SYMPATHETIC NERVOUS SYSTEM IN NA HYPERTENSION

钠敏感性高血压与内源性或强加的 导致钠潴留的肾功能异常。 一 提出了一个模型，其中积累的钠是负责 激活中枢神经系统以刺激交感神经 系统活动。 交感神经流出的增加导致了 包括肾血管阻力在内的总外周阻力。 的 增加的肾血管阻力导致进一步保留 钠在中枢神经系统上形成正反馈回路。 随着持续的交感神经刺激，动脉压升高 肾灌注压和重建钠平衡。 换句 换句话说，动脉压-钠排泄关系转移到 高动脉压 因此，要检验的中心假设 这一建议是，钠潴留导致激活 交感神经系统和局部血管阻力增加。 为了评估这个模型，将测试三个特定的假设。 第一项研究将调查增加的数量的假设 钠摄入会导致局部交感神经系统的比例升高， 流出（通过测量去甲肾上腺素周转率确定）和 局部血管阻力（如通过多普勒血流探头在 肾动脉、髂动脉和肠系膜动脉）。 因此，钠消耗将 打开模型中提出的反馈回路，预防高血压。 第二项研究将检验交感神经阻断的假设， 通过肾脏去神经支配流出到肾脏将防止 通过干扰肾去甲肾上腺素的增加来治疗高血压 周转率和随后的血管阻力上升。 因此 将防止钠的滞留。 最后的研究将检查 直接假设增加的肾血管阻力是 与钠潴留有关。 肾神经的作用 这一过程将通过研究一组肾脏失神经支配的 大鼠 这些研究将为理解这种关系提供基础 钠诱导的高血压和与之相关的血流动力学变化之间的关系 交感神经系统的激活。 获得的信息 将提供对事件序列的重要见解， 高血压的过程

Sodium-sensitive hypertension is associated with an intrinsic or imposed aberration in renal function which results in the retention of sodium. A model is proposed in which the accumulated sodium is responsible for the activation of the central nervous system to stimulate sympathetic nervous system activity. This increase in sympathetic outflow causes an elevation in total peripheral resistance including renal vascular resistance. The increased renal vascular resistance results in a further retention of sodium creating a positive feedback loop on the central nervous system. With continued sympathetic stimulation, arterial pressure rises increasing renal perfusion pressure and reestablishing sodium balance. In other words, the arterial pressure-sodium excretion relationship is shifted to a higher arterial pressure. Thus, the central hypothesis to be examined in this proposal is that sodium retention causes an activation of the sympathetic nervous system and increase in regional vascular resistance. To evaluate this model, three specific hypotheses will be tested. The first study will investigate the postulate that increasing amounts of sodium intake will cause a proportional elevation in regional sympathetic outflow (as determined by measurements of norepinephrine turnover rate) and regional vascular resistance (as estimated by Doppler flowprobes on the renal, iliac and mesenteric arteries). Accordingly, sodium depletion will open the feedback loop proposed in the model and prevent the hypertension. The second study will test the hypothesis that interruption of sympathetic outflow to the kidneys by renal denervation will prevent the development of hypertension by interfering with the increase in renal norepinephrine turnover rate and subsequent rise in vascular resistance. Thus, the retention of sodium will be prevented. The final study will examine directly the hypothesis that the increased renal vascular resistance is associated with a retention of sodium. The role of the renal nerves in this process will be determined by studying a group of renal denervated rats. These studies will provide a foundation for understanding the relationship between sodium-induced hypertension and hemodynamic changes associated with the activation of the sympathetic nervous system. The information gained will provide significant insights into the sequence of events comprising the hypertensive process.