Presystemic signals in the control of thirst, salt appetite, and vasopressin secretion

Stricker, Edward M.; Hoffmann, Myriam L.

doi:10.1016/j.physbeh.2007.04.007

Cited by 73 publications

(60 citation statements)

References 55 publications

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“…Recent experiments have found that DOCA-treated rats drank different volumes of 0.15 M -0.50 M NaCl solution depending on its concentration, with less consumed the more concentrated the fluid was (16). These and other results suggested that saline-drinking bouts are terminated by early inhibitory signals associated with increases in the osmolality of fluid emptied from the stomach (as might be detected by visceral osmoreceptors) and/or in the volume of fluid contained in the stomach and small intestine (as might be detected by stretch receptors on those organs) (16,20). The present experiments examined the generality of those findings by determining whether presystemic signals also inhibit NaCl consumption by Na + -deprived adrex rats.…”

mentioning

confidence: 78%

“…4). If visceral osmo-or Na + -receptors are located in that proximal portion of the small intestine, as suggested recently (13,20), then those receptors may be stimulated before intestinal stretch receptors can detect distension.Increasing intestinal distension allows for an expanded surface area from which fluid can be absorbed into the mesenteric vasculature. Inspection of Fig.…”

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confidence: 86%

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Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Bykowski

Smith

Stricker

2007

Physiology & Behavior

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Adrenalectomized (adrex) rats adaptively increase NaCl intake to compensate for the uncontrolled loss of Na + in urine due to the absence of aldosterone. After a period of NaCl deprivation, they ingest saline avidly but stop drinking before hyponatremia is repaired. The present experiments determined whether presystemic signals inhibit further NaCl intake, and whether gastric emptying of Na + is modulated according to the concentration of ingested NaCl solution. After overnight deprivation, adrex rats consumed 0.05 M and 0.15 M NaCl at a maximally fast rate (~1.7 ml/min) and emptied ingested fluid from the stomach at a slower but maximally fast rate (~1.1 ml/min). When 0.30 M NaCl was consumed instead, fluid intake still was maximally fast but gastric emptying slowed in proportion to concentration so that the emptying of Na + was comparable to that observed when 0.15 M NaCl was ingested (~0.13 meq/min). When 0.50 M NaCl was consumed, intake slowed proportionately so that Na + consumption was comparable to that observed when 0.30 M NaCl was ingested (~0.5 meq/min). NaCl intake appeared to be inhibited both by the concentration of saline emptied from the stomach and by the volume of ingested fluid in the stomach and small intestine. Gastric emptying also slowed proportionately when 0.50 M NaCl was consumed, as if the rats were regulating the delivery of Na + to the small intestine. These results suggest that adrex rats can detect the volume and concentration of ingested NaCl solution and integrate these two variables, and thereby modulate the rates of Na + intake and gastric emptying. Keywords adrenalectomy; DOCA; gastric distension; gastric emptying; salt appetite Adrenalectomized (adrex) rats adaptively compensate for the uncontrolled loss of Na + in urine due to the absence of aldosterone by consuming sufficient NaCl solution to maintain Na + balance (12). When adrex rats are deprived of dietary NaCl and become Na + -deficient, they drink a large bout of saline when it becomes available again but stop before their physiological need for Na + has been fully satisfied (9). The issues under investigation in the present experiments are the bases for the termination of that initial drinking bout and the fate of the ingested fluid.A pronounced salt appetite also is seen in rats given daily injections of the synthetic mineralocorticoid, deoxycorticosterone acetate (DOCA) (11), even though those animals have Address for editorial correspondence: Dr. Edward M. Stricker, Department of Neuroscience, 360 Langley Hall, University of Pittsburgh, Pittsburgh, PA 15260, Phone: 412/624-4569, Fax: 412/624-9198, e-mail: stricker@bns.pitt.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors m...

