Post-ingestive signals and satiation of water and sodium intake of male rats

Abstract

This study investigated the role of post-ingestive signals in the satiation of thirst or salt appetite. Postingestive signals, defined as those arising from the passage of fluid into the duodenum and proximal jejunum, were manipulated by implanting rats with gastric fistulas. After recovery, rats were water deprived and the following day gastric fistulas were opened (sham-drinking) or closed (control). Deprivation-induced thirst significantly increased water intake with sham-drinking rats consuming four-fold more than controls after 120 min access. Subsequently, rats were given sodium deficient chow for 48 h and the next day were administered furosemide and urine was collected. Twenty-four hours later, gastric fistulas were manipulated and rats were given water and 0.5 M NaCl and intakes were measured. After 120 min of access, rats were sacrificed and plasma sodium (pNa) and plasmarenin-activity (PRA) were measured. Furosemide resulted in a loss of 2.2 mEq of sodium in urine and sham-drinking rats consumed significantly more water and 0.5 M NaCl when compared to controls. At 120 min sham-drinking rats consumed 7.5 mEq of sodium nearly twice that of controls but had significantly lower pNa and significantly increased PRA. Interestingly, the ratio of water to 0.5 M NaCl intake was similar in both groups, with each making a mixture of ≈ 0.25 M NaCl. The results suggest that post-ingestive signals are necessary for the satiation of thirst and salt appetite.

Dehydration followed by sham rehydration contributes to reduced neuronal activation in vasopressinergic supraoptic neurons after water deprivation

“…Further, the ingested volume for sham-rehydrated rats was increased compared with rehydrated rats with closed fistulas. These data suggest persistent thirst during sham rehydration with either water or saline, as others have reported (36,61), which is consistent with hyperosmolality and elevated hematocrit. Dehydration reportedly increases sodium appetite (17,18) and stimulates natriuresis (30); however, we were unable to uncover a significant increase in saline intake following dehydration and osmolality in saline-rehydrated rats returned to normal.…”

Roux-en-Y gastric bypass does not affect daily water intake or the drinking response to dipsogenic stimuli in rats

“…Studies by Miller et al (32) showed that the act of drinking was more satiating than the infusion of the same volume of fluid directly into the gut, suggesting that there is some feedback generated by the act of drinking itself. On the other hand, sham drinking, in which a gastric fistula allows ingested fluid to drain from the stomach before causing gastric fill, increases drinking behavior in dehydrated rats (25,39). This could be seen to support the hypothesis that gastric fill is required for drinking termination, but confining water to the stomach, thereby exaggerating distention, does not decrease behavior (15,16,20).…”

“…Regulation of saline intake, for instance, appears to use a different satiating mechanism than that employed for water intake, and testing the effect of RYGB on saline intake remains an important area for future study. Indeed, the mechanism underlying saline intake satiety remains controversial, with some studies suggesting a minor, if any, role of postingestive signaling in sodium intake termination (18,34) and others suggesting that the signaling is primarily postingestive (25,38,40). The knowledge that the water component of any saline intake measured is unaffected by the RYGB procedure could help with the interpretation of future studies.…”

Heat acclimation and thirst in rats

“…; Johnson ; Stricker and Hoffmann ; Krause et al. ; Thornton ). Determination of the role of these factors was beyond the scope of this study.…”

“…An increased drinking response to angiotensin II may also explain the increased water intake in the heat-acclimated rats following water deprivation. However, the regulation of water intake is complex and involves both peripheral and central components and thirst satiation involves both presystemic and systemic factors (Stricker and Sved 2000;McKinley et al 2004;Johnson 2007;Stricker and Hoffmann 2007;Krause et al 2010;Thornton 2010). Determination of the role of these factors was beyond the scope of this study.…”