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      Depression of Contractions of Rabbit Aorta and Guinea Pig Vena cava by Mesudipine and Other Slow Channel Blockers

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          The effects of several drugs having Ca<sup>++</sup>-antagonistic and vasodilating properties were compared in arterial and venous smooth muscles. Developed force (phasic component) was recorded from isolated rings (about 2 mm wide) of blood vessel wall taken from rabbit aorta or guinea pig inferior vena cava. The vascular smooth muscle (VSM) was stimulated to contract for a sustained period by elevating the extracellular K<sup>+</sup> concentration ([K]<sub>o</sub>) to 100 mM or by exposure to norepinephrine (NE). All drugs depressed the K<sup>+</sup>-induced contractures in a dose-dependent manner between 10-9 and 10–5 M. The order of potency in aorta was: mesudipine = verapamil > diltiazem > nifedipine. Of the three drugs studied in vena cava, the order of potency was: mesudipine > verapamil > bepridil. It is concluded that, in both preparations of arterial and venous VSM, mesudipine is the most potent inhibitor of K<sup>+</sup>-induced contractions. Aortic contractions to 10<sup>-7</sup> M NE were depressed at concentrations of Ca<sup>++</sup> antagonists 2 or 3 orders of magnitude less than those needed to depress contractions to 10–5 M NE. The NE-induced contractions were depressed by the drugs to about the same extent as the K<sup>+</sup>-induced contractions when 10<sup>-7</sup> M NE was used, but were depressed to a much smaller extent when 10–5 M NE was used. This may reflect the involvement of intra-cellular Ca<sup>++</sup> storage sites in contractions induced by high NE concentrations. It is likely that these drugs depress and block Ca<sup>++</sup> influx through the cell membrane.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          19 September 2008
          : 20
          : 4
          : 172-183
          Department of Physiology, University of Virginia School of Medicine, Charlottesville, Va., USA
          158471 Blood Vessels 1983;20:172–183
          © 1983 S. Karger AG, Basel

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          Pages: 12
          Research Paper


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