Subfornical organ lesion decreases sodium appetite in the sodium-depleted rat

Weisinger, R. S.; Denton, Derek A.; Nicolantonio, R. Di; Hards, D.K.; McKinley, Michael J.; Oldfield, Brian J.; Osborne, P.G.

doi:10.1016/0006-8993(90)90245-7

Cited by 100 publications

(63 citation statements)

References 18 publications

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“…Others have shown that behaviors such as feeding and osmotically stimulated drinking are not affected by ablation of the SFO (16,20), and the inhibitory effects of SFO lesions on drinking apparently are specific for dipsogenic agents that act on specific receptors located on neurons in the SFO to stimulate drinking.…”

Section: Discussionmentioning

confidence: 99%

Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat

Sunn

Egli

Burazin

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Relaxin, a peptide hormone secreted by the corpus luteum during pregnancy, exerts actions on reproductive tissues such as the pubic symphysis, uterus, and cervix. It may also influence body fluid balance by actions on the brain to stimulate thirst and vasopressin secretion. We mapped the sites in the brain that are activated by i.v. infusion of a dipsogenic dose of relaxin (25 g͞h) by immunohistochemically detecting Fos expression. Relaxin administration resulted in increased Fos expression in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus, and magnocellular neurons in the supraoptic and paraventricular nuclei. Ablation of the SFO abolished relaxininduced water drinking, but did not prevent increased Fos expression in the OVLT, supraoptic or paraventricular nuclei. Although ablation of the OVLT did not inhibit relaxin-induced drinking, it did cause a large reduction in Fos expression in the supraoptic nucleus and posterior magnocellular subdivision of the paraventricular nucleus. In vitro single-unit recording of electrical activity of neurons in isolated slices of the SFO showed that relaxin (10 ؊7 M) added to the perfusion medium caused marked and prolonged increase in neuronal activity. Most of these neurons also responded to 10 ؊7 M angiotensin II. The data indicate that bloodborne relaxin can directly stimulate neurons in the SFO to initiate water drinking. It is likely that circulating relaxin also stimulates neurons in the OVLT that influence vasopressin secretion. These two circumventricular organs that lack a blood-brain barrier may have regulatory influences on fluid balance during pregnancy in rats.R elaxin is a peptide hormone secreted by the corpus luteum of the ovary during pregnancy. Relaxin acts on reproductive tissues such as the pubic symphysis, uterus, and cervix (1, 2), but it may also influence the brain (3). Evidence of this influence is presented in reports that the intracerebroventricular (i.c.v.) (1) injection of relaxin results in stimulation of oxytocin and vasopressin secretion, water drinking, and a pressor response (3-8). i.c.v. administration of relaxin also stimulates increased expression of c-fos in groups of neurons in the supraoptic nucleus (SON) and hypothalamic paraventricular nucleus (PVN), as well as in the subfornical organ (SFO), median preoptic nucleus (MnPO), and organum vasculosum of the lamina terminalis (OVLT) (9). Circulating relaxin probably has endocrine actions on the brain, because high-affinity-binding sites for relaxin are present in the SFO and OVLT of the rat (10), two brain regions that are accessible to circulating relaxin because they lack a blood-brain barrier (11). Also, i.v. infusion of relaxin causes vasopressin secretion and water drinking in the rat, effects that may be mediated through brain angiotensinergic mechanisms (12,13). Evidence that relaxin [together with other hormones such as angiotensin II (Ang II) and vasopressin] plays a physiological role in regulating body fluid homeostasis d...

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Section: Discussionmentioning

confidence: 99%

Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat

Sunn

Egli

Burazin

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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“…Fos activation in the same areas occurs during water deprivation (26,41,49). These areas have been implicated by ablation and pharmacological studies to be involved in ANG II-and Na ϩ -depletion-induced Na ϩ intake (3,6,12,13,15,38,39,43,47). The integrity of preoptic periventricular areas such as the OVLT and MnPO, which send projections to the SON, is also necessary for the expression of Fos-ir in the SON in the presence of hyperosmolality or ANG II (49).…”

