The relationship between blood pressure and serum parathyroid hormone with special reference to urinary calcium excretion: The Tromsø study

2006 ◽  
Vol 29 (3) ◽  
pp. 214-220 ◽  
Author(s):  
F. Saleh ◽  
R. Jorde ◽  
J. Svartberg ◽  
J. Sundsfjord
Keyword(s):  
Blood Pressure ◽  
Parathyroid Hormone ◽  
Special Reference ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Serum Parathyroid Hormone ◽  
The Relationship

Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level

1997 ◽  
Vol 93 (2) ◽  
pp. 153-157 ◽  
Author(s):  
Ryoji Ozono ◽  
Tetsuya Oshima ◽  
Hideo Matsuura ◽  
Katsuhiko Ishibashi ◽  
Mitsuaki Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Calcium Metabolism ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Mean Blood Pressure ◽  
Calcium Excretion ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Change In Mean

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

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.

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.

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.

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

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.

scholarly journals The relation between serum parathyroid hormone (PTH) and blood pressure. The Tromsø study

2009 ◽  
Vol 16 (2) ◽  
Author(s):  
Rolf Jorde
Keyword(s):  
Blood Pressure ◽  
Parathyroid Hormone ◽  
Serum Creatinine ◽  
Diastolic Blood Pressure ◽  
Serum Calcium ◽  
Randomized Clinical Trials ◽  
Smoking Status ◽  
Calcium Excretion ◽  
Serum Parathyroid Hormone ◽  
Serum Pth

The objective of the present cross-sectional epidemiological study from Tromsø, North Norway was to evaluate the relation between blood pressure and serum parathyroid hormone (PTH). 10419 subjects were invited to participate in the fifth Tromsø study and 8128 attended. 7954 subjects had serum PTH measured, and among these, information on blood pressure medication was available in 5841 subjects (2554 males) with serum calcium within the reference range 2.20-2.60 mmol/L. In a multiple linear<br />regression model with age, BMI, serum calcium, serum creatinine, and smoking status as covariables, serum PTH was a significant and positive predictor of systolic and diastolic blood pressure in both genders. When dividing the cohort in PTH quartiles, and adjusting for age, BMI, serum calcium, and serum creatinine, the differences between the lowest and highest PTH quartile in systolic and diastolic blood pressure were 5.0 and 3.5 mmHg for males and 4.1 and 2.5 mmHg for females, respectively. In previous studies we have found serum PTH to be a positive predictor for future increase in blood pressure, and also that the association between serum PTH and blood pressure cannot alone be ascribed to a blood pressure induced increase in urinary calcium excretion. To further elucidate the relation between serum PTH and blood pressure, randomized clinical trials with calcium and/or vitamin D supplementation to subjects with increased serum PTH levels are needed

scholarly journals Mini-review: regulation of the renal NaCl cotransporter by hormones

2016 ◽  
Vol 310 (1) ◽  
pp. F10-F14 ◽  
Author(s):  
Lorena Rojas-Vega ◽  
Gerardo Gamba
Keyword(s):  
Blood Pressure ◽  
Parathyroid Hormone ◽  
Angiotensin Ii ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Hormone Signaling ◽  
Acid Base ◽  
Major Pathway ◽  
Physiological Variables ◽  
Nacl Cotransporter

The renal thiazide-sensitive NaCl cotransporter, NCC, is the major pathway for salt reabsorption in the distal convoluted tubule. The activity of this cotransporter is critical for regulation of several physiological variables such as blood pressure, serum potassium, acid base metabolism, and urinary calcium excretion. Therefore, it is not surprising that numerous hormone-signaling pathways regulate NCC activity to maintain homeostasis. In this review, we will provide an overview of the most recent evidence on NCC modulation by aldosterone, angiotensin II, vasopressin, glucocorticoids, insulin, norepinephrine, estradiol, progesterone, prolactin, and parathyroid hormone.

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