NEUROPEPTIDES AND CARDIOVASCULAR REGULATION

描述：（改编自应用程序）许多研究表明， 氯化钠（NaCl）摄入量的增加会增加动脉压， 几种高血压模型部分通过激活交感神经 系统 然而，盐是否在神经元中发挥类似的交感神经兴奋作用， 正常有意识的动物是不清楚的。 因此，本提案对 一般假设，增加饮食中的氯化钠确实会增加交感神经系统 活动，但这一行动通常被抵消的直接和间接 （降低血管紧张素II诱导的交感神经兴奋和压力反射 激活）盐的作用，以减少交感神经活性。 为了验证这一 一般假设，将检查以下具体假设。 第一章 急性增加氯化钠增加交感神经活动，但这种影响是 通常通过循环血管紧张素II（AII）的减少来抵消 和压力反射激活。 2)NaCl摄入量的慢性变化直接影响 与交感神经活性、血管加压素和 下丘脑-肾上腺垂体轴，但这些行动是正常的 通过AII的相互变化来抵消。 3)饮食中NaCl的变化 部分通过激活交感神经受体影响交感神经活性4） 慢性增加氯化钠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， 去甲肾上腺素转运体 5)如果两者之间的平衡 NaCl的交感神经兴奋和交感神经抑制作用被破坏， 会产生高血压。 这些假设将在有意识的 通过检查NaCl摄入量变化的急性和慢性影响， 有和没有固定的活性，肾素-血管紧张素系统， 肾和腰交感神经活动，血浆儿茶酚胺，加压素 皮质酮水平和酪氨酸神经节mRNA水平 羟化酶和去甲肾上腺素转运蛋白。

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.