Roles of taste and post-ingestional factors in the satiation of sodium appetite in rats.

Nachman, Marvin; Valentino, Dominic

doi:10.1037/h0023667

Cited by 70 publications

(34 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, plasma sodium, aldosterone and angiotensin II are not returned to basal levels at the time that rats cease depletion-induced intake of NaCl solutions (Sakai unpublished observations) and studies examining satiation of salt appetite suggest that taste and post-ingestional factors contribute to the cessation of this behavior. For example, early studies of satiation signals demonstrated that direct delivery of NaCl into the stomach did not significantly suppress the NaCl intake of sodium deficient rats (DiCara & Wilson, 1974;Nachman & Valentino, 1966). These results were interpreted to mean that gustatory cues arising from the natural act of ingestion are critical for reducing the drive to consume sodium.…”

Section: Satiation and Inhibition Of Salt Appetitementioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

View full text Add to dashboard Cite

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

show abstract

Section: Satiation and Inhibition Of Salt Appetitementioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

View full text Add to dashboard Cite

show abstract

“…Ingestion accompanied by stimulation of taste receptors by sodium chloride leads to a rapid (Denton, 1965), short-term satiation (Nachman and Valentino, 1966;DiCara and Wilson, 1974) which does not occur without taste receptor stimulation (e.g., when solutions are introduced into the stomach via an esophageal fistula). If cessation of salt intake were simply under control of postingestional effects, peripheral stimulation would not have this effect (Morrison and Young, 1972).…”

Section: Possible Relationships Between Reduced Neural Responsivity Amentioning

confidence: 99%

Sodium deprivation alters neural responses to gustatory stimuli.

Contreras¹,

Frank²

1979

The Journal of General Physiology

199

View full text Add to dashboard Cite

A B S T R A C T The effects of sodium deprivation for 10 d, a period sufficient to induce sodium appetite, on gustatory nerve discharges in rats were determined. Chorda tympani responses to concentration series of sodium chloride, sucrose, hydrochloric acid, and quinine hydrochloride were recorded and analyzed without the experimenter knowing the animal's deprivation condition. After deprivation, both whole nerve and single nerve fiber responses to sodium chloride were smaller; NaCl-best fibers, those more responsive to sodium chloride than to sucrose, hydrochloric acid, or quinine, were most affected. Thresholds had not changed; however, slopes of the stimulus-response functions for sodium chloride were lowered. Comparable changes in responses to the other stimuli did not occur. These results were discussed with respect to a possible relationship between changes in sodium chloride responsivity and changes in sodium intake, differences between methods of inducing sodium appetite, coding of taste quality and intensity, and mechanisms which might effect the responsivity change.

show abstract

“…It can be produced by pharmacological doses of the mineralocorticoids (aldosterone and desoxycorticosterone) which maintain animals in positive Na balance (Fregly & Waters, 1966; Wolf, 1964;Wolf & Handel, 1966), and it is not controlled by manipulations of plasma Na (Beilharz, Denton & Sabine, 1962;Falk, 1961;Nachman & Valentino, 1966). Decreases in the concentration of plasma Na do not appear to be the direct cause of the appetite.…”

Section: Introductionmentioning

confidence: 99%

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

Bryant¹,

Epstein²,

Fitzsimons³

et al. 1980

The Journal of Physiology

149

View full text Add to dashboard Cite

SUMMARY1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2-7 % NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3 % NaCl.2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight.3. Not only did the animals drink large volumes of 3 % NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months).4. The response to continuous infusion of angiotensin II was dose-dependent.Both water and 3 % NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1.The persistence of the sodium appetite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0.5 M-NH4CI and only occasionally drank minimal amounts of 0 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3 % NaCl only during infusion of angiotensin drank copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3 % NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3 % NaCl but did drink some water.

show abstract

Roles of taste and post-ingestional factors in the satiation of sodium appetite in rats.

Cited by 70 publications

References 6 publications

Richter and sodium appetite: From adrenalectomy to molecular biology

Richter and sodium appetite: From adrenalectomy to molecular biology

Sodium deprivation alters neural responses to gustatory stimuli.

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

Contact Info

Product

Resources

About