Sources of activator calcium in rabbit basilar artery.

Abstract

The responses of segments of rabbit basilar and ear arteries to high K+ (K+, 45 mM), norepinephrine (NE, 10(-5) and 10(-7) M), and 5-hydroxytryptamine (5-HT, 10(-7) M) were tested before and after their incubation in calcium (Ca2+)-free Krebs solution for times varying from 2.5 to 60 min. The time course of evolution of the responses to K+ with Ca2+-free conditions in both vessels could be represented by a monoexponential curve. The rates of decline of the responses of amines in the ear artery were similar to K+ at first but then fell off at a slower rate. The decline in K+ contraction and the fast initial decline of the NE contraction may relate to the speed of removal of extracellular calcium, whereas the final slower NE decline reflects depletion of an intracellular pool. In the basilar artery, the NE and K+ response declined in a similar manner, whereas the 5-HT contraction showed a fast and a slow component of decline. These results for the maintained agonist response were confirmed using the Ca2+ influx antagonist, 3-methoxyverapamil (D 600). In addition, a D 600-insensitive phasic contraction was observed in both arteries. These results suggest that the steady-state NE contraction in the basilar artery is almost entirely dependent on loosely bound extracellular Ca2+. This is in contrast to the ear artery, where an additional tightly bound or intracellular Ca2+ pool is used. This source is present in the basilar artery but contributes only to a D 600-insensitive phasic component.