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.

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.

Changes in calcium metabolic indices during long-term treatment of patients with essential hypertension

1988 ◽  
Vol 75 (5) ◽  
pp. 543-549 ◽  
Author(s):  
Andreas Hvarfner ◽  
Reinhold Bergström ◽  
Hans Lithell ◽  
Claes Mörlin ◽  
Leif Wide ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Essential Hypertension ◽  
Parathyroid Hormone ◽  
Free Fatty Acids ◽  
Calcium Metabolism ◽  
Elevated Blood Pressure ◽  
Ionized Calcium ◽  
Elevated Blood ◽  
Metabolic Indices

1. Disturbances of calcium metabolism, mimicking mild, compensated secondary hyperparathyroidism, accompany essential hypertension, but it is not known whether these alterations are primary or only secondary to the elevated blood pressure. 2. Indices of systemic calcium metabolism were followed prospectively during 6 months' treatment with either propranolol, bendroflumethiazide or verapamil in 35 patients with essential hypertension. Multivariate statistical methods were employed to study the effects of blood pressure reduction upon the metabolic indices with adjustment for the effects of the different antihypertensive agents. 3. Propranolol treatment increased the plasma ionized calcium and serum phosphate concentrations, and reduced the serum levels of parathyroid hormone, free fatty acids and glycerol. Neither the total nor the total albumin-modified serum calcium concentration was significantly affected. Thus, presumably the decrease in free fatty acids reduced the calcium complex and the calcium binding to albumin, and consequently increased the plasma ionized calcium, thereby suppressing the secretion of parathyroid hormone. 4. Bendroflumethiazide caused a reduction of the fasting renal calcium excretion to half the pretreatment level, but produced no other significant changes in the various indices of calcium metabolism. 5. During verapamil treatment, the fasting renal excretion of calcium and magnesium increased, whereas the free fatty acids and glycerol concentrations in serum were reduced. These two changes presumably balanced each other, as the plasma ionized calcium and serum parathyroid hormone concentrations were not significantly altered. 6. There were no consistent relationships between the decrease in blood pressure and the changes in the metabolic indices, either in the total sample or within any subgroup. These findings indicate that disturbances of calcium metabolism in essential hypertension are primary to, and not induced by, the elevated blood pressure per se.

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 Primary Hyperparathyroidism in Homozygous Sickle Cell Patients: A Hemolysis-Mediated Hypocalciuric Hypercalcemia Phenotype?

2021 ◽  
Vol 10 (21) ◽  
pp. 5179
Author(s):  
Edmat Akhtar Khan ◽  
Lynda Cheddani ◽  
Camille Saint-Jacques ◽  
Rosa Vargas-Poussou ◽  
Vincent Frochot ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Sickle Cell ◽  
Fractional Excretion ◽  
Urinary Calcium ◽  
High Rate ◽  
Calcium Handling ◽  
Control Group ◽  
Calcium Excretion ◽  
Calcium Reabsorption ◽  
Chronic Hemolysis

Primary hyperparathyroidism (pHPT) has been reported to have a higher prevalence in sickle cell disease (SCD) patients, including a high rate of recurrence following surgery. However, most patients are asymptomatic at the time of diagnosis, with surprisingly infrequent hypercalciuria, raising the issue of renal calcium handling in SCD patients. We conducted a retrospective study including (1) 64 hypercalcemic pHPT non-SCD patients; (2) 177 SCD patients, divided into two groups of 12 hypercalcemic pHPT and 165 non-pHPT; (3) eight patients with a diagnosis of familial hypocalciuric hypercalcemia (FHH). Demographic and biological parameters at the time of diagnosis were collected and compared between the different groups. Determinants of fasting fractional excretion of calcium (FeCa2+) were also analyzed in non-pHPT SCD patients. Compared to non-SCD pHPT patients, our data show a similar ionized calcium and PTH concentration, with a lower plasmatic calcitriol concentration and a lower daily urinary calcium excretion in pHPT SCD patients (p < 0.0001 in both cases). Fasting FeCa2+ is also surprisingly low in pHPT SCD patients, and thus inadequate to be considered hypercalcemia, recalling the FHH phenotype. FeCa2+ is also low in the non-pHPT SCD control group, and negatively associated with PTH and hemolytic biomarkers such as LDH and low hemoglobin. Our data suggest that the pHPT biochemical phenotype in SCD patients resembles the FHH phenotype, and the fasting FeCa2+ association with chronic hemolysis biomarkers strengthens the view of a potential pharmacological link between hemolytic by-products and calcium reabsorption, potentially through a decreased calcium-sensing receptor (CaSR) activity.

scholarly journals Vitamin D metabolite-mediated hypercalcemia and hypercalciuria patients with AIDS- and non-AIDS-associated lymphoma

