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In isolated human pial arteries (diameter 0.4-0.5 mm), contractions were produced by potassium, noradrenaline, serotonin, and prostaglandin F2 alpha. 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 F2 alpha-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 less than 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 F2 alpha activate isolated pial and mesenteric arteries by different calcium-dependent mechanisms and confirm the potent relaxant effects of nifedipine and nimodipine in these vessels.
L Brandt, and
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Nitric oxide : biology and chemistry,
