scholarly journals Effects of calcium-modulating hormones on thiazide receptor density.

1996 ◽  
Vol 7 (7) ◽  
pp. 1052-1057 ◽  
Author(s):  
P Blakely ◽  
D A Vaughn ◽  
D D Fanestil
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Urinary Calcium Excretion ◽  
Ion Concentration ◽  
Calcium Excretion ◽  
Calcitropic Hormones ◽  
Calcium Ion Concentration

Thiazide diuretic drugs act in the distal convoluted tubule (DCT) to inhibit a Na+Cl- cotransporter and enhance reabsorption of luminal calcium. The density of receptors for thiazides in the rat DCT is known to be increased by adrenocortical steroids, furosemide, and bendroflumethiazide, but decreased by ischemia. Because the DCT is a physiologic site of action by calcitonin and parathyroid hormone, this study examined the effects of these calcitropic hormones in thyroparathyroidectomized Sprague-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3H)metolazone to renal membranes, and (2) urinary electrolyte excretion rate. Salmon calcitonin (sCT) (20 to 100 ng/h) (1) increased the density of the renal TZR twofold, an effect that is maximal by 6 h after sCT administration, and (2) decreased urinary calcium excretion rate. Adequate dietary calcium must be provided for the effects of sCT to be observed. Regression analysis demonstrated that renal TZR density correlated negatively with total urinary calcium excretion rate but not with plasma calcium ion concentration. In addition, neither rat calcitonin (rCT), at doses that cause hypocalcemia, nor parathyroid hormone, at doses that cause hypercalcemia, produce direct effects on TZR density in the DCT of the thyroparathyroidectomized rat. Our findings indicate that upregulation of TZR by sCT, which occurs independently of plasma calcium-ion concentration, is likely via a calcitonin-like receptor other than that for rat calcitonin itself.

scholarly journals Recombinant human parathyroid hormone (1–84) is effective in CASR-associated hypoparathyroidism

2020 ◽  
Vol 183 (6) ◽  
pp. K13-K21
Author(s):  
Colin Patrick Hawkes ◽  
Dorothy I Shulman ◽  
Michael A Levine
Keyword(s):  
Parathyroid Hormone ◽  
Traditional Approach ◽  
Calcium Supplementation ◽  
Case Series ◽  
Calcium Sensitivity ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Human Parathyroid Hormone

Introduction Gain-of-function mutations in the CASR gene cause Autosomal Dominant Hypocalcemia Type 1 (ADH1), the most common genetic cause of isolated hypoparathyroidism. Subjects have increased calcium sensitivity in the renal tubule, leading to increased urinary calcium excretion, nephrocalcinosis and nephrolithiasis when compared with other causes of hypoparathyroidism. The traditional approach to treatment includes activated vitamin D but this further increases urinary calcium excretion. Methods In this case series, we describe the use of recombinant human parathyroid hormone (rhPTH)1–84 to treat subjects with ADH1, with improved control of serum and urinary calcium levels. Results We describe two children and one adult with ADH1 due to heterozygous CASR mutations who were treated with rhPTH(1–84). Case 1 was a 9.4-year-old female whose 24-h urinary calcium decreased from 7.5 to 3.9 mg/kg at 1 year. Calcitriol and calcium supplementation were discontinued after titration of rhPTH(1–84). Case 2 was a 9.5-year-old male whose 24-h urinary calcium decreased from 11.7 to 1.7 mg/kg at 1 year, and calcitriol was also discontinued. Case 3 was a 24-year-old female whose treatment was switched from multi-dose teriparatide to daily rhPTH(1–84). All three subjects achieved or maintained target serum levels of calcium and normal or improved urinary calcium levels with daily rhPTH(1–84) monotherapy. Conclusions We have described three subjects with ADH1 who were treated effectively with rhPTH(1–84). In all cases, hypercalciuria improved by comparison to treatment with conventional therapy consisting of calcium supplementation and calcitriol.

