Drinking after intragastric NaCl without increase in systemic plasma osmolality in rats

It was already known that systemic osmolality typically rises before drinking behavior begins. However, no prior work had resolved whether drinking could occur without systemic osmolality changes. Some studies suggested that gastrointestinal signals might trigger drinking independently of blood osmolality. This gap motivated researchers to test if drinking could be initiated by intragastric hypertonic solutions without affecting plasma osmolality. Prior research has shown that drinking is often linked to elevated plasma osmolality. Yet, the role of local osmotic signals in the gut remained unclear. That uncertainty drove the need to isolate and test gastrointestinal mechanisms for thirst. This study aimed to clarify if drinking could be triggered by gut osmolality alone.

The aim was to determine if drinking could be initiated by intragastric hypertonic solutions without systemic osmolality changes. The specific problem was whether osmotic signals in the gut could trigger drinking independently of blood osmolality. This question arose from prior findings that drinking often follows systemic osmolality increases. The motivation was to test if a localized gastrointestinal mechanism could elicit thirst. Researchers wanted to see if drinking could occur without a rise in plasma osmolality. They focused on whether intragastric NaCl could trigger drinking without systemic effects. The study sought to isolate the role of gut osmolality in initiating drinking behavior. This would clarify if drinking could be driven by local gut signals alone.

The study used male Sprague-Dawley rats with gastric catheters for intragastric infusions. A 2-ml volume of solutions with varying osmolality was administered to test drinking responses. Drinking latency and 1-hour water intake were measured after each infusion. Plasma osmolality and other blood parameters were analyzed at the time of drinking initiation. Different solutes were tested to determine if specific ions or osmotic agents triggered drinking. Vagotomy procedures were used to assess the role of vagal innervation in drinking behavior. Total subdiaphragmatic vagotomy and selective gastric or hepatic vagotomy were performed. The experimental design allowed researchers to isolate the contribution of gastrointestinal osmosensors.

Intragastric NaCl at 600, 1,200, and 1,800 mosmol/kg reduced drinking latency and increased 1-hour water intake compared to baseline. Plasma osmolality remained unchanged despite these infusions, even at 1,200 mosmol/kg. Plasma sodium, protein, renin activity, and packed cell volume also remained stable at drinking onset. Sodium bicarbonate, isethionate, potassium chloride, lithium chloride, and mannitol all increased water intake variably. Drinking elicited by intragastric NaCl was abolished by total subdiaphragmatic vagotomy. Selective gastric or hepatic vagotomy reduced drinking under some conditions. These findings suggest a vagally mediated osmosensitive mechanism in the gut or portal region. The results indicate that drinking can be initiated without systemic osmolality changes.

The authors propose that drinking can be initiated by intragastric osmotic signals without changes in systemic osmolality. Their findings suggest a vagally mediated osmosensitive mechanism in the gastrointestinal or hepatic-portal region. This mechanism appears to act independently of systemic osmolality increases. The study supports the hypothesis that gut osmosensors can trigger drinking behavior. The results indicate that intragastric NaCl at 600–1,800 mosmol/kg can elicit drinking without affecting plasma osmolality. Vagotomy experiments showed that vagal innervation is necessary for this drinking response. Different solutes varied in their ability to increase water intake, suggesting specific osmotic effects. These findings imply that localized osmotic signals in the gut may play a role in thirst regulation.