Effect of deoxycorticosterone on sodium appetite of intact and adrenalectomized rats

Wolf, George

doi:10.1152/ajplegacy.1965.208.6.1281

Cited by 94 publications

(68 citation statements)

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“…We also tested whether HSD2 neurons are stimulated by the aldosterone analog DOCA, which dramatically increases sodium appetite even in the absence of a sodium deficit (Rice and Richter, 1943;Wolf, 1965). Vehicle-treated control animals drank very little 3% saline (1.4 Ϯ 0.2 ml/d by 7 d; n ϭ 4), and their HSD2 neurons were not activated (2.2 Ϯ 0.5% c-Fos expression; n ϭ 4).…”

Section: Activation Of Hsd2 Neurons By Diuresis and Docamentioning

confidence: 99%

“…Aldosterone is not required for sodium appetite (Richter, 1936), but it enhances salt intake. Although a small dose in adrenalectomized (adx) rats reduces the sodium losses that otherwise would induce sodium appetite (Fregly and Waters, 1966), higher doses of aldosterone and other adrenal mineralocorticoids increase sodium intake even in the absence of sodium deficiency (Rice and Richter, 1943;Wolf, 1965;Wolf and Handal, 1966). In fact, deoxycorticosterone acetate (DOCA) stimulates a pattern of saline ingestion nearly indistinguishable from adrenalectomy (Stricker et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Geerling¹,

Engeland²,

Kawata³

et al. 2006

J. Neurosci.

130

185

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Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-␤-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.

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Section: Activation Of Hsd2 Neurons By Diuresis and Docamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Geerling¹,

Engeland²,

Kawata³

et al. 2006

J. Neurosci.

130

185

View full text Add to dashboard Cite

show abstract

“…In this regard, Wolf (1965) expanded on Richter's initial observations by examining the NaCl intake of intact and adrenalectomized rats after administration of various doses of DOC. As expected, intact rats increased NaCl intake with elevating doses of DOC.…”

Section: Arousal Of Salt Appetite: Contributions Of Aldosteronementioning

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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“…Because thirst and Na appetite are complementary behavioural responses to extracellular fluid depletion, it has been attractive to postulate a role for A II in Na appetite; the more so since A II increases the secretion of mineralocorticoids which are known to stimulate Na intake (Wolf, 1965;Fregly & Waters, 1966). However, the evidence is 0022-3751/80/7870-0408 $07.50 © 1980 The Physiological Society D. B.…”

Section: Introductionmentioning

confidence: 99%

Increased sodium appetite in the rat induced by intracranial administration of components of the renin‐angiotensin system.

Avrith¹,

Fitzsimons²

1980

The Journal of Physiology

151

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SUMMARY1. Intracranial injections of components of the renin-angiotensin system in rats in normal water and Na balance caused an immediate thirst followed by a progressive increase in Na appetite during a test session which lasted 18 h. The effect on water and Na intake was dose-dependent.2. Long-term (7 day) infusions of angiotensin II into the third cerebral ventricle at rates of 1 or 10 pmol h-' produced large and sustained increases in intake of water and 2*7 % NaCl. Intakes sometimes exceeded 100 ml 2-7 % NaCl per day but quickly fell to normal when the infusion was stopped.3. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of 2-7 % NaCl.4. The Na appetite induced by intracranial injection of angiotensin was specific for Na since rats offered a choice of water and equimolar concentrations of NaCl and KCl took only water and NaCl. This resembles the pattern seen in Na-depleted rats.5. Increased Na appetite was not secondary to increased water intake since it occurred when only 2-7 % NaCl was available to drink.6. Increased Na appetite was not secondary to natriuresis since, first, the angiotensin-stimulated rats went into positive Na balance, secondly, intracranial renin did not cause increased Na excretion in Na-loaded rats and thirdly, anuric rats showed a significant Na appetite in response to renin.7. These results suggest that angiotensin in the brain may play a role in the development of Na appetite.

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Effect of deoxycorticosterone on sodium appetite of intact and adrenalectomized rats

Cited by 94 publications

References 0 publications

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Richter and sodium appetite: From adrenalectomy to molecular biology

Increased sodium appetite in the rat induced by intracranial administration of components of the renin‐angiotensin system.

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