DIFFERENT MECHANISMS OF ACTION OF HISTAMINE IN ISOLATED ARTERIES OF THE DOG

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Abstract
1 In helically-cut strips of dog coronary, superior mesenteric, right gastro-epiploic and renal arteries contracted with prostaglandin F2β (PGF2β), histamine produced a dose-related relaxation, while, in contrast, the amine caused only a contraction of cerebral arterial strips 2 The contractile response of cerebral arteries to histamine was attenuated by chlorpheniramine (10−6M)but was unaffected by cimetidine (10−5m). Relaxant responses to histamine of coronary and renal arteries were significantly attenuated by treatment with cimetidine and to a similar extent by combined treatment with cimetidine and chlorpheniramine. Chlorpheniramine alone was ineffective 3 In mesenteric and gastro-epiploic arteries, relaxant responses to histamine were attenuated only slightly by cimetidine. Chlorpheniramine slowed the development of histamine-induced relaxations but did not alter the magnitude of the relaxations. Combined treatment with these H1- and H2- antagonists attenuated the histamine-induced relaxations to an appreciably greater extent than treatment with cimetidine alone 4 It may be concluded that the cerebroarterial contraction induced by histamine is mediated through H1-receptors and the relaxations of coronary and renal arteries induced by histamine are mediated through H2-receptors. It appears that H1- and H2-receptors interact with each other to produce potentiation of histamine-induced relaxations of mesenteric and gastro-epiploic arteries.