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EVIDENCE AGAINST THE INVOLVEMENT OF PROSTAGLANDINS IN THE VASOCONSTRICTOR ACTION OF CALCIUM ION IN RAT MESENTERIC BLOOD VESSELS
Author(s) -
COUPAR I.M.
Publication year - 1981
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.1476-5381.1981.tb09993.x
Subject(s) - calcium , chemistry , endocrinology , medicine , papaverine , vasoconstriction , mesenteric arteries , prostaglandin , thromboxane a2 , verapamil , agonist , blood vessel , pharmacology , artery , receptor
1 Prostaglandin E 2 (PGE 2 ) has been claimed to be essential to the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels. Since noradrenaline acts by releasing intracellular calcium, experiments have been performed using the perfused rat superior mesenteric artery preparation to determine whether prostaglandin synthesis is necessary for the direct vasoconstrictor action of calcium 2 The cyclo‐oxygenase inhibitors, indomethacin and 5, 8, 11, 14‐eicosatetraynoic acid (ETA), inhibited responses to noradrenaline and calcium but both were less effective in inhibiting the response to calcium than to noradrenaline 3 PGE 2 (6 ng‐20 μg/ml) failed to overcome the inhibitory effect of indomethacin (62 μg/ml) and ETA (10 μg/ml) on the response to the EC 50 of Ca 2+ (100 μg/ml). The EC 50 of Ca 2+ did not significantly increase PGE 2 ‐like release by the blood vessels from the resting value of 19 ± 8pg of PGE 2 equivalents/min 4 PGA 1 (6 μg/ml) and the thromboxane A 2 agonist, U‐46619 (200ng/ml), both caused full restoration of indomethacin‐depressed responses to calcium, but did not restore responses depressed by ETA. U‐46619 (200ng/ml) also reversed the inhibitory effect of papaverine (4 μg/ml) and caused a 1.6 fold potentiation of Ca 2+ responses 5 The results do not support the hypothesis that prostaglandin synthesis is essential to the vasoconstrictor action of Ca 2+ in rat mesenteric blood vessels.