Wc. Cole et al., REGULATION OF 4 AMINOPYRIDINE-SENSITIVE, DELAYED RECTIFIER K-MUSCLE BY PHOSPHORYLATION( CHANNELS IN VASCULAR SMOOTH), Biochemistry and cell biology, 74(4), 1996, pp. 439-447
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.