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Articles in PresS, published online ahead of print June 26, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.01369.2000
Submitted on December 12, 2000
Accepted on June 24, 2002
1 MDC for Molecular Medicine, Franz Volhard Clinic, Berlin, Berlin, Germany
2 Nephrology, Medical School Hannover, Hannover, Niedersachsen, Germany
* To whom correspondence should be addressed. E-mail: gollasch{at}fvk-berlin.de.
The initiation of contractile force in arterial smooth muscle (SM) is believed to be regulated by the intracellular Ca2+ concentration and SM myosin type II phosphorylation. We tested the hypothesis that SM myosin type II operates as a molecular motor protein in electromechanical, but not in protein kinase C (PKC)-induced contraction, of small resistance-sized cerebral arteries. We utilized a SM type II myosin heavy chain (MHC) knockout mouse model and measured arterial wall Ca2+ concentration ([Ca2+]i) and diameter of pressurized cerebral arteries (30-100 µm) by means of digital fluorescence video imaging. Intravasal pressure elevation caused a graded [Ca2+]i, increase and constricted cerebral arteries of neonatal wild-type mice by 20-30%. In contrast, intravasal pressure elevation caused a graded increase of [Ca2+]i without constriction in (-/-) MHC-deficient arteries. 60 mM KCl induced a further [Ca2+]i increase but failed to induce vasoconstriction of (-/-) MHC-deficient cerebral arteries. Activation of PKC by phorbol ester (PMA, 100 nM) induced a strong, sustained constriction of (-/-) MHC-deficient cerebral arteries without changing [Ca2+]i. These results demonstrate a major role for SM type II myosin in the development of myogenic tone and Ca2+-dependent constriction of resistance-sized cerebral arteries. In contrast, the sustained contractile response did not depend on myosin and intracellular Ca2+, but instead depended on PKC. We suggest that SM myosin type II operates as a molecular motor protein in the development of myogenic tone but not in pharmacomechanical coupling by PKC in cerebral arteries. Thus, PKC-dependent phosphorylation of cytoskeletal proteins may be responsible for sustained contraction in vascular smooth muscle.
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