SYMPATHETIC NERVOUS SYSTEM AND NITRIC OXIDE IN SALT INDUCED HYPERTENSION

盐敏感性/膳食钠与糖尿病发展之间的联系 高血压被广泛接受。然而，尽管广泛的 在这一领域所做的研究，具体机制（S） 参与盐引起的高血压仍不清楚。远景目标 这项研究项目的一个重要目的是检验饮食中的盐 通过改变血管反应性增加血压，部分通过 交感神经活性增强和一氧化氮抑制 活动/功能。具体目标是：（1）审查机制 参与盐性高血压的发病机制， 心血管、血液动力学和血管反应性，男性和女性， 清醒和去髓的Dahl盐敏感和耐盐大鼠。（二） 阐明参与的信号转导途径和离子通道 一氧化氮、环鸟苷酸、神经递质对盐性高血压的影响 释放和Ca/2+。血压和心率 将通过尾部体积描记法间接测量，以及直接测量 清醒的老鼠心输出量和每搏输出量将使用 计算Cardiomax II和总外周阻力。血管 对硝普钠、苯肾上腺素和去甲肾上腺素的反应性， 肾上腺素能受体和交感神经刺激的影响，以及 Ca/2+通道阻滞剂的作用将在清醒和 去髓老鼠流向离散血管床（主动脉、肠系膜和 肾）将使用跨音速流量计测定。血液样本将 从植入股动脉的动脉导管中采集。 血浆中的儿茶酚胺和cGMP水平将通过高浓度的 高效液相色谱电化学检测 放射免疫分析法。cAMP和cGMP水平， 还将在分离大鼠主动脉中测量细胞内Ca/2+ 内皮细胞从这些研究中获得的数据将提供新的 与性别差异以及心血管和细胞 盐诱发高血压的机制。

The link between salt-sensitivity/dietary sodium and the development of high blood pressure is widely accepted. However, in spite of the extensive research that has been done in this area, the specific mechanism(s) involved in salt-induced hypertension remain unclear. The long-term goal of this research project is to examine the hypothesis that dietary salt increased blood pressure by modifying vascular reactivity, in part, via enhancement of sympathetic activity and suppression of nitric oxide activity/function. The specific aims are: 1) Examine the mechanism(s) involved in the pathogenesis of salt-induced hypertension with emphasis on cardiovascular, hemodynamics and vascular reactivity, in male and female, conscious and pithed Dahl salt-sensitive and salt-resistant rats. 2) Elucidate the signal transduction pathways and ion channels involved in salt-induced hypertension by nitric oxide, cyclic GMP, neurotransmitter release and Ca/2+ in the isolated aorta. Blood pressure and heart rate will be measured indirectly by tail plethysmography as well as directly in conscious rats. Cardiac output and stroke volume will be measured using a Cardiomax II and total peripheral resistance calculated. Vascular reactivity to sodium nitroprusside, phenylephrine and norepinephrine as influence by -adrenoceptors and sympathetic stimulation as well as the effect of Ca/2+ channel blocker will be evaluated in both conscious and pithed rats. Blood flow to discrete vascular beds (aortic, mesenteric and renal) will be determined using a Transonic flow-meter. Blood samples will be collected from arterial catheters implanted in the femoral arteries. Plasma levels of catecholamine and cGMP will be assayed by high performance liquid chromatography with electrochemical detection and radio-immunoassay, respectively. Cyclic AMP and cGMP levels and intracellular Ca/2+ will also be measure din isolated rat aorta endothelial cells. Data derived from these studies will provide new insights related to gender differences and cardiovascular and cellular mechanism(s) involved in salt-induced hypertension.