INVOLVEMENT OF ENDOGENOUS PROSTAGLANDIN-I2 IN THE VASCULAR ACTION OF HISTAMINE IN DOGS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 223  (1) , 257-262
Abstract
In helical strips of dog mesenteric and gastroepiloic arteries contracted with prostaglandin (PG) F2.alpha., the addition of histamine (10-6 M) caused a relaxation, which was markedly attenuated by treatment with aspirin, indomethacin or tranylcypromine. Treatment with chlorpheniramine prevented the inhibitory effect of aspirin of tranylcypromine. Combined treatment with chlorpheniramine plus aspirin or trancylprimne slowed the development of histamine-induced relaxations, as did the treatment with chlorpheniramine alone. Relaxations of mesenteric and gastroepiploic arteries induced by histamine were markedly attenuated or abolished by combined treatment with chlorpheniramine and cimetidine. Histamine-induced relaxations of coronary and renal arterial strips were suppressed by cimetidine alone but were unaffected by aspirin. Contractile responses of cerebral arterial strips to histamine were attenuated by chlorpheniramine and potentiated by aspirin. The collagen-induced platelet aggregation was inhibited by treatment with bathing media in which mesenteric arteries were stimulated by histamine; the inhibition was prevented by treatment of the arteries with aspirin. Relaxation of mesenteric and gastroepiploic arteries induced by histamine is mainly associated with the release of PGI2 from the arterial wall, which results from an activation of histaminergic H1 receptors. Histamine-induced cerebroarterial contractions mediated via H1 receptors appear to be partly counteracted by PGI2 released.