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.
CYP1A1 mRNA expression level was significantly higher in residents with sinus tachycardia or bradycardia than in residents with normal heart rate (1.47×10(-3)(0.87×10(-3), 2.77×10(-3)) vs.1.24×10(-3)(0.64×10(-3), 2.31×10(-3)), P<0.05).
Urotensin-II (U-II) receptors are widely distributed in the central nervous system.Intracerebroventricular (i.c.v.) injection of U-II causes hypertension and bradycardia and stimulates prolactin and thyrotropin secretion.
Low-affinity M(2) receptor binding state mediates mouse atrial bradycardia: comparative effects of carbamylcholine and the M(1) receptor agonists sabcomeline and xanomeline.
Participation of AT1 and AT2 receptor subtypes in the tonic inhibitory modulation of baroreceptor reflex response by endogenous angiotensins at the nucleus tractus solitarii in the rat.
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.