Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine.
Genetically hypertensive (GH) rats of the New Zealand strain and normotensive (N) rats were sympathectomized from birth with 6-hydroxydopamine (100 mg/kg,s.c, on alternate days, seven treatments). In adult treated rats from each strain (GHTr and NTr), blood pressure was lower than normal. Functional tests and electron microscopy showed that denervation was virtually complete in mesenteric and hindlimb arteries; the innervation of the renal artery was little affected. Ganglionic blockade still caused a large fall in blood pressure in treated rats. Vascular resistance was higher in blood-perfused hindlimbs and tails of GH rats than in those of N rats; in contrast, resistance was similar in limbs and tails of GHTr and NTr rats and was greater than that found in untreated N rats. Saline-perfused limb vessels had neither neurogenic nor myogenic tone and resistance was higher in GH limbs (whether these were from treated rats or not) than in untreated N limbs. In saline-perfused NTr limbs, there was a paradoxical structural adaptation (probably luminal narrowing) of the hindlimb blood vessels and resistance was higher than in untreated N rats. The resistance of saline-perfused GH and GHTr limbs was similar. A high peripheral resistance appears to be the main mechanism sustaining genetic hypertension, and the integrity of the vasomotor sympathetic nerves is necessary for the development of this form of experimental hypertension.
D000818:Animals; D000831:Animals, Newborn; D001369:Axons / Q000648:ultrastructure; D001794:Blood Pressure / Q000187:drug effects*; D006614:Hindlimb / Q000503:physiopathology; D006892:Hydroxydopamines / Q000494:pharmacology*; D006973:Hypertension / Q000235:genetics*; D008297:Male; D010477:Perfusion; D051381:Rats; D013623:Tail / Q000503:physiopathology; D014655:Vascular Resistance / Q000187:drug effects*; D014666:Vasomotor System / Q000187:drug effects
D006892:Hydroxydopamines