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1 The actions of prostaglandin F2a (PGF2J) and noradrenaline on contraction and 45Ca exchange have been studied in rat mesenteric arteries.2 PGF2,, and noradrenaline contracted rat isolated mesenteric artery preparations to about the same extent. The PGF2,,-stimulated contractions, unlike those produced by noradrenaline, were completely inhibited in calcium-free physiological solution. 3 The calcium entry blocking drugs, cinnarizine and flunarizine, had little effect on the resting exchange of calcium in the arterial smooth muscle, but inhibited PGF2U-stimulated contractions and 45Ca uptake to a similar extent. 4 Flunarizine was about 7 fold more potent as an inhibitor of noradrenaline-than of PGF2,,-mediated contraction and 45Ca uptake and this ratio was about 50 for cinnarizine. 5 EGTA (1.25 mM) produced a relaxation of noradrenaline and PGF2,,-induced maximal contractions. Measured over the first 2 min of EGTA contact, the rate of relaxation was much faster in noradrenaline than in PGF2,z-stimulated preparations.6 Turnover of cellular calcium (influx plus efflux) during the first 2 min of noradrenaline contact was much greater than that produced by PGF2a, largely due to a greater effect of noradrenaline on calcium efflux. 7 The results suggest that PGF2,,-but not noradrenaline-induced contractions are entirely dependent on the influx of extracellular calcium and that the agonists may stimulate calcium gating mechanisms differently.

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