The contractile responses of three artery segments of diminishing diameter in the rabbit ear (i.e., unstretched lumen diameter ~ 300 Î¼ in central ear artery, unstretched lumen diameter ~ 150 Î¼ in main side branch off the central ear artery and unstretched lumen diameter ~ 75 Î¼ in terminal branch off the main side branch) to high K+, norepinephrine (NE) and 5-hydroxytryptamine (5-HT) were tested before and after their incubation in Ca++-free physiologic salt solution for times varying from 3 to 60 min. The time course of reduction of the contractile responses to K+ with Ca++-free conditions in all classes of vessels could be represented by monoexponential curves that were not significantly different from each other. The contractile response of all the ear arteries to NE and 5-HT was biphasic. The first rapid transient phase (phase I) was more resistant to change upon the removal of exogenous Ca++ than the second usually equilibrium-like component (phase II), which was dramatically and rapidly reduced (but not necessarily eliminated by this procedure. The extent of decline upon Ca++ removal in most instances was greater for 5-HT than for NE. The rate of falloff of both phases of contraction to NE and 5-HT was faster in the smaller compared with the larger arteries. These results suggest that, as vessels in the rabbit ear arterial tree get smaller, the contribution of a tightly bound or intracellular Ca++ pool to both phases of amine-induced contraction becomes smaller, but this contribution is greater to the transient compared with the equilibrium phase. However, the sensitivities to the antagonistic effect of nimodipine, a dihydropyridine calcium channel blocker, did not always become greater in the smaller compared with the larger arteries. Changes in the two effects did not occur in parallel, suggesting an importance of considerations other than relative dependence on external Ca++ in susceptibility of amine-induced tone to nimodipine.
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