Michelini L C, Bonagamba L G
Department of Physiology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
Hypertension. 1988 Feb;11(2 Pt 2):I75-9. doi: 10.1161/01.hyp.11.2_pt_2.i75.
To determine whether the central vasopressinergic system at the level of nucleus tractus solitarii (NTS) modulates the reflex control of heart rate, we employed a new method for microinjection into the brainstem of conscious, freely moving rats. Baroreceptor reflex function was assessed during pressure changes induced by intravenous administration of phenylephrine (0.25-8 micrograms/kg) and sodium nitroprusside (0.5-16 micrograms/kg) in rats microinjected, through a permanent cannula into the brainstem, with saline, arginine vasopressin (AVP), or an AVP blocker. Baseline levels of pressure and heart rate were not changed by either peptide pretreatment. Restricted injection of AVP (20 ng-0.2 microliter) into the NTS attenuated the reflex bradycardia during pressure increases, with an upward displacement of the baroreceptor reflex function line (p less than 0.01) without change in the sensitivity. Local blockade of endogenous AVP, d(CH2)5Tyr(Me)AVP (1 microgram-0.2 microliter), depressed baroreceptor reflex sensitivity with intense bradycardia to either small or large pressure increases. Baroreceptor reflex control of heart rate in response to decreases in pressure was preserved during pretreatment with AVP, whereas endogenous blockade of AVP increased baroreceptor reflex sensitivity. These effects were specific to the NTS, since in another four rats there were no effects when the injections were made 1 mm above, into the cerebellum. The changes in baroreceptor reflex control of heart rate in conscious, unrestrained rats caused by administration of AVP and its endogenous blockade provide evidence that central vasopressinergic synapses at the NTS are important physiological modulators of baroreceptor reflex function.
为了确定孤束核(NTS)水平的中枢血管加压素能系统是否调节心率的反射控制,我们采用了一种新方法,对清醒、自由活动的大鼠脑干进行显微注射。在通过永久性套管向大鼠脑干显微注射生理盐水、精氨酸血管加压素(AVP)或AVP阻断剂后,静脉注射去氧肾上腺素(0.25 - 8微克/千克)和硝普钠(0.5 - 16微克/千克)诱导压力变化期间,评估压力感受器反射功能。两种肽预处理均未改变压力和心率的基线水平。向NTS限制性注射AVP(20纳克 - 0.2微升)可减弱压力升高期间的反射性心动过缓,压力感受器反射功能线向上移位(p < 0.01),而敏感性无变化。内源性AVP的局部阻断剂d(CH2)5Tyr(Me)AVP(1微克 - 0.2微升)可降低压力感受器反射敏感性,对小幅度或大幅度压力升高均伴有强烈的心动过缓。在AVP预处理期间,压力感受器反射对压力降低时心率的控制得以保留,而内源性阻断AVP则增加了压力感受器反射敏感性。这些效应是NTS特有的,因为在另外4只大鼠中,注射部位在小脑上方1毫米处时没有出现这些效应。AVP给药及其内源性阻断引起的清醒、不受约束大鼠压力感受器反射对心率控制的变化,为NTS处的中枢血管加压素能突触是压力感受器反射功能的重要生理调节因子提供了证据。