Abstract
The mechanism involved in the development of contracture in an isolated smooth muscle in Na+-depleted saline solution is not clearly understood. Whereas most of the reported studies attribute it to direct myogenic action of Na+ depletion, a few suggested the contracture to be an indirect mechanism through the release of the neurotransmitter from presynaptic nerve endings. The present study employed rat vas deferens and it showed that the slowly developing contracture in Na+-depleted saline solution was blocked by prior treatment with in vitro prazosin and in vivo reserpine. Prior exposure of the tissue to verapamil caused the development of rhythmic contractions in Na+-free medium and these rhythmic contractions were blocked by prazosin. Exposure of the tissue to a Ca2+-free solution abolished the contractures induced by Na+-free solution. Na+-depletion increased the sensitivity of the vas deferens to exogenous noradrenaline. It is concluded that the contractures induced by Na+ depletion result from the stimulation of postjunctional alpha-adrenoceptors by endogenously released catecholamines from the adrenergic nerve terminals innervating the vas deferens smooth muscle. Further, these contractures result from an influx of extracellular Ca2+ through both voltage-dependent and receptor-operated calcium channels.
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Schedule a callMore From: Quarterly journal of experimental physiology (Cambridge, England)
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