Increased salt preference in adult offspring raised by mother rats consuming excessive amounts of salt and water

Vijande, M.; Brime, J.I.; López-Sela, P.; Costales, M.; Argüelles, Juan

doi:10.1016/0167-0115(96)00042-0

Cited by 31 publications

(21 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Maternal vomiting during gestation, infantile diuresis, diarrhea, vomiting, and inadequate infant formula electrolytes, have all been linked to long-term increased sodium appetite in humans (9,10,23,27,30,44) and are consistent with findings in animals (4,16,26,29,48).…”

Section: Discussionsupporting

confidence: 71%

“…Yet attempts in rats to relate early sodium intake to long-term salt preference have yielded inconsistent results (11,29,37). Similarly, in humans, studies on the determinants of individual variability in salt preference and intake that have concentrated on exposure, acculturation, and learning, particularly in infancy and childhood, have not revealed the determinants of individual variability in salt preference (7, 18, 34) although they have shown how a particular salty food becomes preferred (47).On the other hand, in rats, long-term increases in salt intake have been found consequent on varied instances of perinatal mineralofluid loss: offspring of dams that during pregnancy were dehydrated, lost sodium, or had their hormones of sodium conservation activated, or rats that were acutely sodium deprived postnatally, all show increased sodium intake in adulthood (4,16,26,29,48). Similarly, in humans, maternal vomiting during pregnancy increases offspring salt preference, as do childhood vomiting, diarrhea, salt wasting, and electrolyte deficient feeding (9,10,23,27,42).…”

mentioning

confidence: 99%

“…On the other hand, in rats, long-term increases in salt intake have been found consequent on varied instances of perinatal mineralofluid loss: offspring of dams that during pregnancy were dehydrated, lost sodium, or had their hormones of sodium conservation activated, or rats that were acutely sodium deprived postnatally, all show increased sodium intake in adulthood (4,16,26,29,48). Similarly, in humans, maternal vomiting during pregnancy increases offspring salt preference, as do childhood vomiting, diarrhea, salt wasting, and electrolyte deficient feeding (9,10,23,27,42).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Shirazki

Weintraub²,

Reich³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

with low birth weight of 1,218.2 Ϯ 36.6 g (range, 765-1,580 g) were selected from hospital archives on the basis of whether they had received neonatal diuretic treatment or as healthy matched controls. The children were tested for salt appetite and sweet preference, including rating of preferred concentration of salt in tomato soup (and sugar in tea), ratings of oral spray (NaCl and sucrose solutions), intake of salt or sweet snack items, and a food-seasoning, liking, and dietary questionnaire. Results showed that sodium appetite was not related to neonatal diuretic treatment, birth weight, or gestational age. However, there was a robust inverse correlation (r ϭ Ϫ0.445, P Ͻ 0.005) between reported dietary sodium intake and the neonatal lowest serum sodium level (NLS) recorded for each child as an index of sodium loss. The relationship of NLS and dietary sodium intake was found in both boys and girls and in both Arab and Jewish children, despite marked ethnic differences in dietary sources of sodium. Hence, low NLS predicts increased intake of dietary sodium in low birth weight children some 8 -15 yr later. Taken together with other recent evidence, it is now clear that perinatal sodium loss, from a variety of causes, is a consistent and significant contributor to long-term sodium intake. dietary sodium; humans; hyponatremia; neonates; perinatal programming; sodium appetite THE SOURCE OF INDIVIDUAL VARIATION in salt appetite and why many people ingest an excess of salt are not known. Early development is considered to be a crucial period for establishing individuality in behavior and may similarly determine individual differences in salt preference. Yet attempts in rats to relate early sodium intake to long-term salt preference have yielded inconsistent results (11,29,37). Similarly, in humans, studies on the determinants of individual variability in salt preference and intake that have concentrated on exposure, acculturation, and learning, particularly in infancy and childhood, have not revealed the determinants of individual variability in salt preference (7, 18, 34) although they have shown how a particular salty food becomes preferred (47).On the other hand, in rats, long-term increases in salt intake have been found consequent on varied instances of perinatal mineralofluid loss: offspring of dams that during pregnancy were dehydrated, lost sodium, or had their hormones of sodium conservation activated, or rats that were acutely sodium deprived postnatally, all show increased sodium intake in adulthood (4,16,26,29,48). Similarly, in humans, maternal vomiting during pregnancy increases offspring salt preference, as do childhood vomiting, diarrhea, salt wasting, and electrolyte deficient feeding (9,10,23,27,42).Much of the human data are based on recall, and it thus remains to be proven that confirmed neonatal sodium deficit increases salt appetite enduringly in humans. In an earlier attempt, we tested children who had received neonatal diuretic therapy, and found that five children who had received neonatal di...

show abstract

Section: Discussionsupporting

confidence: 71%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Shirazki

Weintraub²,

Reich³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Both sodium and potassium levels in the milk of rats can be altered by feeding them a low-salt or a high-salt diet (Dlouha et al, 1973;Vijande et al, 1996). When a high-salt diet (about 13%) was fed to pregnant ewes there was no change in the sodium concentration in their milk but, chloride levels in the milk increased (Meyer and Weir, 1954).…”

