• 1 January 1982
    • journal article
    • research article
    • Vol. 256  (1) , 36-48
Abstract
The isolated rat tail artery, exposed to noncumulatively increased K+ concentrations, underwent concentration-related sustained contractions. When the K+ concentration was cumulatively elevated, the amplitude of the contractions was significantly lower. Cocaine potentiated the effects of the noncumulatively increased K+ concentration, whereas after .alpha.-blockade or using reserpine-pretreated arteries, the responses were small, short lasting contractions. Reduction of the external Na+ to 25 mM, potentiated the responses to the lower range of K+ concentrations and decreased those to the higher concentrations. In .alpha.-blocked arteries, low Na+ reduced the responses to all the K+ concentrations. The increase of the Ca2+ concentration to 2.5 mM enhanced the responses to K+ and produced a significant leftward shift of the frequency-response curve to electrical stimulation. Evidently, to establish the actual responses to high external K+, noncumulative dose-response curves must be determined. The actions of K+ are mainly exerted through the release of endogenous catecholamines, the electromechanical coupling seeming to be unable to evoke sustained contractures. The changes of the ionic environment differentially alter the direct and indirect effects of K+, and the release of norepinephrine induced by K+ or by field-electric stimulation appears to have different ionic requirements.

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