Webb R L, Osborn J W, Cowley A W
Am J Physiol. 1986 Dec;251(6 Pt 2):H1244-51. doi: 10.1152/ajpheart.1986.251.6.H1244.
Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were recorded during graded infusions of arginine vasopressin (AVP), angiotensin II (ANG II), and phenylephrine (PE) in conscious, unrestrained, sinoaortic-denervated (SAD) and normal rats. Base-line MAP, CO, and TPR values before infusion were not different between groups. HR values were significantly higher in SAD rats. Dose-response curves indicated that there was a similar enhancement in pressor sensitivity to AVP, ANG II, and PE in the absence of the baroreceptors. Pressor responses to AVP were buffered by offsetting decreases of CO. Similar elevations in MAP evoked a 50% greater reduction in CO with AVP, and HR decreased 1.5 times as much with AVP than with ANG II or PE. The dose of AVP required to raise MAP by 25 mmHg in control rats resulted in similar falls of CO in SAD rats, whereas HR responses to AVP were attenuated significantly in SAD rats. We conclude that baroreceptor buffering of AVP-induced pressor responses is due principally to reflex reduction of TPR. Furthermore, CO suppression was not baroreflex-mediated, whereas bradycardia was reflex dependent. Finally, in rats, AVP does not appear to interact with the baroreceptor reflexes in a manner unique from other vasoconstrictor agents to buffer MAP.
在清醒、未束缚、去窦主动脉神经支配（SAD）和正常大鼠中，在分级输注精氨酸加压素（AVP）、血管紧张素II（ANG II）和去氧肾上腺素（PE）期间记录平均动脉压（MAP）、心率（HR）、心输出量（CO）和总外周阻力（TPR）。输注前的基线MAP、CO和TPR值在各组之间无差异。SAD大鼠的HR值显著更高。剂量反应曲线表明，在没有压力感受器的情况下，对AVP、ANG II和PE的升压敏感性有类似增强。对AVP的升压反应通过抵消CO的降低而得到缓冲。MAP的类似升高引起AVP使CO降低的幅度比ANG II或PE大50%，并且AVP使HR降低的幅度是ANG II或PE的1.5倍。在对照大鼠中使MAP升高25 mmHg所需的AVP剂量在SAD大鼠中导致类似的CO下降，而SAD大鼠对AVP的HR反应显著减弱。我们得出结论，压力感受器对AVP诱导的升压反应的缓冲主要是由于TPR的反射性降低。此外，CO抑制不是压力反射介导的，而心动过缓是反射依赖性的。最后，在大鼠中，AVP似乎不会以与其他血管收缩剂不同的方式与压力感受器反射相互作用来缓冲MAP。
