Elsevier

Brain Research

Volume 543, Issue 2, 15 March 1991, Pages 296-300
Brain Research

Sympathetic inhibition and attenuation of spontaneous hypertension by PVN lesions in rats

https://doi.org/10.1016/0006-8993(91)90040-3Get rights and content

Abstract

To determine whether the paraventricular nucleus (PVN) contributes to the development of hypertension in spontanenously hypertensive rats (SHR), we compared cardiovascular responses to ganglionic blockade with hexamethonium or vasopressin antagonism with dPVAVP in sham-operated or PVN lesioned SHR and Wistar-Kyoto rats (WKY). Lesions were produced electrolytically when the rats were 5 weeks old. During the next 3 weeks, tail-cuff measurements showed that the development of hypertension in SHR was inhibited, while systolic pressure in WKY was unaffected. Mean pressures recorded directly from the femoral artery at 8 weeks of age were lower in lesioned than in sham-operated SHR (141 ± 5vs110 ±_3mm Hg, P < 0.05), but not did not differ in corresponding WKY groups (110 ± 4vs112 ± 5mm Hg). Depressor responses to ganglionic blockade induced by i.v. injection of hexamethonium (25 mg/kg) were significantly larger in sham-operated than in lesioned SHR (−41 ± 4%vs−28 ± 3%, P < 0.05). By contrast, vasopressin antagonism with dPVAVP did not alter blood pressure in all rat groups. In 24-h urine samples, excretion of vasopressin was unaffected, but that of norepinephrine was significantly reduced in lesioned SHR. These findings suggest that the PVN contributes to the development of spontaneous hypertension by sympathetic activation without increasing vasopressin secretion.

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