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1 Pharmacology, Physiology & Therapeutics, University of North Dakota School of Medicine & Health Sciences, Grand Forks, ND, USA
* To whom correspondence should be addressed. E-mail: jbenoit{at}mail.und.nodak.edu.
The ability of arterial smooth muscle to respond to vasoconstrictor stimuli is reduced in chronic portal hypertension (PHT). Additional evidence supports the existence of a post-receptor defect in vascular smooth muscle excitation contraction coupling. However, the nature of this defect is unclear. Recent studies have shown that vasoconstrictor stimuli induce actin polymerization in smooth muscle and that the associated increase in F-actin is necessary for force development. In the present study we have tested the hypothesis that impaired actin polymerization contributes to reduced vasoconstrictor function in small mesenteric arteries derived from rats with chronic prehepatic portal hypertension. In vitro studies were conducted on small mesenteric artery vessel rings isolated from normal and PHT rats. Isometric tension responses to incremental concentrations of phenylephrine were significantly reduced in PHT arteries. The ability to polymerize actin in portal hypertensive mesenteric arteries stimulated by phenylephine was attenuated when compared to control. Inhibition of cAMP dependent protein kinase (PKA) restored agonist-induced actin polymerization of arteries from portal hypertensive rats to normal levels. Depolymerization of actin in arteries from normal rats reduced maximal contractile force, but not myosin phosphorylation, suggesting a key role for the dynamic regulation of actin polymerization in the maintenance of vascular smooth muscle contraction. We conclude that reductions in agonist-induced maximal force development of PHT vascular smooth muscle is due, in part, to impaired actin polymerization; and prolonged PKA activation may underlie these changes.
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