Korner P I, Oliver J R, Reynoldson J A, Head G A, Carson V J, Walker M M
Eur J Pharmacol. 1978 Dec 15;53(1):83-93. doi: 10.1016/0014-2999(78)90270-4.
Acute effects of 6-hydroxydopamine (6-OHDA, 400--900 microgram kg-1 intracisternally, i.c.i.) consisted of bradycardia and hypertension, maximal 2--3 h after injection and preceded after some doses by a phase of hypotension. This pattern was obtained in completely conscious rabbits and after propanidid and sodium pentobarbitone anesthesia. After 600 microgram kg-1 i.c.i. 6-OHDA the peak rise in blood pressure (25 +/- 3.8 mm Hg) was due to a rise in peripheral resistance involving particularly renal and intestinal beds. Suprapontine mechanisms contributed to both hypertension and bradycardia. Giving pontine rabbits 6-OHDA elicited a short-latency fall in blood pressure, resembling the hypotensive phase in intact animals. Chronic effects 7 days after 600 microgram kg-1 included a rapid loss of 10% of body weight associated with reduction in food and water intake. To avoid secondary circulatory effects the rabbits were artificially fed, halving the weight loss. At 7 days blood pressure had fallen by 7.4 +/- 2.3 mm Hg probably owing to this residual weight loss. From experiments involving administration of phenotolamine and clonidine in intact rabbits and the responses of pontine animals it is likely that both descending and ascending catecholaminergic pathways have inhibitory effects on blood pressure, though some of the pathways may also be excitatory. Absence of specific chronic circulatory changes may be due to compensation through parallel pathways involving other transmitters.