Effects of Parathyroid Hormone on the Distribution and Transport of Calcium in Cultured Kidney Cells*

Borle, A. B.; Uchikawa, T.

doi:10.1210/endo-102-6-1725

Cited by 77 publications

(19 citation statements)

References 17 publications

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“…Because our results (Fig. 6) (14,19,20,26 (27,28). In the proximal tubule cells neither dibutyryl-cAMP, 3-isobutyl-l-methylxanthine, nor forskolin reproduced the effects of PTH (14).…”

Section: Time Controlsmentioning

confidence: 64%

Effects of parathyroid hormone on cytosolic free calcium concentration in individual rabbit connecting tubules.

Bourdeau

Lau²

1989

J. Clin. Invest.

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“…Because our results (Fig. 6) (14,19,20,26 (27,28). In the proximal tubule cells neither dibutyryl-cAMP, 3-isobutyl-l-methylxanthine, nor forskolin reproduced the effects of PTH (14).…”

Section: Time Controlsmentioning

confidence: 64%

Effects of parathyroid hormone on cytosolic free calcium concentration in individual rabbit connecting tubules.

Bourdeau

Lau²

1989

J. Clin. Invest.

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“…Therefore, increased PTH levels are likely to be found in a number of elderly subjects within the upper normal distribution of serum calcium levels. PTH could stimulate calcium channels to increase calcium influx, increasing the levels of intracellular calcium [33,34], thereby influencing insulin sensitivity.…”

Section: Possible Mechanisms For Observed Associationsmentioning

confidence: 99%

Serum calcium is independently associated with insulin sensitivity measured with euglycaemic–hyperinsulinaemic clamp in a community-based cohort

et al. 2006

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Aims/hypothesis Diabetes mellitus type 2 is associated with altered calcium metabolism. Moreover, in diseases with supranormal serum calcium levels, such as primary hyperparathyroidism, the prevalence of diabetes is increased. Relatively little is known about the relationship between serum calcium concentration and the underlying causes of diabetes-insulin resistance and defective insulin secretionin the normocalcaemic general population. Materials and methods We investigated associations between serum calcium concentration and insulin sensitivity and secretion in a population-based cohort of elderly men (Uppsala Longitudinal Study of Adult Men, n=961). Insulin sensitivity index (M/I; glucose disposal rate [M] divided by mean insulin concentration [I]) was assessed using euglycaemic-hyperinsulinaemic clamp, and insulin secretion was estimated from the early insulin response (EIR) during an OGTT.Results In a multivariable linear regression model adjusting for BMI, physical activity, smoking, consumption of tea, alcohol, coffee and dietary calcium, serum phosphate and serum creatinine, 1 SD increase in serum calcium was associated with 0.17 mg kg −1 min −1 (mU/l) −1 × 100 (0.024 mg kg −1 min −1 [pmol/l] −1 ×100) decrease in M/I (p=0.01). The results remained robust in individuals with normal fasting glucose, normal glucose tolerance and serum calcium within the normal range (n=413, regression coefficient for 1 SD increase −0.45, p=0.001). Serum calcium was not associated with EIR. Dietary intake of calcium was not independently associated with insulin sensitivity or EIR. Conclusion/interpretation Our data support the notion that endogenous calcium may be involved early in the development of diabetes and that this effect is mediated mainly through effects on insulin sensitivity rather than defective insulin secretion. Dietary intake of calcium does not seem to influence insulin sensitivity.

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“…Epithelial (luminal) cell membrane permeability to sodium is thought to fall as cytosolic calcium rises, perhaps through a direct effect of calcium on the cell membrane (Manery, 1966;Ellory, Flatman & Stewart, 1983). On this basis, PTH-induced increases in cell permeability to calcium (Borle, 1973;Borle & Uchikawa, 1978), might be expected to raise cytosolic calcium and thereby inhibit tubular reabsorption of sodium. Sodium-calcium exchange across the contraluminal cell membrane, a largely passive process dependent upon active sodium-potassium exchange, may be a major regulator of cytosolic calcium (Taylor & Windhager, 1979).…”

Section: Methodsmentioning

confidence: 99%

Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits.

Peart¹,

Roddis²,

Unwin³

1986

The Journal of Physiology

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SUMMARY1. Following a random block experimental design in each case, three repeated measurement studies were carried out in three different groups of conscious rabbits, to investigate the renal effects of increasing doses of intravenous calcium chloride (CaC12) and bovine parathyroid hormone (PTH).2. In the first study, each rabbit received either CaCl2 (0415, 0 3, 0-5 or 1D0 mg kg-' min-) or vehicle alone (control) for 160 min. In the second study, rabbits were given either PTH (0415 ,ug kg-' min'), CaCl2 (1D0 mg kg-' min-), PTH plus CaCl2 (0415 jug kg-' min-and 1-0 mg kg-' min-, respectively) or vehicle alone; PTH was infused for just over 60 min. In the third study, a much smaller dose (005 mg kg-' min-) of CaCl2 was infused for 100 min.3. CaCl2 infusion produced a striking fall in fractional excretion of sodium of at least 50 % (P < 0-01), but this was not dose related, being almost maximal at the smaller doses infused. Although this effect was evident in the absence of any changes in total plasma calcium concentration at the lower doses of CaCl2, renal calcium excretion was increased between 2-and 20-fold (P < 001) at all doses infused. Fractional excretion of chloride doubled at the two higher doses of CaCl2 (P < 0.01), but potassium excretion was unchanged. There were no consistent alterations in mean arterial blood pressure, effective renal plasma flow, glomerular filtration rate or plasma renin activity (PRA); total plasma calcium concentration was consistently elevated only during infusion of the high dose by just under 1 mmol 1-1.4. PTH infusion had no measured effect on fractional excretion of sodium or renal calcium excretion, but doubled fractional potassium excretion (P < 0 05). Heart rate and PRA increased (P < 0-01 and < 0-05, respectively), the latter by 50 %, but systemic pressure and renal haemodynamics were not significantly affected. By contrast, PTH infused with CaCl2 produced a 4-fold rise in fractional sodium excretion and although renal calcium excretion remained increased, it was reduced by ca. 80 % when compared with renal calcium excretion during infusion of CaCl2 alone. Infusion of PTH alone increased PRA, but when PTH and CaCl2 were infused together, PRA did not change.5. These observations are not fully explained, but may involve PTH-related changes in renal tubular and juxtaglomerular cell permeability to calcium, cytosolic calcium concentration and a sodium-calcium exchange process.

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Effects of Parathyroid Hormone on the Distribution and Transport of Calcium in Cultured Kidney Cells*

Cited by 77 publications

References 17 publications

Effects of parathyroid hormone on cytosolic free calcium concentration in individual rabbit connecting tubules.

Effects of parathyroid hormone on cytosolic free calcium concentration in individual rabbit connecting tubules.

Serum calcium is independently associated with insulin sensitivity measured with euglycaemic–hyperinsulinaemic clamp in a community-based cohort

Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits.

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