Intracisternally applied angiotensin II does not excite reticulospinal vasomotor neurons in anesthetized rats.

M K Sun, D J Reis

Index: Eur. J. Pharmacol. 304(1-3) , 63-71, (1996)

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Abstract

We examined whether vasomotor neurons in the rostroventrolateral reticular nucleus of the medulla oblongata might be responsible for an acute increase in arterial pressure, elicited by application of angiotensin II in the central nervous system, as suggested by others. In urethane-pentobarbital-anesthetized and ventilated rats, intracisternal administration of angiotensin II (1-30 nmol, infused over a period of 30 s) produced a dose-dependent pressor response, which was abolished by intracisternal application of [Sar1, Thr8]angiotensin II (100 nmol), an angiotensin II receptor antagonist. The pressor response, however, was neither preceded by nor associated with increased discharges of vasomotor neurons with slow- and fast-conduction axons in the rostroventrolateral reticular nucleus and of lumbar sympathetic chain and renal sympathetic nerves. Intravenous injections of [beta-mercapto-beta, beta-cyclopentamethylenepropinyl1,-O-Et-Tyr2, Val4, Arg8]vasopressin, a vasopressin receptor antagonist, largely abolished the central angiotensin II-induced pressor response, while a blockade of ganglionic transmission with hexamethonium and disruption of descending sympathoexcitatory output were ineffective. We conclude that central administration of angiotensin II, under the experimental conditions and at the doses, evokes an acute pressor response largely through the release of vasopressin, not by exciting vasomotor and sympathetic neurons.