It is concluded that a beta-endorphin-containing pathway projecting from the arcuate nucleus to the ipsilateral dorsal vagal complex is involved in depressor cardiovascular regulation and in the facilitation of baroreflex bradycardia.
Glucagon administered either intravenously (iv) (100-1000 micrograms/kg) or intracerebroventricularly (icv) (5 micrograms) significantly attenuated morphine-induced (200 micrograms/kg, iv) bradycardia without producing any alterations in cardiovascular parameters when given alone.
Both dynorphin (1-13) and Leu-enkephalin administered s.c. to normal and morphine-tolerant rats, 30 min before blood vessel cannulation and testing, lowered the morphine ED50 for bradycardia.
In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia.
In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia.
In contrast, intraventricular administration of prolactin caused bradycardia, hypotension and an enhancement in the epinephrine-induced reflex bradycardia in conscious rats.