Zhang X, Abdel-Rahman A R, Wooles W R
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858.
Eur J Pharmacol. 1992 Nov 3;222(1):81-91. doi: 10.1016/0014-2999(92)90466-h.
This study examined the effects of microinjection of [Arg8]vasopressin (AVP) into the area postrema (AP) on baroreceptor reflex control of heart rate (HR) and sympathetic efferent discharge (SED) in anesthetized rats. Comparable increments in blood pressure evoked by systemic AVP, as opposed to phenylephrine, were associated with significantly greater reflex bradycardia. Similarly, AVP augmented the baroreflex-mediated sympathoinhibition; however, this effect was evident only with the lower increments in arterial pressure (< 45 mm Hg) i.e. following systemic administration of small doses of AVP. Beyond 45 mm Hg there was no further augmentation of baroreflex-mediated sympathoinhibition showing the non-linearity of the response compared to phenylephrine which was linear over a wide range of induced pressure increases. Microinjection of AVP into the AP produced a differential effect on HR and SED responses to baroreceptor activation by systemically administered phenylephrine, the baroreflex slope of HR response was attenuated whereas that of SED was enhanced. Microinjection of the V1 antagonist AVPX (d(CH2)5Tyr(Me)-AVP) into the AP abolished the inhibitory effect of AVP on the baroreceptor-HR response suggesting that V1 receptors are involved in this response. Further, AVPX inhibited the baroreceptor-SED response suggesting that V1 receptors in the AP are tonically involved in modulating the baroreceptor reflex control of SED. Qualitatively similar but smaller responses were obtained following microinjection of AVP into the nucleus tractus solitarii (NTS) suggesting involvement of neural input from the AP to the NTS in AVP-evoked responses in the AP. It is concluded that the AVP receptors in the AP differentially modulates the baroreceptor reflex control of HR and SED.
本研究检测了向麻醉大鼠的最后区(AP)微量注射[精氨酸8]血管加压素(AVP)对心率(HR)压力感受器反射控制及交感神经传出放电(SED)的影响。与去氧肾上腺素不同,全身应用AVP引起的血压同等升高与显著更强的反射性心动过缓相关。同样,AVP增强了压力感受器介导的交感神经抑制;然而,这种效应仅在动脉压升高幅度较小(<45 mmHg)时明显,即小剂量全身应用AVP后。超过45 mmHg时,压力感受器介导的交感神经抑制不再进一步增强,表明与去氧肾上腺素在较宽的诱导压力升高范围内呈线性关系相比,该反应具有非线性。向AP微量注射AVP对全身应用去氧肾上腺素激活压力感受器时的HR和SED反应产生了不同影响,HR反应的压力感受器斜率减弱,而SED的斜率增强。向AP微量注射V1拮抗剂AVPX(d(CH2)5Tyr(Me)-AVP)消除了AVP对压力感受器-HR反应的抑制作用,提示V1受体参与了该反应。此外,AVPX抑制了压力感受器-SED反应,提示AP中的V1受体持续参与调节压力感受器对SED的反射控制。向孤束核(NTS)微量注射AVP后获得了定性相似但较小的反应,提示AP至NTS的神经输入参与了AP中AVP诱发的反应。结论是,AP中的AVP受体对HR和SED的压力感受器反射控制具有不同调节作用。