Patel K P, Schmid P G
Department of Physiology and Pharmacology, School of Medicine, University of South Dakota, Vermillion 57069.
Am J Physiol. 1988 Jun;254(6 Pt 2):H1172-8. doi: 10.1152/ajpheart.1988.254.6.H1172.
To determine whether neural traffic through the median preoptic nucleus (MnPO) is involved in arginine vasopressin (AVP)-mediated bradycardia and sympathoinhibition, we recorded reflex decreases in heart rate (HR) and lumbar sympathetic nerve activity, in response to increases in arterial pressure induced either by intravenous phenylephrine (PE) or AVP before, during, and after local administration of lidocaine (200 nl, 2%) in the MnPO of chloralose-anesthetized rabbits. Base-line blood pressure and HR did not change in response to administration of lidocaine into the MnPO. Blockade of neural traffic (by lidocaine) in the MnPO produced an attenuation of AVP-mediated bradycardia but not the baroreflex-mediated bradycardia caused by PE. Lidocaine in the MnPO did not alter the sympathoinhibition produced with AVP. These results indicate that part of the bradycardia produced by AVP is mediated via forebrain structures such as the MnPO and is selective for bradycardia. Additionally, this response was mimicked by administration of yohimbine, an alpha 2-antagonist, into the MnPO, which suggests that noradrenergic mechanisms are involved in the baroreflex-mediated facilitation of bradycardia by AVP at the level of the MnPO.
为了确定通过视前正中核（MnPO）的神经冲动是否参与精氨酸加压素（AVP）介导的心动过缓和交感神经抑制，我们记录了在氯醛糖麻醉的家兔MnPO局部注射利多卡因（200 nl，2%）之前、期间和之后，静脉注射去氧肾上腺素（PE）或AVP诱导动脉压升高时，心率（HR）和腰交感神经活动的反射性降低。向MnPO注射利多卡因后，基线血压和HR未发生变化。MnPO中神经冲动的阻断（通过利多卡因）使AVP介导的心动过缓减弱，但未使PE引起的压力反射介导的心动过缓减弱。MnPO中的利多卡因并未改变AVP引起的交感神经抑制。这些结果表明，AVP引起的部分心动过缓是通过诸如MnPO等前脑结构介导的，并且对心动过缓具有选择性。此外，向MnPO注射α2拮抗剂育亨宾可模拟这种反应，这表明去甲肾上腺素能机制参与了AVP在MnPO水平介导的压力反射性心动过缓促进作用。
