Role of the alpha(1)- and alpha(2)-adrenoceptors of the paraventricular nucleus on the water and salt intake, renal excretion, and arterial pressure induced by angiotensin II injection into the medial septal area

In this study we investigated the influence of cu-adrenergic antagonists injections into the paraventricular nucleus (PVN) of the hypothalamus on the thirst and salt appetite, diuresis, natriuresis, and presser effects of angiotensin II (ANG II) stimulation of medial septal area (MSA). ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and presser responses. The previous injection of prazosin (an alpha (1)-adrenergic antagonist) into the PVN abolished, whereas previous administration of yohimbine (an alpha (2)-adrenergic antagonist) into the PVN increased the water and sodium intake, urinary, natriuretic, and presser responses induced by ANG ii injected into the MSA. Previous injection of a nonselective alpha -adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and presser responses induced by ANG II injected into the MSA. The present results suggest that alpha -adrenergic pathways involving the PVN are important for the water and sodium excretion, urine and sodium excretion, and presser responses, induced by angiotensinergic activation of the MSA. (C) 2001 Elsevier B.V.

Water deprivation-induced sodium appetite and differential expression of encephalic c-Fos immunoreactivity in the spontaneously hypertensive rat

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Lipopolysaccharide reduces sodium intake and sodium excretion in dehydrated rats

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Episodes of water deprivation enhance daily hypertonic NaCl intake in rats

Water and 1.8% NaCl intake was recorded daily in adult male rats (N = 6) submitted to four water deprivations plus four sodium appetite tests, each at the end of each 7-day interval, or in controls (non-deprived, N = 6). Water deprivation was achieved by removing water and 1.8% NaCl for 24 h. Water was then offered for 2 h. At the end of this period, 1.8% NaCl was also offered in addition to water (sodium appetite test). Average daily 1.8% NaCl intake was enhanced from 5.2 ± 1.0 to 15.7 ± 2.5 ml from the first to the fifth week in the experimental group and was unchanged in the control group. Daily water intake was not altered in either group. Thus, repeated episodes of water deprivation enhance daily NaCl intake.

Effects of central imidazolinergic and alpha2-adrenergic activation on water intake

Non-adrenergic ligands that bind to imidazoline receptors (I-R), a selective ligand that binds to alpha2-adrenoceptors (alpha2-AR) and mixed ligands that bind to both receptors were tested for their action on water intake behavior of 24-h water-deprived rats. All drugs were injected into the third cerebral ventricle. Except for agmatine (80 nmol), mixed ligands binding to I-R/alpha2-AR such as guanabenz (40 nmol) and UK 14304 (20 nmol) inhibited water intake by 65% and up to 95%, respectively. The selective non-imidazoline alpha2-AR agonist, alpha-methylnoradrenaline, produced inhibition of water intake similar to that obtained with guanabenz, but at higher doses (80 nmol). The non-adrenergic I-R ligands histamine (160 nmol, mixed histaminergic and imidazoline ligand) and imidazole-4-acetic acid (80 nmol, imidazoline ligand) did not alter water intake. The results show that selective, non-imidazoline alpha2-AR activation suppresses water intake, and suggest that the action on imidazoline sites by non-adrenergic ligands is not sufficient to inhibit water intake.

Inhibition of sodium appetite by lipopolysaccharide: involvement of alpha(2)-adrenoceptors

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Damage to the central amygdala produces differential encephalic c-fos expression in the water deprivation-partial rehydration protocol

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Involvement of the intermediate nucleus of the lateral septal area on angiotensin II-induced dipsogenic and pressor responses

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Lesions in the central amygdala impair sodium intake induced by the blockade of the lateral parabrachial nucleus

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Lateral parabrachial nucleus and central amygdala in the control of sodium intake

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Moxonidine into the lateral parabrachial nucleus reduces renal and hormonal responses to cell dehydration

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Role of the medial septal area on pilocarpine-induced salivary secretion and water intake

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Serotonergic receptor blockade in the lateral parabrachial nucleus: Different effects on hypertonic and isotonic NaCl intake

Hypertonic NaCl intake is produced by serotonin receptor antagonism in the lateral parabrachial nucleus (LPBN) of dehydrated rats or in rats pretreated with a mineralocorticoid, for example deoxycorticosterone (DOCA), that receive an intracerebroventricular injection (icv) of angiotensin II (ang II). The objective of the present work was to find out whether these two mechanisms are also involved with isotonic NaCl intake. Serotonin receptor blockade by methysergide in the LPBN (4 mu g/0.2 mu l bilaterally) had no effect on 0.15 M NaCl (methysergide: 19.3 +/- 5.2 ml/60 min; vehicle: 19.3 +/- 4.2 ml/60 min; n=7) or water (methysergide: 3.4 +/- 1.4 ml/ 60 min; vehicle 2.2 +/- 0.6 ml/60 min) intake induced by systemic diuretic furosemide combined with low dose of captopril (Furo/Cap). Methysergide treatment 4 days later in the same animals produced the expected enhancement in the 0.3 M NaCl intake induced by Furo/Cap (methysergide: 16.6 +/- 3.5 ml/60 min; vehicle: 6.6 +/- 1.5 ml/60 min). Similar result was obtained when another group was tested first with 0.3 M NaCl and later with 0.15 M NaCl. Isotonic NaCl intake induced by icv ang II was however enhanced by prior DOCA treatment. A de novo hypertonic NaCl intake was produced in another group by the same combined treatment. The results suggest that a facilitatory mechanism like the mineralocorticoid/ang II synergy may enhance NaCl solution intake at different levels of tonicity, while the action of an inhibitory mechanism, like the LPBN serotonergic system, is restricted to the ingestion at hypertonic levels. (c) 2007 Elsevier B.V. All rights reserved.

Central muscarinic receptor subtypes involved in pilocarpine-induced salivation, hypertension and water intake

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Water deprivation-induced sodium appetite

A water deprived animal that ingests only water efficiently corrects its intracellular dehydration, but remains hypovolemic, in negative sodium balance, and with high plasma renin activity and angiotensin II. Therefore, it is not surprising that it also ingests sodium. However, separation between thirst and sodium appetite is necessary to use water deprivation as a method to understand the mechanisms subserving sodium appetite. For this purpose, we may use the water deprivation-partial repletion protocol, or WD-PR. This protocol allows performing a sodium appetite test after the rat has quenched its thirst; thus, the sodium intake during this test cannot be confounded with a response to thirst. This is confirmed by hedonic shift and selective ingestion of sodium solutions in the sodium appetite test that follows a WD-PR. The separation between thirst and sodium appetite induced by water deprivation permits the identification of brain states associated with sodium intake in the appetite test. One of these states relates to the activation of angiotensin II All receptors. Other states relate to cell activity in key areas, e.g. subfornical organ and central amygdala, as revealed by immediate early gene c-Fos immunoreactivity or focal lesions. Angiotensin II apparently sensitizes the brain of the water deprived rat to produce an enhanced sodium intake, as that expressed by spontaneously hypertensive and by young normotensive rat. The enhancement in sodium intake produced by history of water deprivation is perhaps a clue to understand the putative salt addiction in humans.The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009. (C) 2010 Published by Elsevier B.V.