Blood ◽  
1989 ◽  
Vol 73 (1) ◽  
pp. 235-239 ◽  
Author(s):  
JS Adams ◽  
M Fernandez ◽  
MA Gacad ◽  
PS Gill ◽  
DB Endres ◽  
...  
Keyword(s):  
Los Angeles ◽  
Medical Center ◽  
Elevated Serum ◽  
Urinary Calcium ◽  
Disease Stage ◽  
Additional Patient ◽  
Calcium Excretion ◽  
Adult T Cell Leukemia ◽  
Severe Hypercalcemia ◽  
Excretion Rates

Abstract Fifteen patients with lymphoma and hypercalcemia (greater than or equal to 11.0 mg/dL) were identified by screening the serum chemistry profile obtained from patients upon admission to the Los Angeles County/USC Medical Center. Seven of the 15 (47%) possessed a frankly elevated serum concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2-D]. An additional patient with severe hypercalcemia (16.2 mg/dL) had a serum 1,25-(OH)2-D concentration in the midnormal range, not a suppressed value. To examine the potential existence of hypercalciuria in absence of overt hypercalcemia, prospective screening of 23 normocalcemic patients with lymphoma was undertaken. Four of the 23 patients (17%) had increased fractional urinary calcium excretion rates (0.35 +/- 0.3 mg calcium/100 mL glomerular filtrate [GF], mean +/- SE; normal, less than 0.16 mg/100 mL GF); two of the hypercalciuric patients had a frankly elevated serum 1,25-(OH)2-D concentration. Of the 19 hypercalcemic/hypercalciuric lymphoma patients identified, none had an elevated serum immunoreactive parathyroid hormone concentration. Fourteen of the 19 hypercalcemic/hypercalciuric patients (74%) suffered from B-cell neoplasms, three had Hodgkin's lymphoma, and two had adult T-cell leukemia/lymphoma. All hypercalcemic/hypercalciuric patients had widespread disease (stage III or IV). Six patients, four with hypercalcemia and two with hypercalciuria, had acquired immunodeficiency syndrome (AIDS). These data suggest that the deregulated synthesis of a 1,25-(OH)2-D-like metabolite is a common cause of hypercalcemia and hypercalciuria in patients with lymphoma including patients with AIDS-associated tumors.

Effects of thyroparathyroidectomy, parathyroid hormone, and PTHrP on kidneys of ovine fetuses

1993 ◽  
Vol 264 (1) ◽  
pp. E37-E44 ◽  
Author(s):  
R. J. MacIsaac ◽  
R. S. Horne ◽  
I. W. Caple ◽  
T. J. Martin ◽  
E. M. Wintour
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Excretion Rate ◽  
Plasma Concentrations ◽  
Free Water ◽  
Total Calcium ◽  
Fetal Plasma ◽  
Parathyroid Hormone Related Protein ◽  
Fetal Urine ◽  
Excretion Rates

The fetal parathyroid glands and parathyroid hormone-related protein (PTHrP) have been shown to be important regulators of fetal calcium metabolism through their actions on the placenta and bone. This study examined the effects of fetal thyroparathyroidectomy (with thyroxine replacement) and exogenous infusion of human parathyroid hormone [PTH-(1–34)], PTHrP-(1–34), and PTHrP-(1–141) on the urinary excretion of calcium in chronically cannulated ovine fetuses during the last one-fifth of gestation. Fetal plasma total and ionized calcium concentrations were significantly lower in thyroparathyroidectomized (TxPTx) fetuses when compared with intact fetuses, but there were no significant differences in urinary excretion rates of total calcium. However, TxPTx produced a significant increase in the fractional excretion rate of total calcium and a significant decrease in the excretion of adenosine 3',5'-cyclic monophosphate (cAMP) compared with intact fetuses. Infusions of PTH-(1–34), PTHrP-(1–34), and PTHrP-(1–141) into the jugular vein of TxPTx fetuses (n = 5) at the rate of 1 nmol/h for 2 h, after a 1-nmol loading dose, significantly decreased the excretion rate of total calcium and increased the excretion rate of cAMP in fetal urine. Infusions of all three peptides resulted in significant increases in the concentration of total calcium in fetal plasma but had no effect on the plasma concentrations or urinary excretion rates of phosphate. Infusion of either PTH-(1–34), PTHrP-(1–34), or PTHrP-(1–141) also resulted in an increase in fetal urine osmolality and pH and a decrease in free water clearance in TxPTx fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations of dietary calcium intake as a therapeutic modality in essential hypertension

1986 ◽  
Vol 64 (6) ◽  
pp. 803-807 ◽  
Author(s):  
Lawrence M. Resnick
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Calcium Metabolism ◽  
Calcium Supplementation ◽  
Ionized Calcium ◽  
Therapeutic Modality ◽  
Dietary Calcium Intake ◽  
Vitamin D Metabolites ◽  
Dietary Salt ◽  
Hypertensive Disease

Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin–angiotensin system and in the pathophysiology of human hypertension.

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