Reduction of a centrally induced pressor response by neurohypophyseal peptides: the involvement of lower brainstem mechanisms.

Pressor and bradycardiac responses induced by electrical stimulation of the mesencephalic reticular formation in urethane-anesthetized rats were used as model of neurogenic hypertension. Oxytocin (OXT) and prolyl-leucyl-glycinamide (OXT-(7-9] administered into the fourth cerebral ventricle markedly attenuated the magnitude of the pressor response. OXT-(7-9) was somewhat more potent than OXT and its effect was dose-dependent. Microinjection of OXT-(7-9) into the dorsal raphe nucleus reduced the pressor response as well. [Arg8]vasopressin (AVP) did not affect the pressor response when administered via this route, while prolyl-arginyl-glycinamide (AVP-(7-9] had an action that was similar to that of OXT-(7-9). None of these peptides affected the magnitude of the bradycardiac response. It is suggested that OXT and related fragments modulate neurogenic hypertensive responses through lower brainstem mechanisms.