A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men

1997 ◽  
Vol 83 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
Noriko Ashizawa ◽  
Rei Fujimura ◽  
Kumpei Tokuyama ◽  
Masashige Suzuki
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Bone Resorption ◽  
Resistance Exercise ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Osteoclastic Bone Resorption ◽  
Calcium Excretion ◽  
Repetition Maximum ◽  
Renal Tubular

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, and Masashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men. J. Appl. Physiol. 83(4): 1159–1163, 1997.—Metabolic acidosis increases urinary calcium excretion in humans as a result of administration of ammonium chloride, an increase in dietary protein intake, and fasting-induced ketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as a result of increase in blood lactate concentration. In this study we investigated changes in renal calcium handling, plasma parathyroid hormone concentration, and osteoclastic bone resorption after a single bout of resistance exercise. Ten male subjects completed a bout of resistance exercise with an intensity of 60% of one repetition maximum for the first set and 80% of one repetition maximum for the second and third sets. After exercise, blood and urine pH shifted toward acidity and urinary calcium excretion increased. Hypercalciuria was observed in the presence of an increased fractional calcium excretion and an unchanged filtered load of calcium. Therefore, the observed increase in urinary calcium excretion was due primarily to decrease in renal tubular reabsorption of calcium. Likely causes of the increase in renal excretion of calcium are metabolic acidosis itself and decreased parathyroid hormone. When urinary calcium excretion increased, urinary deoxypyridinoline, a marker of osteoclastic bone resorption, decreased. These results suggest that 1) strenuous resistance exercise increased urinary calcium excretion by decreasing renal tubular calcium reabsorption, 2) urinary calcium excretion increased independently of osteoclast activation, and 3) the mechanism resulting in postexercise hypercalciuria might involve non-cell-mediated physicochemical bone dissolution.

Hypocalcaemic disorders, hypoparathyroidism, and pseudohypoparathyroidism

2011 ◽  
pp. 675-686 ◽  
Author(s):  
Rajesh V. Thakker
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Common Causes ◽  
Abnormal Metabolism ◽  
Serum Pth ◽  
Calcium Ion Concentration

Extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) on kidney and bone (Fig. 4.5.1). The intact peptide is secreted by the parathyroid glands at a rate that is appropriate to and dependent upon the prevailing extracellular calcium ion concentration. The causes of hypocalcaemia (Box 4.5.1) can be classified according to whether serum PTH concentrations are low (that is hypoparathyroid disorders) or high (that is disorders associated with secondary hyperparathyroidism) (1–6). The most common causes of hypocalcaemia are hypoparathyroidism, a deficiency or abnormal metabolism of vitamin D, acute or chronic renal failure, and hypomagnesaemia. This chapter will initially review the clinical features and management of hypocalcaemia, and then discuss the specific hypocalcaemic disorders.

scholarly journals Role of 1,25-Dihydroxy Vitamin D3and Parathyroid Hormone in Urinary Calcium Excretion in Calcium Stone Formers

2014 ◽  
Vol 55 (5) ◽  
pp. 1326 ◽  
Author(s):  
Won Tae Kim ◽  
Yong-June Kim ◽  
Seok Joong Yun ◽  
Kyung-Sub Shin ◽  
Young Deuk Choi ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Calcium Stone ◽  
Stone Formers

Dissociation of membrane potential and hormone secretion in bovine parathyroid cells

1983 ◽  
Vol 245 (1) ◽  
pp. E102-E105
Author(s):  
J. J. Morrissey ◽  
S. Klahr
Keyword(s):  
Parathyroid Hormone ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Calcium Ion ◽  
Cell Function ◽  
Hormone Secretion ◽  
Ion Concentration ◽  
Parathyroid Cell ◽  
High Potassium ◽  
Calcium Ion Concentration

