Changes in volemia and natremia and onset of sodium appetite in sodium depleted rats

Ferreyra, María del Carmen Colín; Chiaraviglio, Emma

doi:10.1016/0031-9384(77)90327-4

Cited by 34 publications

(19 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other studies, however, have shown that a reduction of plasma volume in rats does not necessarily initiate the onset of sodium appetite (Ferreyra & Chiaraviglio, 1977). We did not measure blood volume directly in the current experiments but in sodium-deficient calves hypovolaemia develops with a reduction in e.c.f.…”

Section: Discussionmentioning

confidence: 97%

The effect on salt appetite and the renin—aldosterone system on replacing the depleted ions to sodium‐deficient cattle

Bell

Drury

Sly

1981

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO3 rewards showed change in sodium appetite.2. Sodium-depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 1.) in a few minutes, or as an isotonic solution (16 1.) usually within 30 min.3.-When the ionic deficit was restored by either i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (41.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium-deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO3 with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only 0022-3751/81/4490-1106 $07.50

show abstract

Section: Discussionmentioning

confidence: 97%

The effect on salt appetite and the renin—aldosterone system on replacing the depleted ions to sodium‐deficient cattle

Bell

Drury

Sly

1981

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…For example, previous studies have employed dialysis, diuretic treatment, or administration of hyperoncotic colloids (10,11,17,36). Such protocols have the advantage of producing Na ϩ depletion and need-induced Na ϩ intake under clearly defined initial conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Such protocols have the advantage of producing Na ϩ depletion and need-induced Na ϩ intake under clearly defined initial conditions. These initial conditions invariably involve hypovolemia and hyponatremia and subsequent hormonal responses, in particular activation of the renin-angiotensin-aldosterone system and inhibition of oxytocin release (9,11,42). In these protocols, sodium appetite typically occurs only after a delay of several hours subsequent to an earlier development of thirst.…”

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

View full text Add to dashboard Cite

. 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...

show abstract

“…The technique, described previously (11), consisted of an intraperitoneal injection of a 5% glucose solution warmed to 37°C in a volume equivalent to 10% of rat body weight. After 1 h, the ascitic fluid was recovered by inserting a needle into the peritoneal cavity.…”

Section: Methodsmentioning

confidence: 99%

Sodium appetite and Fos activation in serotonergic neurons

Franchini

Johnson

Olmos

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

2000.-We evaluated serotonergic hindbrain groups of cells for their involvement in the generation and inhibition of sodium appetite. For that purpose, we analyzed the number of Fos-immunoreactive (Fos-ir) cells and double-labeled Fosserotonin (5-HT)-ir neurons within different nuclei of the hindbrain raphe system and the area postrema (AP). Sodium depletion and sodium appetite were induced by peritoneal dialysis. Twenty-four hours after peritoneal dialysis, a 2% NaCl solution intake test was given to peritoneal dialyzed animals [PD-with access (PD-A) group] and to control dialyzed animals [CD-with access (CD-A) group]. Two additional groups of animals received either peritoneal dialysis or control dialysis but were not given access to the 2% NaCl [CD-no access (CD-NA) group or PD-no access (PD-NA) group]. The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. The PD-NA group had significantly fewer double-labeled cells along the raphe system compared with the animals in near-normal sodium balance (CD-NA and CD-A) or in the process of restoring sodium balance by consuming NaCl (PD-A). The AP of the PD-A group showed a significant increase in the number of Fos-ir and Fos-5-HT-ir cells compared with the PD-NA and CD groups. Our results suggest that serotonergic pathways with cell bodies in the AP and the raphe system are involved in the control of sodium appetite.Fos-serotonin immunoreactivity; area postrema; raphe system RECENTLY, there has been increased interest in identifying the neural network subserving sodium appetite. Forebrain structures such us the circumventricular organs (CVOs) of the lamina terminalis, the organum vasculosum of the lamina terminalis, and the subfornical organ have been identified as key targets processing angiotensin-, osmotic-, and sodium-related information involved in the control of sodium appetite.A hindbrain system has also been recently implicated in the inhibitory control of sodium appetite. This system includes the neural circuitry of the area postrema (AP), nucleus of the solitary tract (NTS), and lateral parabrachial nucleus (LPBN). Ablation of the AP and the immediately adjacent medial NTS (mNTS) increases induced and ad libitum sodium intake (7, 9, 16). Electrolytic or chemical lesions of the LPBN, which receives afferent projections from the AP/mNTS, also enhance drinking induced by intracerebroventricular ANG II as well as other ANG II-related stimuli (10,28,29). Several studies suggest that a serotonergic hindbrain circuit including the LPBN may normally exert an inhibitory action on several models of reninangiotensin-dependent sodium and water intake (6,22,23; see Ref. 18 for review). In addition, previous evidence has indicated that there are central serotonergic influences on sodium and water intake and excretion (24,27,34,37).Serotonergic neurons are located within several nuclei in the midbrain and the brain stem and have dif...

show abstract

Changes in volemia and natremia and onset of sodium appetite in sodium depleted rats

Cited by 34 publications

References 12 publications

The effect on salt appetite and the renin—aldosterone system on replacing the depleted ions to sodium‐deficient cattle

The effect on salt appetite and the renin—aldosterone system on replacing the depleted ions to sodium‐deficient cattle

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

Sodium appetite and Fos activation in serotonergic neurons

Contact Info

Product

Resources

About