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The spontaneously hypertensive rat (SHR) has an intense consumption of NaCl solution. Water deprivation (WD) followed by water intake to satiety induces partial rehydration (PR)-the WD-PR protocol-and sodium appetite. In the present work, WD produced similar water intake and no alterations in arterial pressure among spontaneously hypertensive rat (SHR), Wistar-Kyoto, and Holtzman strains. It also increased the number of cells with positive c-Fos immunoreactivity (Fos-IR) in the lamina terminalis and in the hypothalamic supraoptic (SON) and paraventricular (parvocellular, PVNp) nucleus in these strains. The WD and WD-PR produced similar alterations in all strains in serum osmolality and protein, plasma renin activity, and sodium balance. The SHR ingested about 10 times more 0.3 M NaCl than normotensives strains in the sodium appetite test that follows WD-PR. After WD-PR, the Fos-IR persisted, elevated in the lamina terminalis of all strains but notably in the subfornical organ of the SHR. The WD-PR reversed Fos-IR in the SON of all strains and in the PVNp of SHR. It induced Fos-IR in the area postrema and in the nucleus of the solitary tract (NTS), dorsal raphe, parabrachial (PBN), pre-locus coeruleus (pre-LC), suprachiasmatic, and central amygdalar nucleus of all strains. This effect was bigger in the caudal-NTS, pre-LC, and medial-PBN of SHRs. The results indicate that WD-PR increases cell activity in the forebrain and hindbrain areas that control sodium appetite in the rat. They also suggest that increased cell activity in facilitatory brain areas precedes the intense 0.3 M NaCl intake of the SHR in the sodium appetite test.

Gavage of 2 M NaCl (IG 2 M NaCl), a procedure to induce cell-dehydration-and water and 0.15 M NaCl intake in a two-bottle choice test-is also a potential gastric irritant. In this study, we assessed whether mineral intake induced by IG 2 M NaCl is associated with gastric irritation or production of pica in the rat. We first determined the amount of mineral solution (0.15 M NaCl, 0.15 M NaHCO3, 0.01 M KCl and 0.05 mM CaCl2) and water ingested in response to IG 2 M NaCl in a five-bottle test. Then, we used mineral solutions (0.01 M KCl and 0.15 M NaHCO3), whose intakes were significantly increased compared to controls, and water in three-bottle tests to test the gastric irritation hypothesis. The IG 2 M NaCl induced KCl and NaHCO3 intake that was not inhibited by gavage with gastric protectors Al(OH)3 or NaHCO3. IG 2 M NaCl or gavage of 0.6 N acetic acid induced mild irritation, hyperemia, of the glandular part of the stomach. A gavage of 50% ethanol induced strong irritation seen as pinpoint ulcerations. Neither ethanol nor acetic acid induced any fluid intake. Neither IG 2 M NaCl nor acetic acid induced kaolin intake, a marker of pica in laboratory rats. Ethanol did induce kaolin intake. These results suggest that IG 2 M NaCl induced a mineral fluid intake not selective for sodium and independent from gastric irritation or pica.

-Sodium intake occurs either as a spontaneous or induced behavior, which is enhanced, i.e., sensitized, by repeated episodes of water deprivation followed by subsequent partial rehydration (WD-PR). In the present work, we examined whether repeated WD-PR alters hypothalamic transcripts related to the brain renin-angiotensin system (RAS) and apelin system in male normotensive Holtzman rats (HTZ). We also examined whether the sodium intake of a strain with genetically inherited high expression of the brain RAS, the spontaneously hypertensive rat (SHR), responds differently than HTZ to repeated WD-PR. We found that repeated WD-PR, besides enhancing spontaneous and induced 0.3 M NaCl intake, increased the hypothalamic expression of angiotensinogen, aminopeptidase N, and apelin receptor transcripts (43%, 60%, and 159%, respectively) in HTZ at the end of the third WD-PR. Repeated WD-PR did not change the daily spontaneous 0.3 M NaCl intake and barely changed the need-induced 0.3 M NaCl intake of SHR. The same treatment consistently enhanced spontaneous daily 0.3 M NaCl intake in the normotensive Wistar-Kyoto rats. The results show that repeated WD-PR produces alterations in hypothalamic transcripts and also sensitizes sodium appetite in HTZ. They suggest an association between the components of hypothalamic RAS and the apelin system, with neural and behavioral plasticity produced by repeated episodes of WD-PR in a normotensive strain. The results also indicate that the inherited hyperactive brain RAS is not a guarantee for sensitization of sodium intake in the male adult SHR exposed to repeated WD-PR.angiotensin; apelin; neuroplasticity; rat strain; dehydration; spontaneously hypertensive rat WATER DEPRIVATION, WHICH OCCURS IN everyday life in the wild and in cities, increases the need for sodium replacement in humans and animals, and is a subject of concern for public health (16,20,24,25).In the laboratory, repeated episodes of water deprivation (WD) followed by partial rehydration (PR), or WD-PR protocol, sensitize sodium appetite and spontaneous or daily (needfree) NaCl intake in rats (6). The WD-PR is a useful experimental protocol to separate thirst from sodium appetite in water-deprived rats (5, 6, 38), and possibly in humans (16). The PR period, characterized by full restoration of plasma osmolality, but only partial restoration of the extracellular fluid volume, is attained through ingestion of only water to satiety in a thirst test performed at the end of a cycle of WD. The sodium appetite is then expressed by ingestion of NaCl solution in a sodium appetite test performed immediately after the thirst test, thus restoring sodium balance and extracellular volume (5). The ingestion of NaCl in the sodium appetite test is a behavior that results from the production of transient negative sodium balance because of the obligatory sodium loss in urine during dehydration (5). Because of the sodium loss, the behavior also depends on the production of the neuropeptide ANG II and activation of its receptor type 1, the AT 1...

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Sodium intake occurs either as a spontaneous or an induced behavior, which is increased by repeated episodes of water deprivation followed by partial rehydration (WD‐PR). In this work, we quantified transcripts related to RAS in the hypothalamus of rats that had a history of WD‐PR. Adult male Holtzman rats (n=6–12/group) had water and 0.3 M NaCl measured daily. The animals were submitted to one or three episodes of WD‐PR, with 7‐day interval among the three episodes. The animals were sacrificed at the end of the 1st or 3rd WD‐PR (dehydrated) or four days after none, 1st, or 3rd WD‐PR (hydrated). The hypothalamus was dissected and level of mRNA for components of the RAS was determined by qRT‐PCR. Dehydrated animals had increased hypothalamic transcripts of angiotensinogen, aminopeptidase N, ANG II receptor type‐1‐associated protein, ANG receptor like‐1 or apelin receptor by 43%, 60%, 36%, and 159%, respectively, in the 3rd versus 1st WD‐PR. There was no difference in the hypothalamic mRNA content of RAS among hydrated animals. The 0.3 M NaCl intake was enhanced in the 3rd compared to the 1st sodium appetite test in a distinct group. These data suggest that enhancement in the induced sodium intake is associated with alterations in gene expression related to RAS in the hypothalamus. Therefore, hypothalamic RAS may play a role in the long‐term changes of sodium appetite. Research supported by CNPq and FAPESP.

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