Abstract

Several studies of the quantitative relationship between sodium need and sodium intake in rats are reviewed. Using acute diuretic treatment 24 h beforehand, intake matches need fairly accurately when intake is spread out in time by using a hypotonic solution of NaCl. In contrast, using a hypertonic solution, intake is typically double the need. Using the same diuretic treatment, although the natriuresis occurs within ~1 h, the appetite appears only slowly over 24 h. Increased plasma levels of aldosterone parallel the increased intake; however, treatment with metyrapone blocks the rise in aldosterone but has no effect on appetite. Satiation of sodium appetite was studied in rats using sodium loss induced by chronic diuretic treatment and daily salt consumption sessions. When a simulated foraging cost was imposed on NaCl access in the form of a progressive ratio lever press task, rats showed satiation for NaCl (break point) after consuming an amount close to their estimated deficit. The chronic diuretic regimen produced hypovolemia and large increases in plasma aldosterone concentration and renin activity. These parameters were reversed to or toward non-depleted control values at the time of behavioral satiation in the progressive ratio protocol. Satiation mechanisms for sodium appetite thus do appear to exist. However, they do not operate quantitatively when concentrated salt is available at no effort, but instead allow overconsumption. There are reasons to believe that such a bias toward overconsumption may have been beneficial over evolutionary time, but such biasing for salt and other commodities is maladaptive in a resource-rich environment.

Highlights

  • In the laboratory, sodium appetite most usually is studied using rats and access to hypertonic solutions of NaCl that normally would be unpalatable

  • We examined the characteristics of intake of a high (300 mM) and low (30 mM) NaCl solution in rats treated 24 h previously with furosemide, timed so that the test began at lights out [10]

  • plasma renin activity (PRA) peaked at the earliest point and decreased at the later times, and was not correlated with appetite. This temporal correlation between aldosterone and sodium appetite does not reflect causality because we found that treatment with metyrapone, a selective inhibitor of aldosterone synthesis that was fully effective to block elevations in plasma aldosterone, was without effect on the induced sodium appetite

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Summary

Introduction

Sodium appetite most usually is studied using rats and access to hypertonic solutions of NaCl that normally would be unpalatable. The sodium appetite that develops as a result of this abrupt depletion has several important characteristics: it is taste-guided and relatively specific for the taste of sodium; it matures over several hours to reach a maximal level after 12-24 h (provided that the animals receive sodium-free food so they cannot replete in the interim); the maximal level reached is excessive, typically two to three times the actual sodium loss. The first of these characteristics is most likely due to the presence of specific sodium-sensitive fibers in the gustatory system [3]. We will consider three conditions that affect the amount of sodium consumed, and the matching of intake to need: concentration, time, and effort

Concentration of sodium offered
Temporal maturation of appetite
Study B
Findings
Discussion
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