INCREASE IN SYMPATHETIC TONE DUE TO HIGH SALT INTAKE

我们将确定高(325 MeQ氯化钠/天)和中等高(161 食盐摄入量会导致血压升高和交感神经 正常血压和二肾一夹Goldblatt高血压患者的血管张力 狗。全身动脉压(BP)和髂动脉或肾血流量 将在动物处于放松状态时进行监测。BP被拿下了 通过植入的导管测量血流量 连接在髂骨或肾脏上的流量探头的电磁流量计 动脉。交感神经张力在高盐前后会被量化。 摄入量引起的血压和髂动脉阻力(IVR)的下降 α1受体阻滞剂与腰椎IVR的降低 普鲁卡因致交感神经麻痹。增强型交叉点 高盐饮食引起的声调可归因于中枢或外周 机制(S)将是研究的一个主要目标。另外，有可能 对肾脏的盐诱导效应，然后将信号传输到 中枢神经系统激活交感神经流出会增加 探索过了。最后，我们将调查高血压的可能性 由正常和Goldblatt高血压患者盐摄入量增加所致 狗可能部分是由于心输出量的增加。我们的长期合作 目标是了解盐的摄入量必须达到什么程度和持续多长时间 升高到高于正常水平会导致有害的心血管影响， 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.