Hasser E M, Bishop V S
Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri-Columbia.
Circ Res. 1990 Aug;67(2):265-71. doi: 10.1161/01.res.67.2.265.
This study investigated the effect of micropressure injection of the V1 arginine vasopressin (AVP) receptor antagonist into the area postrema on the ability of circulating AVP to augment baroreflex inhibition of renal sympathetic nerve activity (RSNA) in urethane-anesthetized rabbits. In addition, the effects of micropressure injections of AVP into the area postrema on RSNA, arterial pressure, heart rate, and baroreflex control of RSNA were evaluated. Injection of 100 ng (in a 10-nl volume) of AVP antagonist into the area postrema abolished the ability of AVP to enhance baroreflex inhibition of RSNA compared with phenylephrine (-8.84 +/- 0.89 before antagonist versus -4.83 +/- 0.44 %RSNA/mm Hg after antagonist). Normal baroreflex inhibition to phenylephrine (-3.95 +/- 0.26 versus -4.10 +/- 0.33 %RSNA/mm Hg) was unaltered. This dose of AVP antagonist given intravenously or into the adjacent medial nucleus tractus solitarius was without effect. Micropressure injection of AVP directly into the area postrema produced a dose-dependent decrease in RSNA without significant effects on arterial pressure or heart rate. Local injection of 4 +/- 0.6 ng (in a 4-nl volume) of AVP produced an average 27 +/- 3% decrease in resting RSNA. Continuous injection of AVP into the area postrema using short-duration, low-frequency pressure pulses significantly augmented the baroreflex inhibition of RSNA during phenylephrine infusion (during AVP injection, -7.12 +/- 1.60%RSNA/mm Hg; control, -3.38 +/- 0.55 %RSNA/mm Hg). These data support the hypothesis that circulating AVP acts at the area postrema to augment baroreflex inhibition of RSNA by a V1 receptor mechanism.
本研究探讨了向延髓后区微量注射血管升压素（AVP）V1受体拮抗剂对在氨基甲酸乙酯麻醉兔中循环AVP增强压力感受性反射对肾交感神经活动（RSNA）抑制能力的影响。此外，还评估了向延髓后区微量注射AVP对RSNA、动脉血压、心率以及RSNA的压力感受性反射控制的影响。与去氧肾上腺素相比，向延髓后区注射100 ng（10 nl体积）的AVP拮抗剂消除了AVP增强压力感受性反射对RSNA抑制的能力（拮抗剂注射前为-8.84±0.89，注射后为-4.83±0.44 %RSNA/mmHg）。对去氧肾上腺素的正常压力感受性反射抑制（-3.95±0.26与-4.10±0.33 %RSNA/mmHg）未改变。静脉内或向相邻的孤束核内侧核注射该剂量的AVP拮抗剂无效。向延髓后区直接微量注射AVP可使RSNA呈剂量依赖性降低，而对动脉血压或心率无显著影响。局部注射4±0.6 ng（4 nl体积）的AVP可使静息RSNA平均降低27±3%。在去氧肾上腺素输注期间，使用短持续时间、低频压力脉冲向延髓后区持续注射AVP可显著增强压力感受性反射对RSNA的抑制（在AVP注射期间，-7.12±1.60%RSNA/mmHg；对照，-3.38±0.55 %RSNA/mmHg）。这些数据支持以下假设：循环中的AVP通过V1受体机制作用于延髓后区，以增强压力感受性反射对RSNA的抑制。
