INCREASE IN SYMPATHETIC TONE DUE TO HIGH SALT INTAKE

我们将确定是否高（325 meq NaCl/天）和中等高（161 meq NaCl/天）盐摄入量导致血压升高和交感神经系统 正常血压与两肾一夹高血压的血管张力 狗 全身动脉血压（BP）和髂动脉或肾动脉血流量 将在动物处于放松状态时进行监测。 BP被拿走了 通过植入的导管，用 与髂动脉或肾动脉上的流量探头耦合的电磁流量计 动脉 在高盐之前和之后将对交感神经张力进行定量 通过降低血压和髂血管阻力（IVR）引起的摄入 α 1受体阻滞剂和腰椎间盘突出症产生的IVR降低 普鲁卡因导致交感神经麻痹 是否增强了症状 高盐饮食引起的紧张可归因于中枢或外周 机制将是研究的一个主要目标。 另外， 盐对肾脏的诱导作用，然后将信号传输到 中枢神经系统激活增加交感神经流出将是 探讨了 最后，我们将研究高血压 由于正常和高血压患者盐摄入量增加 狗可能部分是由于心输出量的增加。 我们的长期 目标是了解盐的摄入量必须达到什么程度和多长时间， 高于正常水平，导致有害的心血管效应， 这些影响的机制。

We will determine whether high (325 meq NaCl/day) and moderately high (161 meq NaCl/day) salt intake causes increased blood pressure and sympathetic vascular tone in normotensive and 2-kidney one clip Goldblatt hypertensive dogs. Systemic arterial blood pressure (BP) and iliac or renal blood flow will be monitored while the animals are in a relaxed state. BP is taken through an implanted catheter and blood flow is measured with an electromagnetic flowmeter coupled to a flow probe on the iliac or renal artery. Sympathetic tone will be quantitated before and after high salt intake by the decrease in BP and iliac vascular resistance (IVR) caused by Alpha1-receptor blockade and the decrease in IVR produced by lumbar sympathetic nerve paralysis with procaine. Whether enhanced symphatetic tone caused by high salt diet is attributable to central or peripheral mechanism(s) will be a major objective of the study. Also, the possibility of a salt-induced effect on the kidney which then transmits a signal to the central nervous system to activate increased sympathetic outflow will be explored. Lastly, we will investigate the possibility that hypertension resulting from increased salt intake in normal and Goldblatt hypertensive dogs may be due in part to an increase in cardiac output. Our long-term objectives are to learn to what degree and for how long salt intake must be elevated above normal to cause deleterious cardiovascular effects and the mechanism of these effects.