Influence of prostaglandin-synthesis inhibitors on carbachol- and histamine-induced vasodilatation in perfused rat hindquarters.
In perfused rat hindquarters, in which vascular tone was maintained by norepinephrine, carbachol-induced dilatations were blocked by atropine (10(-7) M), while histamine dilatations were inhibited as well by mepyramine (10(-6) M) as by cimetidine (10(-5) M) indicating a histamine effect through both H1- and H2-receptors. This double-receptor histamine effect was confirmed by the observation that specific H1- and H2-receptor agonists, respectively PEA (2-pyridyl-ethyl-aminedihydrochloride) and dimaprit also produced a vasodilatation. Carbachol- and histamine-induced dilatations were also inhibited by ETYA (5,8,11,14-eicosatetraynoic acid) and quinacrine but not by indomethacin. The inhibition of the histamine vasodilatation appeared to rest on an interference with the H1-receptor mechanism. It is concluded that metabolites of arachidonic acid possibly mediate the dilating effect of carbachol, acting through muscarine receptors, and of histamine, acting through H1-receptors.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology*; D006614:Hindlimb / Q000098:blood supply*; D006632:Histamine / Q000494:pharmacology*; D006633:Histamine Antagonists / Q000494:pharmacology; D008297:Male; D010477:Perfusion; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011796:Quinacrine / Q000494:pharmacology; D051381:Rats / Q000502:physiology*; D011968:Receptors, Histamine / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
D001095:Arachidonic Acids; D006633:Histamine Antagonists; D011448:Prostaglandin Antagonists; D011968:Receptors, Histamine; D006632:Histamine; D002217:Carbachol; D011796:Quinacrine