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. Post-ingestive 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 0.5M NaCl and intakes were measured. After 120 min of access, rats were sacrificed and plasma sodium (pNa) and plasma-renin-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 0.5M 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 0.5M NaCl intake was similar in both groups, with each making a mixture of approximately 0.25 M NaCl. The results suggest that post-ingestive signals are necessary for the satiation of thirst and salt appetite.

Figure 1

Cumulative intake of control and sham-drinking rats during 120 min access to water. At 15, 30, 60 and 120 min sham-drinking rats had greater intakes when compared to controls. Water intakes of controls ceased to significantly increase after 30 min whereas the intakes of sham-drinking rats increased over time. * = significantly greater than controls P < 0.05; † = significantly greater than the previous time point P < 0.05.

Figure 2

Cumulative intakes of control and sham-drinking rats during 120 min access to 0.5 M NaCl (left) and water (right). Control and sham-drinking rats consume similar amounts of 0.5 M NaCl and water after injection of saline. Administration of furosemide significantly increases 0.5 M NaCl and water intake. Sham-drinking rats consume significantly more 0.5 M NaCl and water at 30, 60 and 120 min when compared to controls. The intakes of sham-drinking significantly increased across time. * = significantly greater than closed P < 0.05; † = significantly greater than the previous time point P < 0.05.

Figure 3

Ratio of 0.5 M NaCl to water intake (mol of Na⁺ / L of water). Rats treated with furosemide make similar mixtures of 0.5 M NaCl and water, regardless of condition (control vs sham-drinking).

Figure 4

Amount of Na⁺ lost and consumed after furosemide and 120 min access to 0.5 M NaCl and water. As can be seen, furosemide-treatment caused ≈ 2.2 mEq of Na⁺ to be lost in urine, which is similar to the amount consumed by controls. In contrast, sham-drinking rats ingested ≈ 7.5 mEq of Na⁺ nearly twice the amount of that lost in urine or consumed by controls. * = significantly greater than Na⁺ lost in urine or consumed by controls rats P < 0.05.

Figure 5

pNa of control and sham-drinking rats treated with furosemide and given 120 min access to 0.5 M NaCl and water. Despite consuming twice the amount of Na⁺, sham-drinking rats have significantly lower pNa when compared to their control counterparts. * = significantly less than closed P < 0.05.

Figure 6

PRA of control and sham-drinking rats treated with furosemide and given 120 min access to 0.5 M NaCl and water. PRA of sham-drinking rats remains significantly elevated when compared to that of controls. * = significantly less than open P < 0.05.