Salt Appetite Is Reduced by a Single Experience of Drinking Hypertonic Saline in the Adult Rat

Abstract

Salt appetite, the primordial instinct to favorably ingest salty substances, represents a vital evolutionary important drive to successfully maintain body fluid and electrolyte homeostasis. This innate instinct was shown here in Sprague-Dawley rats by increased ingestion of isotonic saline (IS) over water in fluid intake tests. However, this appetitive stimulus was fundamentally transformed into a powerfully aversive one by increasing the salt content of drinking fluid from IS to hypertonic saline (2% w/v NaCl, HS) in intake tests. Rats ingested HS similar to IS when given no choice in one-bottle tests and previous studies have indicated that this may modify salt appetite. We thus investigated if a single 24 h experience of ingesting IS or HS, dehydration (DH) or 4% high salt food (HSD) altered salt preference. Here we show that 24 h of ingesting IS and HS solutions, but not DH or HSD, robustly transformed salt appetite in rats when tested 7 days and 35 days later. Using two-bottle tests rats previously exposed to IS preferred neither IS or water, whereas rats exposed to HS showed aversion to IS. Responses to sweet solutions (1% sucrose) were not different in two-bottle tests with water, suggesting that salt was the primary aversive taste pathway recruited in this model. Inducing thirst by subcutaneous administration of angiotensin II did not overcome this salt aversion. We hypothesised that this behavior results from altered gene expression in brain structures important in thirst and salt appetite. Thus we also report here lasting changes in mRNAs for markers of neuronal activity, peptide hormones and neuronal plasticity in supraoptic and paraventricular nuclei of the hypothalamus following rehydration after both DH and HS. These results indicate that a single experience of drinking HS is a memorable one, with long-term changes in gene expression accompanying this aversion to salty solutions.

Effects of chronic dietary exposure to monosodium glutamate on feeding behavior, adiposity, gastrointestinal motility, and cardiovascular function in healthy adult rats

“…This might be due to an osmotic effect induced by the proportional increase in sodium intake in MSG‐treated rats (sodium constitutes 12% of MSG), compared to control animals (i.e., thirst stimulation) . In rats, fluid intake increased about 50% when a solution with 0.9% NaCl (3.6 g/L sodium) was offered for drinking instead of water . In our case, although the solution offered for drinking had 0.48 g/L, still increased fluid intake by 18%, not by the expected 6–7% (corresponding to those 7–8 times less sodium).…”

Water deprivation-partial rehydration induces sensitization of sodium appetite and alteration of hypothalamic transcripts

“…The apelin receptor mRNA is also highly expressed in hypothalamic nuclei where ANG II acts to stimulate vasopressin and oxytocin release (28). Water deprivation also induces plastic changes in mRNA expression of neurohypophysial hormones in these nuclei (15).…”

“…Several factors like age, sex, and taste influence sodium intake (8,15,19,41). In addition, ANG II is an established key mediator of sodium appetite sensitization associated with sodium loss (3,17,31,36).…”

Endogenous opioid dependence after intermittent use of glucose, sodium chloride, and monosodium glutamate solutions

“…We used the same concentration of glucose solution as Colantuoni et al (2002). Three different concentrations of sodium chloride were chosen as rats under normal conditions prefer hypotonic to normotonic sodium chloride solutions (Greenwood, Greenwood, Paton, & Murphy, 2014;Omouessi et al, 2016). Solutions of MSG were isomolar compared to solutions of sodium chloride.…”