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confidence: 78%

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confidence: 86%

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Bykowski

Smith

Stricker

2007

Physiology & Behavior

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“…The first is the presence of anticipatory mechanisms: osmotically induced hormonal or behavioral responses occur much faster than any other change detected in the ECF, that is, before the information can reach the central osmosensors. Thus, water drinking quenches thirst, [155][156][157][158] and changes in gastric osmotic load due to water or food intake modulate AVP secretion 159 -161 before any alteration in ECF osmolarity. Second, local changes in osmotic concentration (for example, due to oral or intragastric sodium or water load) elicit larger regulatory responses than what the same load provokes when administered intravenously 162 Based on these findings, peripheral osmoreceptors have been proposed to localize to the oropharyngeal area, 163 along the gastrointestinal tract (stomach, duodenum), 159,164,165 in the liver, 166 portal vein, 167,168 and splanchnic mesentery.…”

Section: Peripheral Osmosensorsmentioning

confidence: 99%

Osmosensory Mechanisms in Cellular and Systemic Volume Regulation

Pedersen

Kapùs

Hoffmann

2011

Journal of the American Society of Nephrology

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Osmotic water flux across the plasma membrane, resulting in altered cellular volume and ionic strength, severely affects cell function. Most vertebrates counteract such perturbations by maintaining a remarkably stable osmolarity in the extracellular fluid (ECF; in mammals, close to 300 mOsm) and by possessing a variety of generally indirect mechanisms of volume regulated ion transport that allow individual cells to monitor and recover their volume following osmotic swelling or shrinkage. The purpose of this review is to outline the current evidence on how cells sense volume perturbations, with particular focus on mechanisms relevant to the kidneys and to ECF osmolarity/whole body volume homeostasis. The signaling events downstream from the osmosensor and the volume regulatory ion transport proteins involved in the process of regulatory volume decrease (RVD) and regulatory volume increase (RVI) after osmotic swelling and shrinkage, respectively, have been reviewed in detail elsewhere. [1][2][3][4] We also discuss a variety of pathophysiological consequences to disturbances in cell-volume sensing.Two terms are used to describe the osmotic relation between the cell and its surroundings: osmolarity and tonicity. Osmolarity is an absolute term that can be measured typically by freezing-point depression, whereas tonicity is defined by the osmotic gradient across a membrane; by definition, hypertonic exposure causes cell shrinkage, and hypotonic exposure causes cell swelling. In contrast, exposure of a cell to a fully permeable osmolyte has an osmotic effect, but no tonicity effect, and does not alter cell volume. In this review, we will use the terms osmosensor and osmosensing unless there is direct experimental evidence that the modality sensed is tonicity that perturbs cell volume. Tonicity will be used for describing the experimental perfusion of a cell with an anisotonic solution or for processes in which a direct dependence on cell volume, rather than osmolarity, is established. BASAL MECHANISMS IN CELLULAR VOLUME SENSINGArguably the most fundamental issue in osmosensing is precisely what is sensed when a cell is exposed to osmotic stress. Surprisingly, this issue is still not resolved completely. At least three types of osmotic stress signals can be identified in eukaryotic cells: changes in macromolecular crowding, ionic strength, and mechanical or chemical changes in the lipid bilayer or the extracellular matrix (ECM) and the cytoskeleton to which it is tethered. 1,5-7 Osmosensory systems respond to these signals, resulting in a series of signal transduction events that, in turn, activate volume regulatory, protective, and adaptive events. 1 All three types of osmotic stress signals can be part of the osmosensory machinery in various model systems, and, in some cases, several signals may contribute to a given response, as examples that follow will show.A poorly understood issue in volume sensing is where, subcellularly, the sensors are located and how that impacts on the signals that can be perceived. As discu...