An increase in the calcium ion concentration of the medium from 0.5 to 2.0 mM is associated with a 65% decrease in the secretion of parathyroid hormone from dispersed parathyroid cells. This maneuver also depolarized the cell membrane from -55 to -21 mV as measured by the distribution of [3H]tetraphenylphosphonium ion between cells and medium. An increase in the potassium ion concentration of the medium to 50 mM caused a 67% increase in hormone secretion at 0.5 mM calcium and depolarized the cell to -31 mV. The high potassium did not significantly change hormone secretion or the membrane potential at 2.0 mM calcium. Chlorpromazine inhibited hormone secretion by 40% and depolarized the cell to -30 mV at 0.5 mM calcium in the medium. Chlorpromazine did not change hormone secretion or membrane potential in cells incubated at 2.0 mM calcium. These results suggest that depolarization of the cell by calcium cannot account by itself for the inhibition of hormone secretion and chlorpromazine mimics the effect of an increase in calcium on parathyroid cell function.

Update – Kalziumstoffwechsel

2019 ◽  
Vol 144 (16) ◽  
pp. 1125-1132
Author(s):  
Christof Schöfl
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Free Calcium ◽  
Calcium Excretion ◽  
Calcium Balance ◽  
Stomach Pain ◽  
Free Calcium Concentration

AbstractA finely balanced control system keeps the extracellular calcium concentration within narrow limits. Disorders of calcium metabolism are often based on altered parathormone levels. Symptoms are not always clear, sometimes they are even missing: the more it is important to know possible associated diseases. The author presents basics, current diagnostics and concrete therapy options. Central hormone for the regulation of the calcium balance is the parathyroid hormone. With decreasing calcium, PTH leads to an increase in extracellular free calcium concentration in three ways. The classic symptoms of pHPT (polyuria, polydipsia, “stone, leg, and stomach pain”) are rare now, as the condition is diagnosed much earlier. Treatment of choice in all symptomatic patients with pHPT is surgery. FHH and pHPT are both characterized by hypercalcaemia and increased parathyroid hormone. The differential diagnosis of urinary calcium excretion, which is usually lower in FHH but normal or elevated in pHPT, is crucial. In primary hypoparathyroidism, parathyroid failure interferes with calcium homeostasis at a central location. Consequences are hypocalcaemia, hyperphosphatemia and lack of active vitamin D. Due to increased urinary calcium excretion, patients with ADH are at high risk for kidney stones, nephrocalcinosis and the development of renal insufficiency. Recently, rhPTH 1-84 has been available for the treatment of hypoparathyroidism. However, long-term data is still lacking to provide a safe indication, considering potential effects and side effects.

Abnormalities of Calcium Metabolism in Essential Hypertension

1983 ◽  
Vol 65 (2) ◽  
pp. 137-141 ◽  
Author(s):  
P. Strazzullo ◽  
V. Nunziata ◽  
M. Cirillo ◽  
R. Giannattasio ◽  
L. A. Ferrara ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Calcium Handling ◽  
Ionized Calcium ◽  
Calcium Excretion ◽  
Hypertensive Patients ◽  
Excretion Rates

1. Calcium metabolism has been investigated in patients with essential hypertension and normal renal function to evaluate the renal calcium handling and the reported increase in renal calcium loss. 2. In 55 hypertensive and 55 sex- and age-matched healthy normotensive subjects creatinine clearance, serum total and ionized calcium, plasma parathyroid hormone and 24 h urinary excretion of calcium, sodium and cAMP were measured. In a subgroup of 20 hypertensive patients and 20 controls the fasting calcium excretion rate was also measured. 3. Both 24 h and fasting calcium excretion rates were higher in the hypertensive group; so also were plasma parathyroid hormone and urinary cAMP. Serum total and ionized calcium levels were not different in the two groups. 4. After intravenous calcium infusion (15 mg 3 h−1 kg−1) in seven hypertensive patients and controls, the hypertensive patients excreted more calcium at all serum calcium concentrations. 5. These results support the hypothesis of primary renal calcium leak in essential hypertension. Enhanced urinary calcium excretion rate may cause compensatory parathyroid overactivity.

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