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Regulation of NaCl solution intake and gastric emptying by adrenalectomized rats

Adrenalectomized (adrex) rats adaptively increase NaCl intake to compensate for the uncontrolled loss of Na+ in urine due to the absence of aldosterone. They ingest saline readily after a period of NaCl deprivation, but the drinking bout stops before hyponatremia is repaired. The present experiments...

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Bibliographic Details
Published in:The FASEB journal 2007-04, Vol.21 (5), p.A511-A511
Main Authors: Bykowski, Michael R, Hoffmann, Myriam L, Smith, James C., Stricker, Edward M.
Format: Article
Language:English
Online Access:Get full text
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Summary:Adrenalectomized (adrex) rats adaptively increase NaCl intake to compensate for the uncontrolled loss of Na+ in urine due to the absence of aldosterone. They ingest saline readily after a period of NaCl deprivation, but the drinking bout stops before hyponatremia is repaired. The present experiments determined whether pre‐systemic signals inhibit further NaCl intake, and whether gastric emptying of Na+ is modulated according to the concentration of the ingested NaCl solution. After overnight deprivation, rats consumed 0.05 M – 0.30 M NaCl at a similar rate (in ml/min) that was faster than when they consumed 0.50 M NaCl. However, the rate of Na+ intake (in meq/min) was similar whether rats drank 0.30 M NaCl or 0.50 M NaCl, suggesting that the animals were regulating intake when ingesting concentrated saline solution (but not when ingesting more dilute solutions). The intakes appeared to be inhibited both by the concentration of saline emptied from the stomach and by the volume of ingested fluid in the stomach and small intestine. Gastric emptying (in meq Na+/min) was similar when rats drank 0.15 M, 0.30 M, or 0.50 M NaCl, as if they were regulating the delivery of Na+ to the small intestine. Thus, adrex rats seem able to detect the volume and concentration of ingested NaCl solution and to integrate these two variables, and thereby modulate the rates of Na+ intake and gastric emptying.
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.21.5.A511-a