Abstract
In pithed and vagotomized rats, the electrically induced vasopressor response was not affected by 2-(2-thiazolyl)ethylamine and dimaprit but was inhibited by Nα-methylhistamine (NαMH) in a thioperamidesensitive manner. NαMH did not affect the vasopressor response to exogenously added noradrenaline. NαMH produced a biphasic effect on basal diastolic blood pressure, i.e. a vasodepressor response (abolished by dimethindene plus ranitidine) and a subsequent vasopressor effect (counteracted by dimethindene or adrenalectomy). Basal heart rate was increased by NαMH (effect abolished by propranolol, dimethindene or adrenalectomy). In conclusion, presynaptic H3, but not H1 or H2, receptors are detectable in the resistance vessels of the rat. NαMH allows the characterization of another four histamine receptor-mediated effects, i.e vasodepressor effects mediated via H1 and H2 receptors and an increase in blood pressure and heart rate mediated via catecholamine-releasing H1, receptors in the adrenal medulla.
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