Berecek K H
J Cardiovasc Pharmacol. 1986;8 Suppl 7:S76-80. doi: 10.1097/00005344-198600087-00015.
Using techniques of intracerebroventricular administration of vasopressin, microinjection of vasopressin into specific brain nuclei, electrical stimulation, and ablation of specific nuclei, we found that vasopressin, through an effect on central neural structures, increases mean arterial pressure and heart rate via an increase in sympathetic outflow and that deoxycorticosterone acetate (DOCA)-salt hypertensive rats show increased sensitivity and responsiveness to the central effects of vasopressin. Furthermore, we found that an important central target area for the cardiovascular effects of vasopressin is the pontine nucleus locus coeruleus. Ablation of the locus coeruleus markedly attenuates the cardiovascular effects of vasopressin as well as the development of DOCA-salt hypertension. Taken together, our results suggest a link between vasopressin, the locus coeruleus, and the sympathetic nervous system in normal cardiovascular regulation as well as in the pathogenesis of DOCA-salt hypertension. Our studies support the hypothesis that vasopressin modifies sympathetic drive through an action on central neural target areas, such as the locus coeruleus controlling sympathetic outflow. Our data further suggests that vasopressin may participate in the pathogenesis of DOCA-salt hypertension by inducing stimulation of the sympathetic nervous system at the region of the locus coeruleus in this model.
运用脑室内注射加压素、向特定脑核微量注射加压素、电刺激以及损毁特定脑核等技术,我们发现,加压素通过作用于中枢神经结构,经由增加交感神经传出冲动来升高平均动脉压和心率,并且醋酸脱氧皮质酮(DOCA)-盐高血压大鼠对加压素的中枢效应表现出更高的敏感性和反应性。此外,我们发现,加压素对心血管系统产生作用的一个重要中枢靶区是脑桥蓝斑核。损毁蓝斑核可显著减弱加压素的心血管效应以及DOCA-盐高血压的发展。综上所述,我们的结果表明,在正常心血管调节以及DOCA-盐高血压的发病机制中,加压素、蓝斑核和交感神经系统之间存在联系。我们的研究支持这样一种假说,即加压素通过作用于中枢神经靶区(如控制交感神经传出冲动的蓝斑核)来改变交感神经驱动。我们的数据进一步表明,在该模型中,加压素可能通过在蓝斑核区域诱导交感神经系统兴奋而参与DOCA-盐高血压的发病机制。