| Research Abstract |
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
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(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
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