Effect of Variations in Sodium Intake on Calcium Excretion in Normal Humans.

Bohannan, J.; Bernstein, D.; Ling, Shun M.; Maxwell, M H

doi:10.3181/00379727-115-28821

Cited by 155 publications

(51 citation statements)

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“…In fact, enhanced sodium excretion in HCa-SHR might have been anticipated on theoretical grounds, in view of the well-known close association between the handling of sodium and calcium at the proximal tubule 27 and the observed positive correlation between net urinary sodium and calcium excretion. 28 The high calcium diet in this study resulted in a sustained negative sodium balance that could account, perhaps along with a relative sodium-volume depletion, for the lower rate of weight gain and growth in HCa-SHR. Although measurements of the extracellular and blood volume were not obtained, the negative sodium balance might have led to some contraction of the extracellular and intravascular compartments.…”

mentioning

confidence: 68%

Effects of high calcium intake on blood pressure and calcium metabolism in young SHR.

Stern¹,

Lee²,

Silis³

et al. 1984

Hypertension

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SUMMARY Increased dietary calcium intake in the adult spontaneously hypertensive rat (SHR) has been reported to correct low serum ionized calcium concentration ([Ca ++ ]) and to result in a significant amelioration of the prevailing hypertension. In the present study we examined several parameters of calcium metabolism in young (6-week-old) SHR and compared them with those observed in normotensive Wistar-Kyoto (WKY) rats fed equal amounts of a diet containing normal quantities of calcium (0.4%, wt/wt) for 4 weeks. A separate group of SHR was placed on an equal amount of a high calcium (2.8%, wt/wt) but otherwise identical diet. In SHR and WKY eating a normal calcium diet, serum total calcium concentration was not different, but [Ca + + ] was lower in SHR (1.58 ± 0.06 vs 1.91 ± 0.07 mmol/liter, p< 0.01). Serum immunoreactive parathyroid hormone (PTH) was increased in some, but not all, SHR. No difference was noted between the two groups in the following parameters: calcium intake, serum 1,25 dihydroxycholecalciferol (1,25(OH) 2 D 3 ), urinary calcium excretion, fractional stool calcium content ([stool calcium/calcium intake] x 100), and in vitro 4SCa uptake by everted gut sacs constructed from segments of duodenum, mid-jejunum, ileum, and proximal colon. A high calcium diet corrected the abnormal serum [Ca + + ] and PTH but did not alter the progression or severity of the hypertension in SHR. A lower net weight gain was observed in SHR on a high calcium diet when compared to SHR eating normal calcium diet (9.1 ± 1.8 vs 27.0 ± 2.0 g). This was attributed, at least in part, to a consistently higher urinary sodium loss in the former group of rats (p < 0.05-0.001 throughout the study period). The progression of hypertension, even in the face of normalized serum [Ca + + ] in young SHR, suggests that low [Ca + + ] and hypertension do not have a cause-and-effect relationship. Sustained natriuresis caused by the augmented dietary calcium intake and increased urinary calcium excretion may contribute to the blood-pressure-lowering effect reported in adult SHR. (Hypertension 6: 639-646, 1984) KEY WORDS • calcium • 1,25(OH) 2 D • sodium • spontaneously hypertensive rat A LTERATIONS in calcium homeostasis in humans with essential hypertension and in spontaneously hypertensive rats (SHR) have been described in recent years.1 " 3 Similar findings in human and rat hypertension include reduced serum ionized calcium concentration [Ca ++ ], increased immunoreactive parathyroid hormone (PTH) levels, and enhanced urinary calcium excretion. Whereas a unify-

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mentioning

confidence: 68%

Effects of high calcium intake on blood pressure and calcium metabolism in young SHR.

Stern¹,

Lee²,

Silis³

et al. 1984

Hypertension

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“…Across extremes of urinary sodium excretion, the relationship between UcaV and UNaV is nonlinear. The previously noted proportional relationship between UcaV and UNaV is applicable only between a sodium intake of 10 and 300 mEq/day, a range approximating that studied in ear lier investigations [5,7,8,33]. Under the stimulus of profound sodium loading, volume expansion and in creased cardiac index, our subjects achieved an average maximal UcaV of 262 ± 53 mg/day on a fixed calcium intake of 400 mg/day.…”

Section: Discussionmentioning

confidence: 90%

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

et al. 1981

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To elucidate the relationship between the renal regulation of sodium and calcium excretion at extremes of sodium intake, we studied 6 normal men ingesting a fixed, 400 mg/day calcium intake and four levels of sodium intake from 10 to 1,500 mEq/day. Serum ionized calcium was not influenced by sodium intake. Blood pressure and cardiac index increased modestly. Urinary calcium excretion increased to 262 ± 53 mg/day (mean ± SE). Plasma norepinephrine concentration, serum PTH levels, hematocrit, total serum protein concentrations and CO₂ content decreased with increasing sodium intake. Urinary cAMP increased as sodium intake was raised from 10 to 300 mEq/day, but subsequently decreased to basal values. Urinary calcium and sodium excretion were related (p < 0.001) in a nonlinear fashion as were the fractional excretions of these cations (p < 0.001). The filtered calcium load and the fractional calcium excretion were directly and linearly related (p < 0.001). We conclude that the effect of sodium intake on urinary calcium excretion principally reflects changes in the filtered calcium load rather than changes in renal sodium handling. Calcium homeostasis at extremes of sodium intake does not appear to be critically dependent upon PTH-mediated mechanisms. The data suggest that the proximal tubule has a remarkable capacity to dissociate calcium resorption from that of sodium.

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“…Interdependence of sodium and calcium transport in the kidney was suggested by the studies of Walser (42) and others (43)(44)(45)(46)(47). Sodium and calcium reabsorption in the proximal convoluted tubules varies in close concert under a variety of conditions, suggesting either a common transport mechanism or dependence of calcium reabsorption on sodium reabsorption and related water reabsorption (48,49).…”

Section: Discussionmentioning

confidence: 99%

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

DeFronzo¹,

Cooke²,

Andres³

et al. 1975

J. Clin. Invest.

1,035

418

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A B S T R A C T The effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 PU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401±46 (SEM) to 213+18 iteq/min during insulin administration, the change becoming significant (P < 0.02) within the 30-60-min collection period. Free water clearance (CH2o) increased from 10.6±0.6 to 13±0.5 ml/min (P <0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (Ui.V) excretion were also both decreased during insulin administration; UKV decreased from 66±9 to 21±1 Meq/min (P < 0.005), and UrV decreased from 504±93 to 230 ±43 Ag/min (P <0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126±24 to 200±17 ug/min (P < 0.01).These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2o suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.

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Effect of Variations in Sodium Intake on Calcium Excretion in Normal Humans.

Cited by 155 publications

References 0 publications

Effects of high calcium intake on blood pressure and calcium metabolism in young SHR.

Effects of high calcium intake on blood pressure and calcium metabolism in young SHR.

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

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