Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Shelat, SG; Flanagan-Cato, LM; Sj, Fluharty

doi:10.1677/joe.0.1620381

Cited by 30 publications

(19 citation statements)

References 62 publications

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“…Thus the "synergy" hypothesis of salt appetite (4, 7) now includes prominent roles for glucocorticoids and their receptors (6,8). In the brain, glucocorticoids increase ANG II receptor binding while amplifying ANG II-related intracellular signaling processes (3,6,(22)(23)(24)27) and also increase binding to type I mineralocorticoid receptors (8,17,35). Dex in combination with DOCA increases ANG II binding at angiotensin type 1 (AT 1 ) receptors in brain areas involved in mediating responses to circulating ANG II, including the subfornical organ, area postrema, and paraventricular nucleus (22).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Thunhorst¹,

Beltz²,

Johnson³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Glucocorticoids [e.g., corticosterone and dexamethasone (Dex)], when administered systemically, greatly increase water drinking elicited by angiotensin and sodium ingestion in response to mineralocorticoids [e.g., aldosterone and deoxycorticosterone acetate (DOCA)], possibly by acting in the brain. In addition, glucocorticoids exert powerful renal actions that could influence water and sodium ingestion by promoting their excretion. To test this, we determined water and sodium intakes, excretions, and balances during injections of Dex and DOCA and their coadministration (DOCAϩDex) at doses commonly employed to stimulate ingestion of water and sodium. In animals having only water to drink, Dex treatment greatly increased water and sodium excretion without affecting water intake, thereby producing negative water and sodium balances. Similar results were observed when Dex was administered together with DOCA. In animals having water and saline solution (0.3 M NaCl) to drink, Dex treatment increased water and sodium excretion, had minimal effects on water and sodium intakes, and was associated with negative water and sodium balances. DOCA treatment progressively increased sodium ingestion, and both water and sodium intakes exceeded their urinary excretion, resulting in positive water and sodium balances. The combination of DOCAϩDex stimulated rapid, large increases in sodium ingestion and positive sodium balances. However, water excretion outpaced total fluid intake, resulting in large, negative water balances. Plasma volume increased during DOCA treatment and did not change during treatment with Dex or DOCAϩDex. We conclude that increased urinary excretion, especially of water, during glucocorticoid treatment may explain the increased ingestion of water and sodium that occurs during coadministration with mineralocorticoids. thirst; urine volume; dexamethasone; deoxycorticosterone acetate; food intake SYSTEMICALLY ADMINISTERED mineralocorticoids, such as aldosterone and deoxycorticosterone acetate (DOCA), stimulate vigorous sodium ingestion by activating mineralocorticoid receptors in the brain. Glucocorticoids, such as corticosterone, greatly increase this salt appetite response when coadministered with mineralocorticoids (2,17,33,35). Systemically administered glucocorticoids also increase water drinking in response to peripheral and central administration of ANG II (9, 27). The potentiation of salt appetite and thirst by glucocorticoids has been postulated to arise from glucocorticoid actions within the brain, affecting either mineralocorticoid (17, 35) or ANG II (3,6,8,22) receptors. For example, high levels of glucocorticoids are proposed to increase type I mineralocorticoid receptors and thus mineralocorticoid binding in the brain (17,35). Additionally, glucocorticoids may increase the number of ANG II receptors in the brain (22) and thereby augment the central actions of ANG II (which, in turn, may interact with mineralocorticoid receptors).Glucocorticoids also have systemic effects that could facilitate ingest...

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Section: Discussionmentioning

confidence: 99%

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Thunhorst¹,

Beltz²,

Johnson³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Mineralocorticoids have further been shown to upregulate Fos (41,42), angiotensin receptors (51), oxytocin receptors (51), vasopressin (20), and the vasopressin V 1a receptor (41,42). Vasopressin (11) and angiotensin II (9,29,45,50,51) in turn stimulate, whereas oxytocin (53) inhibits, salt intake. Interestingly, the effect of mineralocorticoids or salt depletion on salt appetite may be modified by glucocorticoids (18,34,50) and amphetamine (5).…”

Section: Discussionmentioning

confidence: 99%

“…Vasopressin (11) and angiotensin II (9,29,45,50,51) in turn stimulate, whereas oxytocin (53) inhibits, salt intake. Interestingly, the effect of mineralocorticoids or salt depletion on salt appetite may be modified by glucocorticoids (18,34,50) and amphetamine (5). Moreover, salt appetite has been shown to be dependent on the age of the animal (54).…”

Section: Discussionmentioning

confidence: 99%

SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess

Vallon¹,

Huang²,

Grahammer³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Specifically, rats treated with DOC and dexamethasone consumed more NaCl than when given DOC alone. Furthermore, co-administration of DOC and dexamethasone increased angiotensin II receptor binding in the paraventricular nucleus, subfornical organ and area postrema, but administration of only DOC had no such effect (Shelat et al, 1999a). Accordingly, new models of hormonal regulation of salt appetite incorporate the contributions of mineralcorticoids as well as glucocorticoids.…”

Section: Central Interactions Of Aldosterone and Angiotensin IImentioning

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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Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Cited by 30 publications

References 62 publications

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Glucocorticoids increase salt appetite by promoting water and sodium excretion

SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess

Richter and sodium appetite: From adrenalectomy to molecular biology

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