Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat

Abstract

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.

Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats

“…Because the present results resembled those reported recently (8,13,16), a full discussion of the findings and their implications will not be repeated. However, a few observations were unique to the adrex rat and therefore warrant additional comments.…”

“…4). If visceral osmo-or Na + -receptors are located in that proximal portion of the small intestine, as suggested recently (13,20), then those receptors may be stimulated before intestinal stretch receptors can detect distension.Increasing intestinal distension allows for an expanded surface area from which fluid can be absorbed into the mesenteric vasculature. Inspection of Fig.…”

Diabetes Insipidus: A Review

“…Osmolality is also is detected and influenced peripherally [31,32]. Signals from oropharynx, small intestine and liver all contribute to osmostasis [31,32].…”

“…Signals from oropharynx, small intestine and liver all contribute to osmostasis [31,32]. In the liver, in contrast to central osmosensing, signaling is stimulated by hyposmolality, as opposed to the hyperosmolal stimulated increase in neuron firing found in the OVLT and MNCs.…”

“…It has also been demonstrated in humans that ADH secretion is suppressed by non osmotic influences such as oropharyngeal stimulation caused by drinking. In rats distension of the stomach, and [Na + ] in the small intestine also influence [ADH], anticipatory of imminent osmolal change [32].…”