Section: Introductionmentioning

confidence: 99%

Feeding pregnant ewes a high-salt diet or saltbush suppresses their offspring’s postnatal renin activity

Chadwick

Williams

Vercoe

et al. 2009

Animal

View full text Add to dashboard Cite

If ewes consumed a high-salt diet or saltbush during the last 3 months of pregnancy and for 3 weeks after birth, we expected the renin activity of their lamb to be suppressed at birth and at 3 weeks of age. We also expected an increase in the concentration of cations other than sodium in the ewe's milk and an increase in the plasma Na concentration of the lamb at birth. To test these hypotheses, Merino ewes were fed a high-salt diet (14% NaCl) in an animal house and compared to control ewes eating a control diet (2% NaCl). In addition, we compared ewes grazing saltbush (about 13% salt in diet) to ewes grazing pasture from day 60 of pregnancy to 3 weeks after birth. Lambs born to ewes consuming saltbush had 85% lower ( P , 0.001) renin activity than offspring from ewes consuming pasture at 3 weeks of age. Similarly, lambs born to ewes consuming a high-salt diet had 20% lower renin activity at birth and 3 weeks ( P 5 0.07). Feeding ewes a high-salt diet or saltbush altered the mineral composition of the milk; the largest change was a 10% increase in K levels ( P < 0.05). Consuming a high-salt diet or saltbush lowered the plasma Na of ewes at 130 days of gestation (by 3-5 mmol/l; P , 0.001), but only lambs from ewes fed the high-salt diet had a lower plasma Na at birth ( P , 0.05). Suppression of the renin activity of lambs could lead to permanent physiological changes in salt balance in later life.

show abstract

“…The enhancement is, however, not related to the anteroventral periventricular tissue surrounding the third ventricle, an area important for the angiotensin II-induced component of sodium intake, since lesion of this area does not alter either daily NaCl intake or its enhancement (10). The print might be related to organizational changes in the brain because pregnancy and neonatal sodium depletion or hypovolemia produce offspring with enhanced need-free intake during adulthood (11)(12)(13). The failure to obtain significant enhancement of need-induced NaCl intake with repeated water deprivations contrasts with the experiments of extracellular models in which need-induced intake is clearly enhanced by only one prior episode of sodium depletion (1,3,9,10).…”

mentioning

confidence: 99%

Episodes of water deprivation enhance daily hypertonic NaCl intake in rats

Pereira

David

Menani

et al. 2002

Braz J Med Biol Res

View full text Add to dashboard Cite

Water and 1.8% NaCl intake was recorded daily in adult male rats (N = 6) submitted to four water deprivations plus four sodium appetite tests, each at the end of each 7-day interval, or in controls (nondeprived, N = 6). Water deprivation was achieved by removing water and 1.8% NaCl for 24 h. Water was then offered for 2 h. At the end of this period, 1.8% NaCl was also offered in addition to water (sodium appetite test). Average daily 1.8% NaCl intake was enhanced from 5.2 ± 1.0 to 15.7 ± 2.5 ml from the first to the fifth week in the experimental group and was unchanged in the control group. Daily water intake was not altered in either group. Thus, repeated episodes of water deprivation enhance daily NaCl intake. Key wordsMechanisms subserving need-induced sodium intake, i.e., the sodium intake that results from sodium depletion, have been studied in models of extracellular dehydration. The rat in these models becomes hypovolemic as a result of administration of intraperitoneal dialysis, hyperoncotic colloids or diuretics (1-4). Enhancement of need-induced sodium intake in the extracellular model is produced in the rat by a prior episode of sodium depletion (1-4). The episode of sodium depletion corresponds to a period of 24 h in negative sodium balance, after which normal hydration balance is restored by allowing the animal to ingest sodium and water (1-4). Daily need-free intake of hypertonic NaCl, i.e., sodium intake in the hydrated state, is also enhanced by episodes of sodium depletion (2,4).Net sodium loss occurs during water deprivation as part of the mechanisms that blunt the increase in extracellular hypertonicity and consequent cell dehydration (5,6). Concurrent hypovolemia and activation of the renin-angiotensin system during water deprivation induce a specific appetite for sodium, clearly distinct from thirst (5-9). It is not known whether episodes of water deprivation also enhance sodium intake. The results of the present study show that daily sodium intake is enhanced by repeated episodes of water deprivation in rats.Male Holtzman rats (280-300 g) were housed under standard laboratory conditions of a 12/12-h light-dark cycle, 23 ± 2ºC and 55 ± 10% humidity. Regular food pellets (Purina chow), water and 1.8% NaCl solution were freely available for consumption unless otherwise stated. Daily intake of water and 1.8% NaCl was recorded using polypropylene tubes graduated to the nearest 1 ml and fitted with stainless steel spouts. Water deprivation and sodium appetite tests were performed as described (8). Briefly, water and 1.8% NaCl were removed from the cages and only food remained available

show abstract

Increased salt preference in adult offspring raised by mother rats consuming excessive amounts of salt and water

Cited by 31 publications

References 9 publications

Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Feeding pregnant ewes a high-salt diet or saltbush suppresses their offspring’s postnatal renin activity

Episodes of water deprivation enhance daily hypertonic NaCl intake in rats

Contact Info

Product

Resources

About