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      Protein Kinase C as a Modulator of Response Amplification in Vascular Smooth Muscle

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          The amplification of α-adrenoceptor-mediated vasoconstriction by angiotensin II was studied in femoral artery rings from rabbits. Threshold concentrations of angiotensin II (0.1 n M) increased the maximal response to clonidine to 139 ± 8% of control and produced a 3.2-fold increase in sensitivity. These effects of angiotensin II were reversed when tissues were pretreated with staurosporine (50 n M), an inhibitor of protein kinase C. The amplification of the α-adrenoceptor-mediated vasoconstrictor effects of thrombin and norepinephrine by angiotensin II were also reversed by pretreatment with staurosporine. Angiotensin II induced a response amplification in vascular smooth muscle known to be a nonspecific phenomenon, implying postreceptor interaction at intracellular transducer systems. Our findings suggest that upon activation of protein kinase C by angiotensin II, arterial responses to α-adrenoceptor agonists are amplified. This provides for nonspecific changes in vascular sensitivity by tonic alterations in postsynaptic modulation by enzyme systems known to regulate Ca<sup>2+</sup>-dependent phenomena, e.g. those related to vascular excitation-contraction mechanisms.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 27
          : 6
          : 333-340
          Department of Pharmacology, and Vermont Center for Vascular Research, University of Vermont, College of Medicine, Burlington, Vt., USA
          158827 Blood Vessels 1990;27:333–340
          © 1990 S. Karger AG, Basel

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          Pages: 8
          Research Paper


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