYRIDINE-SENSITIVE, DELAYED RECTIFIER K-MUSCLE BY PHOSPHORYLATION( CHANNELS IN VASCULAR SMOOTH)

Voltage-gated delayed rectifier K+ current (K-V) that is sensitive to 4-aminopyridine (4AP) block has been identified in all vascular smooth muscle tissues studied to date. These channels conduct outward, hyper polarizing K+ current that influences resting membrane potential and c ontributes to repolarization of action potentials. Smooth muscle cells in most arterial resistance vessels regulate Ca2+ influx and contract ile tone by low amplitude, tonic changes in membrane potential. Block of K-V with 4-aminopyridine leads to contraction and an enhanced myoge nic response to increased intravascular pressure. We investigated the. modulation of K-V currents in isolated, freshly dispersed smooth musc le cells from rabbit portal vein and coronary arteries in whole-cell v oltage clamp experiments. Our findings indicate that K-V channels are regulated by signal transduction mechanisms involving vasoactive agoni sts that activate cAMP-dependent protein kinase (PKA) or protein kinas e C (PKC). In this paper, the properties and potential function of K-V channels in vascular smooth muscle are reviewed. Further, the regulat ion and potential role of alterations in K-V due to beta-adrenoceptor agonists, adenylyl cyclase and PKA, as well as angiotensin II, diacylg lycerol, and PKC are discussed.