MECHANISMS BEHIND THE BIPHASIC CONTRACTILE RESPONSE TO POTASSIUM DEPOLARIZATION IN ISOLATED RAT CEREBRAL-ARTERIES

  • 1 January 1984
    • journal article
    • research article
    • Vol. 228  (1) , 187-195
Abstract
Ring segments of rat basilar and middle cerebral arteries were suspended in a small volume muscle bath and the mechanical activity recorded isometrically. K+ excess (124 mM) evoked a biphasic contractile response, composed of an early rapid phase (phase A) and an ensuing slow phase (phase B), separated by a small transient relaxation. Cooling produced a gradual dissociation of the 2 contraction components and depressed their maxima. Readdition of Ca2+ to arteries previously depolarized by K+ in the absence of external Ca2+ also elicited a biphasic contraction, which excludes the possibility that the initial transient response was initiated by a burst of spikes. Ca2+ removal considerably suppressed and 1 mM La3+ abolished both components of K+ contraction. Prolonged treatment (> 3 h) in Ca2+-free, ethylene glycol bis(.beta.-aminoethyl ether)N,N''-tetraacetic acid (1 mM)-containing medium reduced neither the amplitude of phase A or nor that of phase B of the contraction induced by the simultaneous addition of K+ and Ca2+. The early rapid component was evidently due to a release of intracellularly stored Ca2+. Nifedipine preferentially inhibited phase B of the K+ contraction. The drug also effectively suppressed Ca2+-induced contractions in arteries previously depolarized by K+ in Ca2+-free medium. The inhibition produced by nifedipine consisted of a reduction of both the maximum and the slope of the concentration-response curve for Ca2+. K+ evidently initiates contraction in rat cerebral arteries by promoting the movement of extracellular and/or superficially bound Ca2+ to the cytoplasmic matrix. The 2-component contractile response to K+ evidently reflects the inflow of Ca2+ through 2 separate K+-activated Ca2+ channels in the surface membrane, one permitting a rapid and transient movement of Ca2+ across the smooth muscle membrane (the rapidly activated Ca2+ channel), the other allowing Ca2+ to pass at a slower rate (the slowly activated Ca2+ channel).

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