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

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.

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.

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

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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.

Physiological diversity in tolerance to water deprivation among species of South American desert rodents

Rodents from and and semi-arid deserts are faced with the problem of water conservation. The physiological responses of small rodents to such conditions have been intensively investigated over broad geographically disjunct areas. Despite the presence of xeric habitats in South America since the late Tertiary, some studies suggest that sigmodontine South-American desert rodents do not display the same diversity of physiological responses at the species level as those observed in other desert-dwelling species of rodents. In this paper, we analyzed the physiological responses to water deprivation, at the interespecific and interindividual level, among eight species of sigmodontine desert-dwelling rodents from different geographical areas within South-American deserts. Using randomization tests, we found no significant phylogenetic signal for resistance to water deprivation or for individual variability in this response. Contrary to our initial predictions, we observed that sigmodontine rodents from arid/semi-arid habitats (Monte Desert) had significantly lower rates of body mass loss per day (higher tolerances to water deprivation) than species from the hyperarid deserts. We showed that sigmodontine rodents from South America showed a remarkable diversity of physiological mechanisms for coping with water shortage resulting from different evolutionary adaptive strategies. This diversity, however, displays a rather unexpected pattern in terms of its geographical distribution. (c) 2007 Elsevier Ltd. All rights reserved.

NATRIURESIS, NOT SEIZURES, INDUCED BY CHOLINERGIC STIMULATION OF THE LOCUS-CERULEUS IS AFFECTED BY FOREBRAIN LESIONS AND WATER-DEPRIVATION

Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.

Antagonism of the renin-angiotensin system and water deprivation-induced NaCl intake in rats

Adult male rats (n = 5-7 per group) were water deprived for 24 h with only food available. Then they had access to water for 2 h. At the end of the 2 h, 1.5% NaCl was offered to the animals and the intake was measured for another 2 h. The rats drank an average of 9.8 +/- 3.0 ml/120 min of 1.5% NaCl; water intake during this time was negligible (not more than 1.0 ml/120 min). Captopril injected IP at the doses of 12 and 24 mg/kg induced 60-90% inhibition of the intake. Losartan or PD123319 injected ICV induced 50-80% inhibition of the intake. Losartan (80 nmol) inhibited the intake at a lower dose than PD123319 (160 nmol). Neither losartan nor PD123319 inhibited 10% sucrose intake. The inhibition of 1.5% NaCl intake was not related to alterations in arterial pressure. The results show that the antagonism of the renin-angiotensin system inhibits the 1.5% NaCl intake induced by water deprivation. The inhibition induced by the angiotensin II antagonists suggest that this peptide is important for the control of salt intake induced by water deprivation.

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: influence of sodium intake

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Enhanced Expression of Heme Oxygenase-1 and Carbon Monoxide Excitatory Effects in Oxytocin and Vasopressin Neurones During Water Deprivation

A growing body of evidence indiates that carbon monoxide (CO) acts as a gas neurotransmitter within the central nervous system. Although CO has been shown to affect neurohypophyseal hormone release in response to osmotic stimuli, the precise sources, targets and mechanisms underlying the actions of CO within the magnocellular neurosecretory system remain largely unknown. In the present study, we combined immunohistochemistry and patch-clamp electrophysiology to study the cellular distribution of the CO-synthase enzyme heme oxygenase type 1 (HO-1), as well as the actions of CO on oxytocin (OT) and vasopressin (VP) magnocellular neurosecretory cells (MNCs), in euhydrated (EU) and 48-h water-deprived rats (48WD). Our results show the expression of HO-1 immunoreactivity both in OT and VP neurones, as well as in a small proportion of astrocytes, both in supraoptic (SON) and paraventricular (PVN) nuclei. HO-1 expression, and its colocalisation with OT and VP neurones within the SON and PVN, was significantly enhanced in 48WD rats. Inhibition of HO activity with chromium mesoporphyrin IX chloride (CrMP; 20 mu m) resulted in a slight membrane hyperpolarisation in SON neurones from EU rats, without significantly affecting their firing activity. In 48WD rats, on the other hand, CrMP resulted in a more robust membrane hyperpolarisation, significantly decreasing neuronal firing discharge. Taken together, our results indicate that magnocellular SON and PVN neurones express HO-1, and that CO acts as an excitatory gas neurotransmitter in this system. Moreover, we found that the expression and actions of CO were enhanced in water-deprived rats, suggesting that the state-dependent up-regulation of the HO-1/CO signalling pathway contributes to enhance MNCs firing activity during an osmotic challenge.

The role of leptin and ghrelin in appetite regulation in the Australian Spinifex hopping mouse, Notomys alexis, during long-term water deprivation

Water deprivation of the Spinifex hopping mouse, Notomys alexis, induced a biphasic pattern of food intake with an initial hypophagia that was followed by an increased, and then sustained food intake. The mice lost approximately 20% of their body mass and there was a loss of white adipose tissue. Stomach ghrelin mRNA was significantly higher at day 2 of water deprivation but then returned to the same levels as water-replete (day 0) mice for the duration of the experiment. Plasma ghrelin was unaffected by water deprivation except at day 10 where it was significantly increased. Plasma leptin levels decreased at day 2 and day 5 of water deprivation, and then increased significantly by the end of the water deprivation period. Water deprivation caused a significant decrease in skeletal muscle leptin mRNA expression at days 2 and 5, but then it returned to day 0 levels by day 29. In the hypothalamus, water deprivation caused a significant up-regulation in both ghrelin and neuropeptide Y mRNA expression, respectively. In contrast, hypothalamic GHSR1a mRNA expression was significantly down-regulated. A significant increase in LepRb mRNA expression was observed at days 17 and 29 of water deprivation. This study demonstrated that the sustained food intake in N. alexis during water deprivation was uncoupled from peripheral appetite-regulating signals, and that the hypothalamus appears to play an important role in regulating food intake; this may contribute to the maintenance of fluid balance in the absence of free water.

Differential impact of acclimation and acute water deprivation in the expression of key transcription factors in soybean roots.

2016