Central Oxytocin Mediates Inhibition of Sodium Appetite by Naloxone in Hypovolemic Rats

Blackburn, R. E.; Stricker, Edward M.; Verbalis, Joseph G.

doi:10.1159/000126236

Cited by 61 publications

(27 citation statements)

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“…The OTKO mice also showed elevated intakes after 24 hours of water restriction, a condition that increases both hematocrit and plasma osmolality. 21 These results are supportive of studies in rats that showed that PEG-induced salt intake was inhibited by central OT administration, 9 whereas lesions of the brain OT system increased the response to hyperosmolality. 11 In contrast, an OT antagonist had no effect on PEGinduced salt intake.…”

Section: Discussionsupporting

confidence: 68%

“…11 In contrast, an OT antagonist had no effect on PEGinduced salt intake. 9 Studies that compared the effect of volume expansion with hypertonic mannitol versus saline showed that saline intake was responsive to osmolality changes, rather than sodium. 11 To proceed to the next stage, we determined whether a stimulus to volume receptors alters salt intake in mice and whether the response is changed in the OT gene-disruption model.…”

Section: Discussionmentioning

confidence: 99%

“…Time-course and pharmacologic antagonist studies suggest that PEG-induced OT release inhibits salt intake. 9,10 There is also evidence for an OT-specific response to increased osmolality, rather than sodium. 11 A role for central angiotensin II (Ang II) in mediating the OT responses was suggested, because OT antagonists potentiated the salt intake induced by Ang II.…”

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confidence: 99%

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Salt Appetite and the Renin-Angiotensin System

et al. 2003

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Abstract-To explore the role of oxytocin in the regulation of salt appetite and blood pressure, we conducted studies in oxytocin gene-knockout mice and determined (1) blood pressure and heart rate during day and night periods, (2) salt appetite after iso-osmotic volume depletion, and (3) salt appetite and blood pressure after central injection of angiotensin II. Long-term arterial catheters were inserted, and blood pressure and heart rate were recorded for 24 hours. There was a modest decrease in blood pressure and heart rate in knockout mice. Salt appetite was measured with a 2-bottle choice (water and 2% NaCl), with measurement of licking activity. Mice were injected subcutaneously with 30% polyethylene glycol (0.5 mL), and voluntary intakes were measured for 24 hours. Knockout mice consumed 3 times the amount of NaCl than did controls, 276Ϯ77 vs 90Ϯ38 licks/24 h (PϽ0.05). Water consumption was similar between groups. Angiotensin II (5, 50, and 200 ng/3 L) injected intracerebroventricularly produced dose-related increases in intake, with no differences between the groups. The 50-ng dose of angiotensin II elicited salt and water intakes of 151Ϯ43 vs 160Ϯ33 licks and 250Ϯ53 vs and 200Ϯ51 licks, respectively (control vs knockout). The pressor response to angiotensin II was not different between the groups. Results suggest that oxytocin plays a role in the regulation of blood pressure and salt appetite, specifically as mediated by volume receptors, and that the renin-angiotensin system is not involved in these changes. Key Words: mice Ⅲ blood pressure Ⅲ angiotensin Ⅲ renin-angiotensin system Ⅲ water-electrolyte balance Ⅲ sodium O xytocin (OT) is a posterior pituitary hormone that has a wide range of effects on target tissues from the brain to the vasculature. Although OT is well recognized for its role in reproduction, recent discoveries suggest that OT is also involved in regulation of fluid balance, blood pressure (BP), and cardiac function. [1][2][3][4] Oxytocinergic neurons innervate brain regions important in cardiovascular control, such as the nucleus tractus solitarius, locus ceruleus, dorsal motor nucleus of the vagus, and intermediolateral cell column in the spinal cord. 5-7 OT and OT receptors are present in the vasculature, heart, and kidney, 2 and OT has effects on BP, renal function, and salt intake. 1,3 Hypovolemia is a stimulus for cardiovascular and neuroendocrine reflexes, resulting in sympathetic, adrenal, and hypothalamic activation. 8 Experimentally, volume depletion is often induced by the injection of large-molecular-weight colloids, such as polyethylene glycol (PEG), which acts to draw iso-osmotic fluid from the tissues. Time-course and pharmacologic antagonist studies suggest that PEG-induced OT release inhibits salt intake. 9,10 There is also evidence for an OT-specific response to increased osmolality, rather than sodium. 11 A role for central angiotensin II (Ang II) in mediating the OT responses was suggested, because OT antagonists potentiated the salt intake induced by Ang II. 12,13 I...

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Salt Appetite and the Renin-Angiotensin System

et al. 2003

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“…In fact, when endogenous oxytocin secretion was stimulated by systemic naloxone, sodium appetite was eliminated (Blackburn et al, 1992b). Similarly, central administration of oxytocin abolished the NaCl intake that accompanies hypovolemiainduced by polyethylene glycol (Blackburn et al, 1992b). These findings provided evidence for oxytocin regulation of salt appetite, but whether such a role for oxytocin fit within the framework of stimulatory signals for sodium consumption remained to be determined.…”

Section: Satiation and Inhibition Of Salt Appetitementioning

confidence: 99%

Section: Satiation and Inhibition Of Salt Appetitementioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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Nearly three-quarters of a century ago, Curt Richter removed the adrenal glands from rats and noted that the animal's vitality was dependent on its increased consumption of sodium chloride. In doing so, Richter revealed an innate behavioral mechanism that serves to maintain the hydromineral balance of an animal faced with sodium deficit. This experiment and others like it, led to the development of a field of research devoted to the investigation of salt appetite. The following is a discussion of how Richter's initial observations gave birth to an evolving field that incorporates multiple approaches to examine the drive to consume sodium. KeywordsSalt appetite; Angiotensin; Aldosterone; Corticosterone; Richter The Discovery of Salt AppetiteAt the time that Richter began his career at Johns Hopkins University much of the research examining ingestive behavior focused on the responses of individual organs or closely coordinated systems. Richter's pioneering work initiated a fundamental paradigm shift that moved the focus to adaptations of the organism as a whole. Specifically, he was interested in changes in behavior that compensated for perturbations in the internal environment. His approach toward investigation of such behaviors was as thorough as it was fundamental. Richter manipulated diet, interfered with the nervous system, and removed or replaced glandular secretions in attempt to understand the nutritional, neural, and endocrine signals that contribute to behavior.Richter created disturbances in the nutritional or mineral content of the internal environment with dietary deficiency. Subsequently, "self selection" experiments were performed where choices of different minerals and nutrients were presented for consumption. More often than not, animals would consume minerals and nutrients in amounts that would alleviate their experimentally-induced deficiencies. One of the most striking behaviors that Richter observed was that of rats voluntarily ingesting salt when faced with sodium deficit. Sodium chloride was removed from the rats' food and they were given access to water and 3 % NaCl solution. The intake of the NaCl solution was approximately 1% of the total diet, which remarkably, is the

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