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“…Reduction in gastric emptying may signal satiety for hypertonic NaCl intake (39). LPS reduces gastric emptying, an effect reduced by YOH in mice (21).…”

Section: Protocolsmentioning

confidence: 99%

“…LPS also has the potential to recruit a short-latency peripheral inhibitory mechanism, such as reduction in gastric emptying, thereby increasing satiating signals through osmo-or mechanoreceptors lying in the wall of the stomach to inhibit sodium appetite (39). This idea is consistent with the increased stomach liquid content in the presence of LPS, but contradicted by the experiments with YOH: whereas YOH, an ␣ 2 -adrenoceptor antagonist, failed to influence the reduction in gastric emptying, it nonetheless restored sodium appetite in LPStreated rats.…”

Section: Sodium Appetite Test and Changes In Map And Hr In Sodium-depmentioning

confidence: 99%

Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors

Almeida

David²,

Constancio³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Lipopolysaccharide (LPS), an endotoxin from the wall of Escherichia coli, produces a general behavioral inhibition and affects several aspects of fluid-electrolyte balance. LPS inhibits thirst; however, it is not clear if it also inhibits sodium appetite. The present results show that LPS (0.3-2.5 mg/kg body wt) injected intraperitoneally produces a dose-dependent reduction of sodium appetite expressed as 0.3 M NaCl intake induced by sodium depletion (furosemide plus removal of ambient sodium for 24 h). The high doses of LPS (1.2-2.5 mg/kg) also produced transient hypothermia at the beginning of the sodium appetite test; however, no dose produced hyperthermia. LPS also increased the stomach liquid content (an index of gastric emptying) after a load of 0.3 M NaCl given intragastrically by gavage to sodium-depleted rats. The ␣ 2-adrenoceptor antagonist yohimbine (5 mg/kg ip) abolished the effect of LPS on 0.3 M NaCl intake, without changing the effect of LPS on gastric emptying. Injection of RX-821002 (160 nmol), another ␣ 2-adrenoceptor antagonist, in the lateral cerebral ventricle (LV) also reversed the inhibition of sodium appetite produced by LPS. Yohimbine intraperitoneally or RX-821002 in the LV alone had no effect on sodium intake. Although yohimbine plus LPS produced a slight hypotension, RX-821002 plus LPS produced no change in arterial pressure, suggesting that the blockade of the effects of LPS on sodium intake by the ␣ 2-adrenoceptor antagonists is independent from changes in arterial pressure. The results suggest an inhibitory role for LPS in sodium appetite that is mediated by central ␣ 2-adrenoceptors. sodium intake; endotoxin; arterial pressure; RX-821002; fluid balance; sickness behavior LIPOPOLYSACCHARIDE (LPS), an endotoxin derived from the wall of gram-negative bacteria, triggers an array of behavioral and systemic responses, grouped under the name of "sickness behavior" (7).Sickness behavior has been hypothesized to be an adaptive syndrome of behavioral and physiological responses by animals coping with infectious pathogens (7). Reduced activity, feeding, and drinking are some of the behavioral alterations induced by infection. These alterations may help to shift internal energy production to increase body temperature and sustain fever, an important mechanism to combat infection.It is possible that the reduced drinking that occurs in sickness behavior is also associated with a general effect on body-fluid balance because LPS releases hormones that influence such balance (4) and reduces several aspects related to sodium metabolism: sodium transport in the gut (5), natriuresis (1, 31), and a rapidly developing sodium intake induced by the diuretic furosemide combined with a low dose of the converting enzyme inhibitor captopril or Furo/Cap (1).In the previous study (1), LPS injected before Furo/Cap treatment inhibited sodium intake produced within 2 h, but it also reduced sodium excretion, which may affect sodium intake. Thus it is not possible to definitively conclude if the inhibition of sodiu...

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Presystemic signals in the control of thirst, salt appetite, and vasopressin secretion

Cited by 73 publications

References 55 publications

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Osmosensory Mechanisms in Cellular and Systemic Volume Regulation

Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors

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Presystemic signals in the control of thirst, salt appetite, and vasopressin secretion

Cited by 73 publications

References 55 publications

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

Osmosensory Mechanisms in Cellular and Systemic Volume Regulation

Inhibition of sodium appetite by lipopolysaccharide: involvement of α2-adrenoceptors

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Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors