title: Temporal aspects of Ca(2+) and myosin phosphorylation during myogenic and norepinephrine-induced arteriolar constriction.
abstract: Previous studies demonstrated that maintenance of steady-state myogenic tone requires Ca(2+)-dependent myosin phosphorylation. The present studies furthered these observations by examining temporal relationships among Ca(2+), myosin phosphorylation and vessel diameter during acute increases in intraluminal pressure and norepinephrine stimulation. Rat cremaster muscle arterioles were cannulated and loaded with the Ca(2+)-sensitive indicator fura-2. The extent of myosin phosphorylation was measured using two-dimensional gel electrophoresis. Acute increases in intraluminal pressure caused a biphasic increase in intracellular Ca(2+) ([Ca(2+)](i)), characterized by a transient peak followed by a decline to a steady-state level which remained significantly higher than control values. Peak [Ca(2+)](i) was significantly related to vessel distension and increased with the change in wall tension. Increased intraluminal pressure resulted in a monophasic increase in myosin phosphorylation that was significantly correlated with instantaneous wall tension. In general, norepinephrine induced larger [Ca(2+)](i) transients and a biphasic myosin phosphorylation pattern. The results demonstrate: (a) major roles for Ca(2+) and myosin phosphorylation in arteriolar myogenic and norepinephrine-induced responses; (b) that changes in Ca(2+) and phosphorylation during a myogenic response are related to changes in wall tension, and (c) differences in Ca(2+) and phosphorylation patterns between the two modes of contraction reflect possible differences in underlying signaling mechanisms. The data further emphasize that spontaneous arteriolar tone represents a state of maintained smooth muscle activation that requires increases in [Ca(2+)](i) and myosin light-chain phosphorylation.
authors.affiliation: Department of Physiology, Eastern Virginia Medical School, Norfolk, Va., USA.
authors.forename: H
authors.initials: H
authors.lastname: Zou
authors.forename: P H
authors.initials: PH
authors.lastname: Ratz
authors.forename: M A
authors.initials: MA
authors.lastname: Hill
mesh_terms: D000818:Animals; D001160:Arterioles / Q000187:drug effects* / Q000502:physiology; D001794:Blood Pressure; D020013:Calcium Signaling / Q000502:physiology*; D015180:Electrophoresis, Gel, Two-Dimensional; D008297:Male; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009219:Myosin-Light-Chain Kinase / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology*; D010766:Phosphorylation; D011312:Pressure; D011499:Protein Processing, Post-Translational; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D009219:Myosin-Light-Chain Kinase; D009218:Myosins; D009638:Norepinephrine