Central pressor activity of cimetidine in spontaneously hypertensive rats.
The systemic blood pressure effect of cimetidine given intracerebroventricularly (i.c.v.) in anaesthetized spontaneously hypertensive (SH) rats has been investigated. Cimetidine (250 micrograms i.c.v.) caused a gradual long lasting rise in mean arterial blood pressure with maximum of 31.6 +/- 4.5 mm Hg. Chemical degeneration of catecholaminergic neurons with 6-OHDA treatment, central administration of phentolamine and prazosin, and the bilateral adrenalectomy significantly inhibited the pressor response of cimetidine, while propranolol (i.c.v.) had no effect. From these results it appears that the hypertensive response of cimetidine is mediated by central catecholaminergic pathways and is due to an increase in efferent sympathetic outflow and release of catecholamine from the adrenal medulla.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001921:Brain / Q000187:drug effects*; D002927:Cimetidine / Q000494:pharmacology*; D006892:Hydroxydopamines / Q000633:toxicity; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains
D006892:Hydroxydopamines; D002927:Cimetidine; D016627:Oxidopamine; D009638:Norepinephrine