NEUROPEPTIDES AND CARDIOVASCULAR REGULATION

描述：(根据申请改编)大量研究表明 增加的氯化钠(氯化钠)摄入量增加动脉压。 几种高血压模型部分通过激活交感神经 系统。然而，盐是否在脑内发挥类似的交感兴奋作用 意识正常的动物尚不清楚。因此，这项提案考验着 普遍的假设是增加饮食中的氯化钠确实增加交感神经 活动，但这一行动通常被直接和间接抵消 (减少血管紧张素II引起的交感兴奋和压力感受性反射 激活)盐降低交感神经活性的作用。为了测试这一点 一般假设，我们将检验以下具体假设。1) 氯化钠的急剧增加增加了交感神经的活性，但这种效应是 通常被循环血管紧张素II(AII)的减少所抵消 和压力感受器反射的激活。2)食盐摄入量的慢性变化直接 与交感神经活性、后叶加压素和 下丘脑-肾上腺垂体轴，但这些活动通常是 被所有人的互惠变化所抵消。3)膳食氯化钠的变化 部分通过激活渗透压感受器影响交感神经活动 慢性氯化钠升高对交感神经节后神经元活动的影响 通过改变酪氨酸羟化酶的表达和神经元 去甲肾上腺素转运体。5)如果两者之间的差额 氯化钠的交感兴奋和交感抑制效应被破坏， 就会产生高血压。这些假设将在有意识的情况下得到检验 通过检测氯化钠摄入量变化的急性和慢性影响， 无论是否固定肾素-血管紧张素系统的活性， 肾和腰交感神经活动、血浆儿茶酚胺、加压素 酪氨酸的皮质酮水平和神经节细胞基因水平 羟基酶和去甲肾上腺素转运体。

DESCRIPTION: (Adapted from the application) Numerous studies suggest that increases in sodium chloride (NaCl) intake increase arterial pressure in several hypertensive models in part by activating the sympathetic nervous system. However, whether salt exerts a similar sympathoexcitatory action in normal conscious animals is unclear. Therefore, this proposal tests the general hypothesis that increased dietary NaCl does increase sympathetic activity, but this action is normally counterbalanced by direct and indirect (decreased angiotensin II-induced sympathoexcitation and baroreflex activation) effects of salt to decrease sympathetic activity. To test this general hypothesis, the following specific hypotheses will be examined. 1) Acute increases in NaCl increase sympathetic activity, but this effect is normally counterbalanced by decreases in circulating angiotensin II (AII) and baroreflex activation. 2) Chronic changes in NaCl intake are directly related to changes in sympathetic activity, vasopressin and activity of the hypothalamic-adrenal pituitary axis, but these actions are normally counterbalanced by reciprocal changes in AII. 3) Changes in dietary NaCl influence sympathetic activity in part by activation of osmoreceptors 4) Chronic increases in NaCl influence activity of sympathetic postganglionic neurons by altering expression of tyrosine hydroxylase and the norepinephrine transporter. 5) If the balance between the sympathoexcitatory and sympathoinhibitory effects of NaCl is disrupted, hypertension will be produced. These hypotheses will be tested in conscious rats by examining the acute and chronic effects of changes in NaCl intake, with and without fixing the activity of the renin-angiotensin system, on renal and lumbar sympathetic activity, plasma catecholamines, vasopressin and corticosterone levels and ganglionic mRNA levels for tyrosine hydroxylase and the norepinephrine transporter.