Ventromedial Hypothalamus Lesions Increase the Dipsogenic Responses and Reduce the Pressor Responses to Median Preoptic Area Activation

Bastos, Rosemary; Menani, José Vanderlei; Saad, Wilson Abrão; Renzi, Antonio; Silveira, Jen; Camargo, Luiz Antônio de Arruda

doi:10.1016/s0031-9384(97)88986-x

Cited by 4 publications

(1 citation statement)

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“…The CVOs feed unto midbrain sites and then to bulbospinal pathways that are critical for the control of sympathetic nervous activity 19 . Activity of the median preoptic area (MnPO), a downstream target of the OVLT and SFO, seems to play a role in many models of hypertension, 20–22 salt appetite 23 and drinking behaviour (of interest because drinking is increased in some forms of salt‐sensitive hypertension) 24,25 . The MnPO, in turn, sends projections to the zona incerta (ZI) and to the paraventricular nucleus of the hypothalamus (PVN).…”

Section: Aetiology Of Salt‐sensitive Hypertensionmentioning

confidence: 99%

A Role for Benzamil‐sensitive Proteins of the Central Nervous System in the Pathogenesis of Salt‐dependent Hypertension

Abrams

Osborn

2008

Clin Exp Pharma Physio

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SUMMARY1. While increasing evidence suggests that salt-sensitive hypertension is a disorder of the central nervous system, little is known about the critical proteins (e.g., ion channels or exchangers) that play a role in the pathogenesis of the disease. 2.Central pathways involved in the regulation of arterial pressure have been investigated. In addition, systems such as the renin-angiotensin-aldosterone axis, initially characterized in the periphery, are present in the central nervous system, and seem to play a role in the regulation of arterial pressure. 3.Central administration of amiloride, or its analogue benzamil hydrochloride, has been shown to attenuate several forms of salt-sensitive hypertension. In addition, intracerebroventricular (ICV) benzamil effectively blocks pressor responses to acute osmotic stimuli, such as ICV hypertonic saline. Amiloride or its analogues have been shown to interact with the brain renin-angiotensin-aldosterone system (RAAS) and to effect the expression of endogenous ouabain-like compounds; both could play a role in the interaction between amiloride compounds and arterial pressure. Peripheral treatments with benzamil, even at higher doses than those given centrally, have little or no effect on arterial pressure. These data provide strong evidence that benzamil-sensitive proteins (BSPs) of the central nervous system play a role in cardiovascular responsiveness to sodium. 4.Mineralocorticoids have been linked to human hypertension; many patients with essential hypertension respond well to pharmacological agents antagonizing the mineralocorticoid receptor (MR), and certain genetic forms of hypertension are due to chronically elevated levels of aldosterone. The deoxycorticosterone acetate (DOCA) -salt model of hypertension is a benzamil-sensitive model that incorporates several factors implicated in the etiology of human disease, including mineralocorticoid action and increased dietary sodium. The DOCA-salt model is ideal for investigating the role of BSPs in the pathogenesis of hypertension, because mineralocorticoid action has been shown to modulate the activity of at least one benzamil-sensitive protein, the epithelial sodium channel (ENaC). 5.Characterizing the BSPs involved in the pathogenesis of hypertension may provide a novel clinical target. Further studies are necessary to determine which BSPs are involved, and where in the nervous system they are located.

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