Section: Discussionmentioning

confidence: 99%

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

Luca

Schoorlemmer

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes. Am J Physiol Regulatory Integrative Comp Physiol 282: R552-R559, 2002; 10.1152/ ajpregu.00295.2000. Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 Ϯ 0.8 ml/2 h; n ϭ 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na ϩ ; 2) decreased blood volume; and 3) reduced total body Na ϩ ; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na ϩ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water. salt intake; hypovolemia; circumventricular organs; dehydration; thirst MODELS OF NA ϩ INGESTION based on selective depletion of the extracellular fluid compartment have revealed several potential mechanisms that control Na ϩ ingestion. These models typically employ combinations of Na ϩ deprivation and depletion to induce hypovolemia. In the rat, Na ϩ ingestion after Na ϩ loss in these models is associated with increased levels of circulating ANG II and aldosterone (9), unloading of baroreceptors (20), and inhibition of oxytocin secretion by dilution of body fluids after the Na ϩ -depleted animals have ingested water (42). Water deprivation is another procedure associated with an increased preference for ingesting NaCl solutions (48). During water deprivation, the obligatory excretion of water coupled with increased natriuresis results in dehydration of both the intracellular and extracellular fluid compartments (21,25,35). Like selective extracellular depletion models of Na ϩ ingestion, water deprivation reduces blood volume and increases plasma renin activity (PRA) and levels of circulating ANG II (8,29,30,35). However, in contrast to the selective extracellular dehydration models, water deprivation is accompanied by reductions, or no changes, in plasma levels of aldosterone (29,34) and by increases in plasma Na ϩ concentration ([Na ϩ ]) and osmolality (29,34,35 ] and osmolality levels are reduced after dehydrated animals drink water.Water-deprived animals clearly prefer to drink water, but there is also considerable ingestion of hypertonic saline solutions wh...

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“…Accordingly, investigators considered the SFO and OVLT potential sites of action for angiotensin II arousal of salt appetite. In this regard, ablation of the SFO decreased sodium intake elicited by administration of the furosemide (Thunhorst et al, 1999;Weisinger et al, 1990). Similarly, lesion of the OVLT significantly attenuated NaCl intake induced by sodium depletion (Chiaraviglio & Perez, 1984), and site-specific injection of angiotensin II into the OVLT stimulated NaCl consumption (Fitts & Masson, 1990).…”

Section: Arousal Of Salt Appetite: Contributions Of Angiotensin IImentioning

confidence: 93%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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Nearly three-quarters of a century ago, Curt Richter removed the adrenal glands from rats and noted that the animal's vitality was dependent on its increased consumption of sodium chloride. In doing so, Richter revealed an innate behavioral mechanism that serves to maintain the hydromineral balance of an animal faced with sodium deficit. This experiment and others like it, led to the development of a field of research devoted to the investigation of salt appetite. The following is a discussion of how Richter's initial observations gave birth to an evolving field that incorporates multiple approaches to examine the drive to consume sodium. KeywordsSalt appetite; Angiotensin; Aldosterone; Corticosterone; Richter The Discovery of Salt AppetiteAt the time that Richter began his career at Johns Hopkins University much of the research examining ingestive behavior focused on the responses of individual organs or closely coordinated systems. Richter's pioneering work initiated a fundamental paradigm shift that moved the focus to adaptations of the organism as a whole. Specifically, he was interested in changes in behavior that compensated for perturbations in the internal environment. His approach toward investigation of such behaviors was as thorough as it was fundamental. Richter manipulated diet, interfered with the nervous system, and removed or replaced glandular secretions in attempt to understand the nutritional, neural, and endocrine signals that contribute to behavior.Richter created disturbances in the nutritional or mineral content of the internal environment with dietary deficiency. Subsequently, "self selection" experiments were performed where choices of different minerals and nutrients were presented for consumption. More often than not, animals would consume minerals and nutrients in amounts that would alleviate their experimentally-induced deficiencies. One of the most striking behaviors that Richter observed was that of rats voluntarily ingesting salt when faced with sodium deficit. Sodium chloride was removed from the rats' food and they were given access to water and 3 % NaCl solution. The intake of the NaCl solution was approximately 1% of the total diet, which remarkably, is the

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Subfornical organ lesion decreases sodium appetite in the sodium-depleted rat

Cited by 100 publications

References 18 publications

Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat

Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

Richter and sodium appetite: From adrenalectomy to molecular biology

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