Development of salt-sensitive hypertension in a sensory denervated model: the underlying mechanisms

Wang, Donna H.; Huang, Yan

doi:10.1177/14703203010020012201

Cited by 4 publications

(4 citation statements)

References 15 publications

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“…We have previously shown that development of saltsensitive hypertension induced by sensory denervation can be prevented by AT1 receptor antagonists [2,11]. Direct measurement of plasma renin activity and plasma aldosterone levels confirms that the circulating RAAS is insufficiently suppressed by high salt intake in this model, which may account, at least in part, for the increase in salt sensitivity.…”

Section: Discussionsupporting

confidence: 58%

Increased salt sensitivity induced by impairment of sensory nerves

Wang

Zhao²

2003

Journal of Hypertension

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Despite elimination of urine retention, sensory denervation impairs renal function and leads to an increase in blood pressure in response to high salt intake. The abnormalities in renal function and blood pressure in sensory denervated rats are reversible, at least in part, when high salt intake is withdrawn. These data support the hypothesis that sensory innervation counterbalances the pro-hypertensive systems and serves as a modulator to control salt sensitivity and cardiovascular function.

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Section: Discussionsupporting

confidence: 58%

Increased salt sensitivity induced by impairment of sensory nerves

Wang

Zhao²

2003

Journal of Hypertension

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“…12,13 We showed that neonatal degeneration of capsaicin-sensitive sensory nerves increases blood pressure only when a high salt diet is given. 12,13 Moreover, we have shown that plasma renin activity is higher in sensory denervated rats than in sensory nerve-intact rats in response to a high salt intake, 14 indicating that plasma renin activity is insufficiently suppressed by salt load in the former one. Increased activity of the renin-angiotensin system may stimulate the ET system in this model.…”

Section: Discussionmentioning

confidence: 93%

“…12,13 Moreover, we have shown that plasma renin activity is higher in sensory denervated rats than in sensory nerve-intact rats in response to high salt intake, and that blockade of the AT1 receptors prevents the development of hypertension in this model. 13,14 Angiotensin (Ang II) has been shown to be a stimulus for ET-1 production both in vitro and in vivo. 15,16,17 It is likely that the activated renin-angiotensin system activates the ET system that in turn contributes the development of hypertension in this model.…”

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confidence: 99%

Function and Regulation of Endothelin-1 and Its Receptors in Salt Sensitive Hypertension Induced by Sensory Nerve Degeneration

Wang

2002

Hypertension

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Abstract-To determine the role of endothelin-1 (ET-1) and its receptors in salt-sensitive hypertension induced by sensory nerve degeneration, selective ET A antagonist (ABT-627) and ET B antagonist (A-192621) were used. Newborn Wistar rats were given vehicle or 50 mg/kg capsaicin subcutaneously on the first and second days of life. After the weaning period, male rats were divided into eight groups, and subjected to the following treatments for 2 weeks: control ϩ normal salt diet (ConϩNS, 0.5%), control ϩ high salt diet (ConϩHS, 4%), control ϩ high salt diet ϩ ABT-627 (ConϩHSϩABT-627), control ϩ high salt diet ϩ A -192621 (ConϩHSϩA-192621), capsaicin ϩ normal salt diet (CapϩNS), capsaicin ϩ high salt diet (CapϩHS), capsaicin ϩ high salt diet ϩ ABT-627 (CapϩHSϩABT-627), capsaicin ϩ high salt diet ϩ A -192621 (CapϩHSϩA-192621 Key Words: endothelin Ⅲ receptors, endothelin Ⅲ hypertension, sodium-dependent T he endothelin-1 (ET-1) belongs to a family of endothelium-derived peptides. Endogenous ET-1 is a potent vasoconstrictor and plays a fundamental physiological role in maintenance of blood pressure in human. 1 There are 2 distinct endothelin receptor subtypes, ET A and ET B.2,3 The ET A receptor has a selectively higher expression in vascular smooth muscle cells. 2 Endogenous ET-1 contributes to maintenance of the basal vascular tone and blood pressure via its action on the vascular smooth muscle ET A receptor. 4 ET B receptors are mainly expressed in endothelial cells, as well as in vascular smooth muscle cells and renal epithelium. 2,3,5,6 Endogenous ET-1 via binding to endothelial and renal ET B receptors causes vasodilation and natriuresis that result in a decrease in blood pressure. 4 The overall cardiovascular effect of endogenous ET-1 depends on the balance between ET Aand ET B -mediated effects. 4 In addition to the well-known control by sympathetic nerves, peripheral vascular resistance is regulated by sensory nerves. 7 For example, calcitonin gene-related peptide (CGRP), one of the sensory neurotransmitters, is a potent vasodilator and natriuretic factor. 7 It has been shown that CGRP-containing nerves suppress vasoconstriction mediated by sympathetic nerves. 8 It has also been suggested that the defect in sensory vasodilator function may produce an imbalance that contributes to the development and maintenance of hypertension in spontaneously hypertensive rats (SHR). 9,10,11 In contrast to this genetic model, we have developed a novel salt-sensitive hypertensive model that is sensory nervesdependent. 12,13 We demonstrate that neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to a salt load with a significant increase in blood pressure. 12,13 Moreover, we have shown that plasma renin activity is higher

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“…Moreover, this complex phenomenon of renin and aldosterone in SS or SR will go far toward identifying subjects who will be more susceptible to RAAS-blocking agents. 24…”

Section: Discussionmentioning

confidence: 99%