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 two contraction components and depressed their maxima. Readdition of Ca++ to arteries previously depolarized by K+ in the absence of external Ca++ also elicited a biphasic contraction, which excludes the possibility that the initial transient response was initiated by a burst of spikes. Ca++ removal considerably suppressed and 1 mM La abolished both components of the K+ contraction. Prolonged treatment (greater than 3 hr) in Ca++-free, ethylene glycol bis(beta-aminoethyl ether)N,N'-tetraacetic acid (1 mM)-containing medium reduced neither the amplitude of phase A nor that of phase B of the contraction induced by the simultaneous addition of K+ and Ca++. This indicates that the early rapid component was not due to a release of intracellularly stored Ca++. Nifedipine preferentially inhibited phase B of the K+ contraction. The drug also effectively suppressed Ca++-induced contractions in arteries previously depolarized by K+ in Ca++-free medium. The inhibition produced by nifedipine consisted of a reduction of both the maximum and the slope of the concentration-response curve for Ca++. The results of the present study indicate that K+ initiates contraction in rat cerebral arteries by promoting the movement of extracellular and/or superficially bound Ca++ to the cytoplasmic matrix.(ABSTRACT TRUNCATED AT 250 WORDS)