Humoral-sympathetic interaction in the adaptive regulation of body-fluid balance under central salt loading : involvement of arterial baroreceptor and vasopressin.

各种流行病学研究表明，膳食盐摄入量与血压调节和原发性高血压的患病率和进展相关。然而，盐负荷引起高血压的产生和维持的机制仍有待阐明。本研究使用清醒的自由活动大鼠进行，旨在检验以下假设：肾交感神经活动（RSNA）对盐负荷的反应失败参与肾钠排泄受损，导致高血压。(1)脑室内（i.c.v.）给予高渗盐水（0.3、0.67和1.0M，1 μ l/min）引起抑制，伴随着动脉血压以剂量相关的方式增加，而心率没有改变。(2)在去窦弓神经（SAD）大鼠，RSNA对高渗NaCl的抑制作用明显减弱，但仍显著持续，与对照组相比，RSNA对高渗NaCl的抑制作用明显减弱，但仍显著持续。 ...更多信息 El. (3)用加压素V_1预处理能减弱高渗NaCl对正常大鼠RSNA的抑制作用，但对SAD大鼠则无进一步影响。这一发现表明动脉压力感受器输入参与了加压素诱导的RSNA抑制。(4)为了阐明内源性加压素调节RSNA反应的机制，高渗NaCl中枢灌注诱导的Fos样免疫反应（FLI）在穹窿下器（SF 0），终板血管器（OVLT），最后区（AP），下丘脑室旁核（PUN），视上核（SON）。高渗NaCl的中枢输注以张力依赖性方式增加OVLT、PVN、SON和AP的FLI，但不增加SF0的FLI。用AVP V1受体拮抗剂预处理显著增加PVN的FLI，减少AP的FL1，而其他区域没有变化。这一发现表明，存在一个“反馈”调节环激活加压素通过PVN和AP的RSNA流出到中央盐负荷。少

Various epidemiological studies have suggested a correlation of dietary salt intake with blood pressure regulation and the prevalence and progression of essential hypertension. However, the mechanisms responsible for the generation and maintenance of hypertension in response to salt loading remain to be elucidated. The present study, which was conducted using conscious freely moving rats, purported to test the hypothesis that failure of the renal sympathetic nerve activity (RSNA) response to salt loading participates in impaired renal sodium excretion, leading to hypertension.(1) Intracerebroventricular (i.c.v.) administration of hypertonic saline (0.3, 0.67, and 1.0 M, 1 mu1/min) elicited an inhibition accompanied with an increase in arterial blood pressure in a dose-related manner, while the heart rate did not change.(2) In sinoaortic denervated (SAD) rats, the inhibition in RSNA to hypertonic NaCI was greatly attenuated, but still significantly persisted, compared to the control lev … More el.(3) Pretreatment with vasopressin V_1, but not with a V_2-receptor non-peptide antagonist, attenuated hypertonic NaCI-induced inhibition in RSNA in intact rats but did not further affect the inhibition in SAD rats. This finding suggests the involvement of arterial baroreceptor inputs in the vasopressin-induced inhibition in RSNA.(4) To elucidate the mechanisms responsible for the modulation of RSNA response by endogenous vasopressin to salt loading, Fos-like immunoreactivity (FLI) induced by the central infusion of hypertonic NaCI was measured in the subfornical organ (SF0), the organum vasculosum of the lamina terminalis (OVLT), the area postrema (AP), the hypothalamic paraventricular nucleus (PUN), and the supraoptic nucleus (SON). Central infusion of hypertonic NaCI increased FLI in OVLT, PVN, SON, and AP, but not in SF0 , in a tonicity-dependent manner. Pretreatment with AVP V1-receptor antagonist significantly increased FLI in the PVN and decreased FLl in the AP, while other regions did not change. The finding suggests the existence of a "feedback" modulatory loop activated by vasopressin through the PVN and AP on the RSNA outflow to central salt loading. Less