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      Diminishment of Contractions Associated with Depolarization-Evoked Activation of Ca 2+ Channels in Diabetic Rat Aorta

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          Alterations in contractile responses of aortic rings mediated by activation of Ca<sup>2+</sup> channels were investigated in rats with streptozotocin-induced diabetes. Eight to 12 weeks of diabetes resulted in a marked decrease in the contractile response of aortic rings to high K<sup>+</sup>. In contrast, diabetic aortas exhibited significantly greater contractions in response to noradrenaline compared to age-matched controls. In the presence of 15 ml K<sup>+</sup>, the Ca<sup>2+</sup> channel agonist Bay K 8644 consistently produced concentration-dependent contractions in control aortas. On the other hand, the half of diabetic aortas did not respond to Bay K 8644. As a result, the contractile response to Bay K 8644 was significantly less in diabetic aortas compared to controls. There was no significant difference in basal <sup>45</sup>Ca<sup>2+</sup> uptake between control and diabetic aortas. However, the uptake of <sup>45</sup>Ca<sup>2+</sup> induced by high K<sup>+</sup> was significantly less in diabetic aortas than in controls, and pretreatment with the Ca<sup>2+</sup> channel antagonist nifedipine abolished both responses. The resting membrane potentials were not significantly different between control and diabetic aortas. Furthermore, no difference was found in the magnitude of depolarization evoked by increasing K<sup>+</sup> concentrations between the two groups of tissues. There were no significant differences in the density and the dissociation constant for [<sup>3</sup>H]-(+)-PN200-110, a radiolabeled Ca<sup>2+</sup> channel antagonist, between aortic membranes from control and diabetic rats. These data indicate that the contractile responses to high K<sup>+</sup> and Bay K 8644 are specifically diminished in diabetic aortas. These diminished responses are not due to a difference in the number of Ca<sup>2+</sup> channels, but may be related to an alteration in activation of the channels by membrane depolarization.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          24 September 2008
          : 33
          : 6
          : 454-462
          Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan
          159184 J Vasc Res 1996;33:454–462
          © 1996 S. Karger AG, Basel

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          Pages: 9
          Research Paper


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