abstract
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 speccific H1- and H2-receptor agonists, respectively PEA (2-pyridyl-ethylaminedihydrochloride) and dimaprit also produced a vasodilation.
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.
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Preliminary communication held at the meeting of the Belgian Society for Fundamental and Clinical Physiology and Pharmacology, June 5, 1982 (Arch Int Pharmacodyn 1982, 260:312–313)
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Van de Voorde, J., Leusen, I. Influence of prostaglandin-synthesis inhibitors on carbachol-and histamine-induced vasodilatation in perfused rat hindquarters. Pflugers Arch. 397, 290–294 (1983). https://doi.org/10.1007/BF00580263
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DOI: https://doi.org/10.1007/BF00580263