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In isolated human pial arteries (diameter 0.4–0.5 mm), contractions were produced by potassium, noradrenaline, serotonin, and prostaglandin F 2α . For comparison, experiments were also performed on human mesenteric arteries. Threshold concentration for potassium-induced contraction in pial arteries was about 10 mm; in mesenteric arteries it was 3–5 mm higher. In pial arteries the calcium antagonists nifedipine and nimodipine caused an almost complete relaxation of contractions induced by potassium at drug concentrations relaxing prostaglandin F 2α -contracted vessels to only about 60%. Both nifedipine and nimodipine effectively inhibited contraction elicited by noradrenaline and serotonin in pial arteries. Nifedipine had a higher potency for relaxing cerebral than mesenteric arteries contracted by potassium ( p &lt; 0.001). No such difference was demonstrated for nimodipine. In pial arteries pretreated in a calcium-free medium for 30 min, potassium depolarisation elicited contractions reaching a maximum amplitude of about 40% of that evoked in normal Krebs solution. Both nifedipine and nimodipine effectively inhibited contractions induced by calcium in pial arteries pretreated in a calcium-free medium and depolarised by potassium. The results suggest that potassium, amines, and prostaglandin F 2α  activate isolated pial and mesenteric arteries by different calcium-dependent mechanisms and confirm the potent relaxant effects of nifedipine and nimodipine in these vessels.

Effects of Extracellular Calcium and of Calcium Antagonists on the Contractile Responses of Isolated Human Pial and Mesenteric Arteries