Scheuer D A, Bishop V S
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284, USA.
Am J Physiol. 1996 Jun;270(6 Pt 2):H1963-71. doi: 10.1152/ajpheart.1996.270.6.H1963.
Arginine vasopressin (AVP) has been shown to increase the inhibitory influence of the baroreflex on sympathetic nerve activity by a mechanism involving receptors located in the area postrema. The purpose of these experiments was to study the functional effect of this action of AVP by testing the hypothesis that AVP can buffer its own vasoconstrictor effect by facilitating baroreflex-mediated withdrawal of sympathetic nerve activity. Specifically, we determined 1) if AVP can attenuate increases in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine, and 2) whether the effects of AVP on vascular resistance are associated with appropriate corresponding changes in lumbar sympathetic nerve activity (LSNA). In pentobarbital-anesthetized New Zealand White rabbits the baroreflex was stimulated by phenylephrine-induced elevations in arterial pressure. Baroreflex-mediated changes in heart rate (HR), calculated hindquarter vascular resistance index (R), and LSNA were determined during the simultaneous intravertebral infusion of AVP (0, 0.5, or 1.0 ng.kg-1, min-1). Intravertebral infusion of AVP alone had no effect on resting mean arterial pressure (MAP) but reduced baseline values for LSNA and HR. Intravenous infusion of phenylephrine alone produced dose-dependent increases in MAP and R and decreases in LSNA and HR. The simultaneous infusion of AVP (0.5 or 1.0 ng.kg-1 min-1) and phenylephrine (1.25, 2.5, 5.0, 7.5, and 10.0 micrograms.kg-1.min-1) had no effect on the increase in MAP but attenuated the increases in R and facilitated the reductions in LSNA at all doses of phenylephrine. The higher dose of AVP also enhanced the phenylephrine-induced reductions in HR. In contrast, the intravenous infusion of AVP (1.0 ng.kg-1.min-1) did not alter baroreflex-mediated changes in R, LSNA, or HR. Therefore, we conclude that the action of AVP to increase baroreflex-mediated sympathoinhibition results in an attenuated rise in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine.
精氨酸加压素（AVP）已被证明可通过一种涉及最后区受体的机制，增强压力反射对交感神经活动的抑制作用。这些实验的目的是通过检验AVP可通过促进压力反射介导的交感神经活动撤离来缓冲其自身血管收缩作用这一假设，研究AVP这一作用的功能效应。具体而言，我们确定了：1）AVP是否能在输注另一种血管收缩剂去氧肾上腺素期间减弱后肢血管阻力的增加；2）AVP对血管阻力的影响是否与腰交感神经活动（LSNA）的相应适当变化相关。在戊巴比妥麻醉的新西兰白兔中，通过去氧肾上腺素诱导的动脉压升高来刺激压力反射。在同时经椎内输注AVP（0、0.5或1.0 ng·kg⁻¹·min⁻¹）期间，测定压力反射介导的心率（HR）变化、计算得出的后肢血管阻力指数（R）和LSNA。单独经椎内输注AVP对静息平均动脉压（MAP）无影响，但降低了LSNA和HR的基线值。单独静脉输注去氧肾上腺素使MAP和R呈剂量依赖性增加，使LSNA和HR降低。同时输注AVP（0.5或1.0 ng·kg⁻¹·min⁻¹）和去氧肾上腺素（1.25、2.5、5.0、7.5和10.0 μg·kg⁻¹·min⁻¹）对MAP的升高无影响，但减弱了R的升高，并在所有去氧肾上腺素剂量下促进了LSNA的降低。较高剂量的AVP还增强了去氧肾上腺素诱导的HR降低。相比之下，静脉输注AVP（1.0 ng·kg⁻¹·min⁻¹）并未改变压力反射介导的R、LSNA或HR变化。因此，我们得出结论，AVP增加压力反射介导的交感神经抑制作用，导致在输注另一种血管收缩剂去氧肾上腺素期间后肢血管阻力的升高减弱。
