Neuroendocrine factors in salt appetite

• Autorzy: Stellar E. , Epstein A. N.
• Języki publikacji: EN

Abstrakty

EN

We dedicate this paper to Curt P. Richter, father of the study of salt appetite, who died recently at the age of 94. Richter first demonstrated that the adrenalectomized rat’s voracious appetite for salt kept it alive (1936) and showed the same in humans (1940). Our first paper in 1955 demonstrated that salt appetite was an innate response to salt depletion. Since then, we have pursued the notion that the neuroendocrine consequences of sodium depletion create a brain state that raises salt appetite. In Epstein’s laboratory, it was shown that angiotensin and aldosterone, the hormones of salt retention in the periphery, act synergistically in the brain to produce salt appetite in the rat. Block either hormone and the appetite is reduced by half; block both and the appetite is eliminated despite severe bodily need. With repeated depletions or treatments of the brain with angiotensin and aldosterone, salt ingestion increases, reaching an asymptote by the third depletion. Need-free intake of NaCI also increaes, especially in female rats which ingest more NaCI than male rats. In Stellar’s laboratory, running speed to salt solutions in a runway is used as a measure of salt appetite. When the appetite is raised with large doses of DOCA, a mimic of aldosterone, rats run rapidly for a taste of strong salt solutions as high as 24% (almost 4 molar). Using ingestion as a measure, the role of the atrial natriuretic peptide (ANP), an antagonist of angiotensin’s physiological effect, was investigated as a modulator of salt appetite. When angiotensin is involved is producing salt appetite, following sodium depletion by a diuretic combined with a low-salt diet, ANP reduced salt intake by 40%. When salt appetite was raised by DOCA, however, ANP either had no effect or reduced salt ingestion by only 10%. The subfornical organ, the lateral preoptic area, and the central and medial nuclei of the amygdala are being investigated as major components of the limbic circuit underlying salt appetite produced by the actions of angiotensin, aldosterone and ANP in the brain.

Słowa kluczowe

EN

salt appetite; sodium depletion; angiotensin; aldosterone; atrial natriuretic peptide; limbic system; hypothalamus; angiotensis

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 1991
• Tom: 42
• Numer: 4
• Opis fizyczny: p.345-355,fig.,ref.

Twórcy

autor

Stellar E.

• Departments of Anatomy and Biology, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104-6058, USA

autor

Epstein A. N.

• Departments of Anatomy and Biology, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104-6058, USA

Bibliografia

• 1. Stellar E. The physiology of motivation. Psychol Rev 1954; 61: 5-22.
• 2. Stellar E. Brain Mechanisms and hedonic processes. Acta Neurobiol Exp 1980; 40: 313-324.
• 3. Stellar JR, Stellar E. Neurobiology of Motivation and Reward. New York, Springer-Verlag, 1985.
• 4. Richter CP. Total self regulatory functions in animals and human beings. Harvey Lect 1942-43; 38: 63-103.
• 5. Epstein AN, Stellar E. The control of salt preference in the adrenalectomized rat. J Comp Physiol Psychol 1955; 48: 167-172.
• 6. Richter CP. Increased salt appetite in adrenalectomized rats. AmerJPhysiol 1936; 115:155-161.
• 7. Sakai RR, Fine WB, Frankmann SP, Epstein AN. Salt appetite is enhanced by one prior episode of sodium depletion in the rat. Behav Neurosci 1987; 101: 724-731.
• 8. Sakai RR, Nicolaidis S, Epstein AN. Salt appetite is suppressed by interference with angio- stein II and aldosterone. Amer J Physiol 1986; 251: R762-R768.
• 9. Sakai RR, Epstein AN. Dependence of adrenalectomy-induced sodium appetite on the action of angiostensin II in the brain of the rat. Behav Neurosci 1990; 104: 67-176.
• 10. Sakai RR, Frankmann SP, Fine WB, Epstein AN. Prior episodes of sodium depletion increase the need-free sodium intake of the rat. Behav Neurosci 1989; 103: 186-192.
• 11. Nitabach MN, Schulkin J, Epstein AN. The medial amygdala is part of a minerolcorticoid-sensitive circuit controlling NaCl intake in the rat. Behav Brain Res 1989; 35: 127-134.
• 12. Schulkin J, Marini J, Epstein AN. A role for the medial region of the amygdala in mineralo- corticoid-induced salt-hunger. Behav Neurosci 1989; 103: 178-185.