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，饮食盐摄入量与血压调节以及高血压的流行和进展有关。然而，盐负荷引起高血压的发生和维持的机制仍有待阐明。本研究使用清醒自由活动的大鼠，旨在验证肾交感神经活动(RSNA)对盐负荷的反应失败参与肾钠排泄受损，从而导致高血压的假设。(1)脑室内(I.C.V.)给予高渗盐水(0.3、0.67和1.0M，1MU1/分钟)引起一种抑制，并伴随着动脉血压的升高，呈剂量相关关系，而心率没有变化。(2)在去窦弓神经的大鼠，与对照水平的…相比，RSNA对高张NACI的抑制作用大大减弱，但仍显著持续。(3)预先给予加压素V_1，但不加V_2受体非肽拮抗剂，可减弱高渗NaCI对正常大鼠RSNA的抑制作用，但对SAD大鼠的抑制作用无进一步影响。这一发现提示动脉压力感受器传入参与了加压素对RSNA的抑制作用。(4)为了阐明内源性加压素对盐负荷的RSNA反应的调节机制，我们在穹隆下器(SF0)、终板血管器(OVLT)、最后区(AP)、下丘脑室旁核(PUN)和视上核(SON)观察了中枢注射高张NaCI诱导的Fos样免疫反应(Fos样免疫反应)。中枢输注高渗NaCI可增加OVLT、PVN、SON和AP的FLI，但不能增加SF0的FLI，且呈强直性依赖。预先给予AVP V1受体拮抗剂后，PVN的FLI显著增加，AP的FLL显著降低，其余区域无明显变化。这一发现表明，在RSNA流出到中央盐负荷的过程中，存在一个由加压素通过PVN和AP激活的“反馈”调制环。较少

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