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      Involvement of L-Type Calcium Channels in Hypoxic Relaxation of Vascular Smooth Muscle

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          In the systemic vasculature, hypoxia elicits a local vasodilator response that may be partially mediated by ionic channels on vascular smooth muscle, such as adenosine triphosphate sensitive K<sup>+</sup> channels. Recent electrophysiological studies suggest that hypoxia may also inhibit voltage-dependent Ca<sup>2+</sup> channels (L type) on peripheral vascular smooth muscle cells. We hypothesized that hypoxia elicits relaxation of vascular smooth muscle by inhibiting L-type Ca<sup>2+</sup> channels. In endothelium-denuded rat thoracic aortic rings contracted with phenylephrine, mild and moderate hypoxia (PO<sub>2</sub> 35 and 20 mm Hg, respectively) elicited significant relaxation. Pretreatment with the L-type Ca<sup>2+</sup> channel antagonist nifedipine completely inhibited mild hypoxic relaxation and diminished relaxation under moderate hypoxia, whereas glibenclamide, a blocker of adenosine triphosphate sensitive potassium channels, only attenuated the response to moderate hypoxia. In rings contracted with the L-type Ca<sup>2+</sup> channel agonist (–)BAY K 8644 both mild and moderate hypoxia elicited almost complete relaxation. Furthermore, in rings contracted with hyperkalemic solutions (85 m M K<sup>+</sup> or 120 m M K), mild and moderate hypoxia elicited significant relaxations. Thus, we conclude that hypoxia acts directly on vascular smooth muscle to cause relaxation in part by inhibiting L-type Ca<sup>2+</sup> channels.

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          Vasoconstrictor and vasodilator effects of hypoxia.

          Hypoxia has marked effects on artery calibre, which reflects important physiological control mechanisms that are altered in disease states. Hypoxia modifies the release of mediators, especially from the endothelium, and influences smooth muscle membrane potential and Ca2+ regulation. In this review, Roger Wadsworth evaluates the vasoconstrictor and vasodilator effects of hypoxia studied in vitro. In the future, drugs developed to act on the mediators or smooth muscle may be beneficial in the therapy of, for example, pulmonary hypertension or coronary vasospasm.
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            Pharmacological characteristics of receptor-operated and potential-operated Ca2+ channels in rat aorta


              Author and article information

              J Vasc Res
              Journal of Vascular Research
              S. Karger AG
              August 1998
              07 August 1998
              : 35
              : 4
              : 265-273
              Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, N. Mex., USA
              25593 J Vasc Res 1998;35:265–273
              © 1998 S. Karger AG, Basel

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              Page count
              Pages: 9
              Research Paper


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