Water deprivation-induced sodium appetite and differential expression of encephalic c-Fos immunoreactivity in the spontaneously hypertensive rat

Abstract

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.

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

“…Such resistance may have resulted from prior sensitization produced by their high brain RAS activity. The SHR also have reduced ingestion-contingent negative feedback and more sensitive cells that respond to WD-PR in the subfornical organ, which combined can subserve their strong sodium intake (9,14,32). In the present work, they showed a vigorous need-induced sodium intake that surpassed the need-induced intakes of HTZ and WKY, as previously shown (32).…”

“…Animals were deprived of both water (WD) and 0.3 M NaCl, but maintained free access to regular food in their cages, for 36 h (experiment 1) or 24 h (experiment 2), according to previous studies (5,32). In sequence, animals were weighed and returned to their cages, from which food had been removed, and a glass burette (with 0.1-ml divisions fitted with a stainless-steel spout) containing filtered water was offered for 2 h to allow a partial extracellular volume repletion, or partial rehydration (PR) condition.…”

“…The SHR inherited through selectively breeding a hyperactive brain RAS (46). We have previously reported that SHR responds to a single WD-PR with increased neural activity (e.g., in the subfornical organ) and stronger sodium appetite than rats from normotensive strains (32). However, it is not known how SHR responds to repeated episodes of WD-PR.…”

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: Influence of sodium intake

“…WD increases plasma renin activity (PRA), which remains elevated at the end of PR [3]. WD-PR also changes neuronal activity as measured by Fos immunoreactivity (Fos-ir) in key brain areas that control bodyfluid balance, thirst and sodium appetite [4,[8][9][10].…”

“…Water deprivation activates the lamina terminalis, a structure that forms part of the anterior wall of the third cerebral ventricle [3,4,9]. The lamina terminalis has two sensory circumventricular organs, organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO), which monitor humoral (e.g.…”