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.
journal_name
J Vasc Resjournal_title
Journal of vascular researchauthors
Zou H,Ratz PH,Hill MAdoi
10.1159/000054089keywords:
subject
Has Abstractpub_date
2000-11-01 00:00:00pages
556-67issue
6eissn
1018-1172issn
1423-0135pii
54089journal_volume
37pub_type
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