EFFECTS OF H1, H2 AND H3 AGONISTS ON THE NEUROGENIC VASOPRESSOR RESPONSE IN THE PITHED RAT

In pithed and vagotomized rats, the electrically induced vasopressor r esponse was not affected by 2-(2-thiazolyl)ethylamine and dimaprit but was inhibited by N(alpha)-methylhistamine (N(alpha)MH) in a thioperam ide-sensitive manner. N(alpha)MH did not affect the vasopressor respon se to exogenously added noradrenaline. N(alpha)MH produced a biphasic effect on basal diastolic blood pressure, i.e. a vasodepressor respons e (abolished by dimethindene plus ranitidine) and a subsequent vasopre ssor effect (counteracted by dimethindene or adrenalectomy). Basal hea rt rate was increased by N(alpha)MH (effect abolished by propranolol, dimethindene or adrenalectomy). In conclusion, presynaptic H-3, but no t H-1 or H-2, receptors are detectable in the resistance vessels of th e rat. N(alpha)MH allows the characterization of another four histamin e receptor-mediated effects, i.e. vasodepressor effects mediated via H -1 and H-2 receptors and an increase in blood pressure and heart rate mediated via catecholamine-releasing H-1 receptors in the adrenal medu lla.