Microinjection of SP (1 ng) or NKA (10-100 ng) into the NTS caused prompt, transient hypotension and bradycardia, suggesting that SP and NKA may be neurotransmitters of the baroreceptor reflex in the NTS.
The most sensitive sites where application of SP into the NTS evoked dose-dependent hypotension and bradycardia were at the level of the posterior tip of the area postrema (zero level) and at the level of the obex.
Low-affinity M(2) receptor binding state mediates mouse atrial bradycardia: comparative effects of carbamylcholine and the M(1) receptor agonists sabcomeline and xanomeline.
In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex 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.
ET-1 significantly (P < 0.0005) potentiated the hypertensive response of a low dose (50 micrograms/kg i.v.) of clonidine in cervical-sectioned rats.I.c.v. administration of clonidine (1, 2, 4 and 6 micrograms) produced a dose-dependent decrease in blood pressure and heart rate.ET-1 pretreatment (25 ng i.c.v.) transiently blocked the clonidine-induced decrease in blood pressure and heart rate for about 10 min but the hypotension and bradycardia was observed subsequently.