Inhibition of NaCl appetite when DOCA-treated rats drink saline

Abstract

Marked increases in the consumption of concentrated NaCl solution were elicited in rats by daily injection of the synthetic mineralocorticoid, deoxycorticosterone acetate (DOCA). DOCA-treated rats drank different volumes of NaCl solution depending on its concentration (between 0.15 M and 0.50 M), with less consumed (in milliliters) the more concentrated the fluid was. In consequence, total Na(+) intake (in milliequivalents) was roughly similar in all groups. Gastric emptying of Na(+) also diminished as the concentration of the ingested NaCl solution increased, and the delivery of Na(+) to the small intestine was remarkably similar in all groups. Cumulative volume of ingested fluid in the stomach and small intestine was very closely related to intake (in milliliters) of the concentrated NaCl solutions. Systemic plasma Na(+) levels did not increase until after rats stopped consuming concentrated NaCl solution, although they were elevated at the onset of water ingestion. The situation appeared to be different when 0.15 M NaCl was consumed. This isotonic solution emptied and was absorbed relatively rapidly, and DOCA-treated rats drank larger amounts of it throughout a 1-h test period than when they drank concentrated NaCl solutions. Collectively, these findings suggest that saline consumption by DOCA-treated rats may be inhibited by two presystemic factors, one related to the volume of ingested fluid (i.e., distension of the stomach and small intestine) and one related to its concentration (i.e., elevated osmolality of fluid in the small intestine and/or in adjacent visceral tissue).

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

“…This equation is similar to others that were obtained previously (16,21). The weight of the dry lining of small intestine was considered to be negligible.…”

“…The present study was deliberately designed to resemble recent investigations of rats given either 0.10 M, 0.15 M, 0.20 M, 0.25 M, 0.30 M, 0.40 M, or 0.50 M NaCl to drink when salt appetite was stimulated by daily DOCA treatments (16). In order to evaluate the same issues but in a less comprehensive approach, we used 0.05 M NaCl as the hypotonic solution and only two or three hypertonic NaCl solutions in the following experiments.…”

“…This treatment presumably mimics the marked salt appetite and high blood levels of aldosterone that are seen when intact rats are deprived of dietary Na + (22). Recent experiments have found that DOCA-treated rats drank different volumes of 0.15 M -0.50 M NaCl solution depending on its concentration, with less consumed the more concentrated the fluid was (16). These and other results suggested that saline-drinking bouts are terminated by early inhibitory signals associated with increases in the osmolality of fluid emptied from the stomach (as might be detected by visceral osmoreceptors) and/or in the volume of fluid contained in the stomach and small intestine (as might be detected by stretch receptors on those organs) (16,20).…”

“…Recent experiments have found that DOCA-treated rats drank different volumes of 0.15 M -0.50 M NaCl solution depending on its concentration, with less consumed the more concentrated the fluid was (16). These and other results suggested that saline-drinking bouts are terminated by early inhibitory signals associated with increases in the osmolality of fluid emptied from the stomach (as might be detected by visceral osmoreceptors) and/or in the volume of fluid contained in the stomach and small intestine (as might be detected by stretch receptors on those organs) (16,20). The present experiments examined the generality of those findings by determining whether presystemic signals also inhibit NaCl consumption by Na + -deprived adrex rats.…”

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

“…Thus recent evidence suggests that each solution (isotonic and hypertonic NaCl) has a different way to regulate the termination of sodium appetite, involving one or two presystemic factors, one related to the volume of ingested fluid (i.e., gastrointestinal distension) and one related to its concentration (i.e., increased osmolality of fluid in the small intestine and adjacent visceral tissue) (51).…”