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      Effects of Protein Kinase C Activation on Intracellular Ca 2+ Distribution in Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats

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          Protein kinase C is known to influence contraction in vascular smooth muscle cells by Ca<sup>2+</sup>-dependent and Ca<sup>2+</sup>-independent mechanisms. In the present study, the effect of protein kinase C activation by phorbol 12-myristate 13-acetate on resting cytosolic free Ca<sup>2+</sup> and on cellular Ca<sup>2+</sup> pools was assessed in cultured rat aortic muscle cells using fura 2. Cellular Ca<sup>2+</sup> pools were evaluated with the selective inhibitor of the sarcoplasmic Ca<sup>2+</sup> ATPase, thapsigargin. In normotensive vascular smooth muscle cells, protein kinase C activation caused a redistribution of Ca<sup>2+</sup> from the thapsigargin-sensitive pool into the cytoplasm, whereas, in hypertensive cells, no significant effect of protein kinase C activity on cellular Ca<sup>2+</sup> distribution was found. It is concluded that protein kinase C modulates the amount of Ca<sup>2+</sup> stored in the thapsigargin-sensitive calcium stores. In hypertensive cells, the regulation of Ca<sup>2+</sup> pools by protein kinase C is disturbed.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 30
          : 2
          : 116-120
          Medizinische Universitäts-Poliklinik, Münster, FRG
          158983 J Vasc Res 1993;30:116–120
          © 1993 S. Karger AG, Basel

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          Pages: 5
          Research Paper


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