Salt appetite and lesions of the ventral part of the ventral median preoptic nucleus.

Fitts, Douglas A.; Tjepkes, Darrel S.; Bright, Rochelle O.

doi:10.1037/0735-7044.104.5.818

Cited by 72 publications

(57 citation statements)

References 27 publications

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“…The increase in plasma renin activity induced by hypovolemia remains elevated after thirst satiation; this elevation correlates with c-Fos expression in the subfornical organ and, partially, in the lamina terminalis. Neurons in these two structures are activated by angiotensin II and belong to encephalic circuits that subserve sodium appetite mediated by angiotensin II (19)(20)(21)(22)(23)(24). The WD-PR protocol is instrumental for the execution of acute tests aimed at understanding the mechanisms of sodium appetite because it allows one to distinguish thirst from sodium appetite originating from the same treatment, i.e., water deprivation.…”

Section: Thirst and Sodium Appetite Results From Water Deprivationmentioning

confidence: 99%

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

Luca

Vendramini

Pereira

et al. 2007

Braz J Med Biol Res

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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.

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Section: Thirst and Sodium Appetite Results From Water Deprivationmentioning

confidence: 99%

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

Luca

Vendramini

Pereira

et al. 2007

Braz J Med Biol Res

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“…Angiotensin-induced thirst is primarily mediated in the OVLT, subfornical organ, and median preoptic nucleus, and angiotensin-induced sodium appetite originates in the OVLT and median preoptic nucleus, where central osmoreceptors function to maintain constant extracellular osmotic pressure (2,38,39). It is tempting to speculate that increased concentration of Ang-II in these areas may be involved in the mechanism of altered behavior in these mice.…”

Section: Discussionmentioning

confidence: 99%

Glia- and Neuron-specific Expression of the Renin-Angiotensin System in Brain Alters Blood Pressure, Water Intake, and Salt Preference

Morimoto

Cassell

Sigmund

2002

Journal of Biological Chemistry

107

124

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The purpose of this study is to examine the regulation of blood pressure and fluid and electrolyte homeostasis in mice overexpressing angiotensin II (Ang-II) in the brain and to determine whether there are significant physiologic differences in Ang-II production in neurons or glia. Therefore, we generated and characterized transgenic mice overexpressing human renin (hREN) under the control of the glial fibrillary acidic protein (GFAP) promoter (GFAP-hREN) and synapsin-I promoter (SYN-hREN) and bred them with mice expressing human angiotensinogen (hAGT) under the control of the same promoters (GFAP-hAGT and SYN-hAGT). Both GFAP-hREN and SYN-hREN mice exhibited the highest hREN mRNA expression in the brain and had undetectable levels of hREN protein in the systemic circulation. In the brain of GFAP-hREN and SYN-hREN mice, hREN protein was observed almost exclusively in astrocytes and neurons, respectively. Transgenic mice overexpressing both hREN and hAGT transgenes in either glia or neurons were moderately hypertensive. In the gliatargeted mice, blood pressure could be corrected by intracerebroventricular injection of the Ang-II type 1 receptor antagonist losartan, and intravenous injection of a ganglion blocking agent, but not an arginine vasopressin V1 receptor antagonist, lowered blood pressure. These data suggest that stimulation of Ang-II type 1 receptors in the brain by Ang-II derived from local synthesis of renin and angiotensinogen can cause an elevation in blood pressure via a mechanism involving enhanced sympathetic outflow. Glia-and neuron-targeted mice also exhibited an increase in drinking volume and salt preference, suggesting that chronic overexpression of renin and angiotensinogen locally in the brain can result in hypertension and alterations in fluid homeostasis. The peptide angiotensin II (Ang-II)1 is the main circulating effector hormone of the renin-angiotensin system (RAS) and is able to act not only on peripheral vascular structures but also on the central nervous system (CNS) to increase blood pressure (BP) (1). Substantial evidence has accumulated that Ang-II has actions on the CNS including increasing sympathetic outflow, arginine vasopressin (AVP) release, water intake, and salt appetite (2). Existence of a local RAS in the CNS has been suggested, since all components of this system have been reported in the brain. In addition, several lines of evidence point to a contribution of an overactive brain RAS to the hypertensive state in spontaneously hypertensive rats, deoxycorticosterone acetate (DOCA) salt hypertensive rats, Dahl salt sensitive rats, and renal hypertensive rats (3-6).Despite numerous studies demonstrating the important cardiovascular effects of Ang-II or Ang-II receptor antagonists injected into the brain, it remains unclear whether RAS components synthesized in the brain, in particular renin and angiotensinogen (AGT), have an important role in the local synthesis of Ang-II. In the brain, AGT expression is localized mainly in astrocytes (glia) (7,8). To determine whether l...

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“…Fos activation in the same areas occurs during water deprivation (26,41,49). These areas have been implicated by ablation and pharmacological studies to be involved in ANG II-and Na ϩ -depletion-induced Na ϩ intake (3,6,12,13,15,38,39,43,47). The integrity of preoptic periventricular areas such as the OVLT and MnPO, which send projections to the SON, is also necessary for the expression of Fos-ir in the SON in the presence of hyperosmolality or ANG II (49).…”

Section: Discussionmentioning

confidence: 99%

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

Luca

Schoorlemmer

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes. Am J Physiol Regulatory Integrative Comp Physiol 282: R552-R559, 2002; 10.1152/ ajpregu.00295.2000. Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 Ϯ 0.8 ml/2 h; n ϭ 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na ϩ ; 2) decreased blood volume; and 3) reduced total body Na ϩ ; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na ϩ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water. salt intake; hypovolemia; circumventricular organs; dehydration; thirst MODELS OF NA ϩ INGESTION based on selective depletion of the extracellular fluid compartment have revealed several potential mechanisms that control Na ϩ ingestion. These models typically employ combinations of Na ϩ deprivation and depletion to induce hypovolemia. In the rat, Na ϩ ingestion after Na ϩ loss in these models is associated with increased levels of circulating ANG II and aldosterone (9), unloading of baroreceptors (20), and inhibition of oxytocin secretion by dilution of body fluids after the Na ϩ -depleted animals have ingested water (42). Water deprivation is another procedure associated with an increased preference for ingesting NaCl solutions (48). During water deprivation, the obligatory excretion of water coupled with increased natriuresis results in dehydration of both the intracellular and extracellular fluid compartments (21,25,35). Like selective extracellular depletion models of Na ϩ ingestion, water deprivation reduces blood volume and increases plasma renin activity (PRA) and levels of circulating ANG II (8,29,30,35). However, in contrast to the selective extracellular dehydration models, water deprivation is accompanied by reductions, or no changes, in plasma levels of aldosterone (29,34) and by increases in plasma Na ϩ concentration ([Na ϩ ]) and osmolality (29,34,35 ] and osmolality levels are reduced after dehydrated animals drink water.Water-deprived animals clearly prefer to drink water, but there is also considerable ingestion of hypertonic saline solutions wh...

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Salt appetite and lesions of the ventral part of the ventral median preoptic nucleus.

Cited by 72 publications

References 27 publications

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

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

Glia- and Neuron-specific Expression of the Renin-Angiotensin System in Brain Alters Blood Pressure, Water Intake, and Salt Preference

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

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