ALTERED REFLEX VASODILATATION IN THE HYPERTENSIVE RAT: POSSIBLE ROLE OF HISTAMINE

¹ Deparment of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, Lafayette, Indiana

Reflex vasodilatation in response to norepinephrine administration and carotid sinus stimulation and vasodilatation after compound 48/80 and histamine administration were examined in the perfused hindquarters of the normotensive and hypertensive rat. Previous studies suggested that histamine is involved as a mediator of reflex vasodilatation in this species. The present study was undertaken to determine if a defect in the histaminergic component of reflex vasodilatation may contribute to elevated peripheral resistance in experimental hypertension. Intravenously administered norepinephrine produced a reflex vasodilatation which was significantly reduced by pretreatment with tripelennamine but not by atropine. The antihistamine did not modify hindquarter perfusion pressure responses to carotid occlusion or to i.a. administered nitroglycerin, but blocked the response to i.a. administered histamine. It was demonstrated that reflex vasodilatation induced by norepinephrine administration or electrical stimulation of the carotid sinus was significantly reduced in the renal- or deoxycorticosterone acetate-hypertensive rat when compared to normotensive controls. There was also a significant reduction in vasodilatation induced by i.a. administered compound 48/80 in the hypertensive rat, but no difference between the two groups in vascular sensitivity to administered histamine. These data indicate that an abnormality in the histaminergic component of reflex vasodilatation may contribute to the elevated peripheral resistance characteristic of experimental hypertension in the rat.