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ACTIONS OF PROSTAGLANDIN F 2α AND NORADRENALINE ON CALCIUM EXCHANGE AND CONTRACTION IN RAT MESENTERIC ARTERIES AND THEIR SENSITIVITY TO CALCIUM ENTRY BLOCKERS
Author(s) -
GODFRAIND T.,
MILLER R.C.
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb08777.x
Subject(s) - flunarizine , contraction (grammar) , calcium , endocrinology , egta , medicine , chemistry , verapamil , mesenteric arteries , bay k8644 , nifedipine , cinnarizine , muscle contraction , extracellular , calcium channel , artery , biochemistry , chromatography
1 The actions of prostaglandin F 2α (PGF 2α ) and noradrenaline on contraction and 45 Ca exchange have been studied in rat mesenteric arteries. 2 PGF 2α and noradrenaline contracted rat isolated mesenteric artery preparations to about the same extent. The PGF 2α ‐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 PGF 2α ‐stimulated contractions and 45 Ca uptake to a similar extent. 4 Flunarizine was about 7 fold more potent as an inhibitor of noradrenaline‐ than of PGF 2α ‐mediated contraction and 45 Ca uptake and this ratio was about 50 for cinnarizine. 5 EGTA (1.25 m m ) produced a relaxation of noradrenaline and PGF 2α ‐induced maximal contractions. Measured over the first 2 min of EGTA contact, the rate of relaxation was much faster in noradrenaline than in PGF 2α ‐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 PGF 2α , largely due to a greater effect of noradrenaline on calcium efflux. 7 The results suggest that PGF 2α ‐ but not noradrenaline‐induced contractions are entirely dependent on the influx of extracellular calcium and that the agonists may stimulate calcium gating mechanisms differently.