Induction of chronic arterial hypertension in rats by repeated transient hypertensive rises in blood pressure. Possible pathogenetic role of delayed hypersensitivity against arteries and arterioles.
Repeated transient rises in blood pressure to hypertensive levels were induced by intravenous injections of angiotensin once or twice weekly. This procedure induced chronic arterial hypertension in five of fourteen rats (36%) within 4-6 weeks of starting the injections. Intracutaneous tests using homogenized common carotid arteries and histological examination of the kidneys gave support to the hypothesis that the transient rises in blood pressure to hypertensive levels resulted in a delayed hypersensitivity (DHS) reaction against components in small arteries and arterioles. This DHS reaction seemed to be responsible for an increased permeability of arterial vessels to plasma components causing exudative thickening of the walls of small arteries and arterioles and thereby narrowing of their lumina. When the lumina of small arteries and arterioles are narrowed, peripheral resistance to blood flow increases, and arterial hypertension results.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D002199:Capillary Permeability; D005260:Female; D006968:Hypersensitivity, Delayed / Q000139:chemically induced / Q000150:complications*; D006973:Hypertension / Q000139:chemically induced / Q000209:etiology*; D007668:Kidney / Q000473:pathology; D008297:Male; D051381:Rats
D000804:Angiotensin II