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We determined sources of activator calcium for prostanoid-induced cerebrovascular constriction by measuring isometric tension and calcium-45 (45Ca) fluxes in bovine middle cerebral arteries. Constriction induced by prostaglandin F2 alpha or the stable thromboxane A2 analogue SQ-26,655 was near-maximally inhibited in calcium-deficient solutions but only partially inhibited by calcium antagonists (10(-5) M verapamil or 3.3 x 10(-7) M nifedipine). Studies of 45Ca binding at different external Ca2+ concentrations showed that cerebral arteries possess two calcium binding sites, a high-affinity site and a low-affinity site. Each prostanoid significantly increased low-affinity 45Ca uptake (external Ca2+ concentration = 1.2 mmol/l) during 5 minutes of 45Ca loading; for prostaglandin F2 alpha 45Ca uptake increased from 69 to 108 nmol/g and for SQ-26,655, from 78 to 141 nmol/g. The prostanoid-induced increases in low-affinity 45Ca uptake were completely abolished by pretreatment with verapamil or nifedipine. Prostaglandin F2 alpha, SQ-26,655, verapamil, and nifedipine had no effect on high-affinity 45Ca uptake (external Ca2+ concentration = 45 mumol/l) or 45Ca efflux (after 60 minutes' preincubation in calcium-deficient media). Prostaglandin F2 alpha and SQ-26,655 each appear to constrict cerebral arteries by two mechanisms: first, by promoting calcium uptake from low-affinity binding sites through receptor-operated channels sensitive to the calcium antagonists, and second, by releasing calcium from depletable internal stores.

Effects of prostaglandin F2 alpha and thromboxane A2 analogue on bovine cerebral arterial tone and calcium fluxes.