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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormalities in Ca metabolism in genetic hypertension have been suggested by studies of the spontaneously hypertensive rat and of humans with essential hypertension. A state of relative Ca deficiency in genetic hypertension was previously hypothesized to explain the reduced serum ionized Ca, increased serum parathyroid hormone levels, and the association between oral Ca loading and mild reduction in blood pressure. Renal Ca leak, reduced intestinal Ca absorption, and diminished Ca intake were further postulated to account for the Ca deficient state. This hypothesis, however, is not supported by the following lines of evidence in genetic hypertension: the absence of fasting hypercalciuria owing to intrinsic tubular defects, increased net Ca absorption in vivo despite greater Ca retention before and during established hypertension, increased intracellular free Ca concentrations, the failure to aggravate the hypertension by 50% reduction in dietary Ca intake, and the failure to ameliorate the hypertension by maneuvers that augment Ca balance (parenteral Ca administration, a high Mg diet, and 1,25-dihydroxyvitamin D3 injections). The available literature may be explained by the alternative hypothesis that genetic hypertension is characterized by generalized membrane defects in Ca regulation, resulting in a relative increase in cytosolic free Ca. The mechanism (or mechanisms) and physiological consequences of the disturbances in Ca homeostasis, however, remain to be defined.
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PMID:The nature and role of disturbances in calcium metabolism in genetic hypertension. 353 40

The effect of calcium supplementation on blood pressure was studied in three groups: eight normotensive subjects, 14 borderline essential hypertensive subjects, and 11 established essential hypertensive subjects (EEH). All subjects were outpatients and were given 6 g of calcium lactate (779 mg of elemental calcium) daily for 16 weeks. In EEH, systolic blood pressure was decreased significantly by 6 mmHg, but diastolic blood pressure was not decreased significantly (2 mmHg). In other groups, blood pressure was not reduced significantly. In all groups, urinary excretion of calcium was increased significantly but urinary excretion of other electrolytes, such as sodium, potassium and phosphate did not change. Serum electrolytes, various hormones, such as parathyroid hormone, 1-25(OH)2D3, 25OHD3, plasma renin activity, plasma aldosterone, plasma norepinephrine and epinephrine, and cardiac output did not change throughout this study. There were no adverse effects observed during this trial. From these results, it was concluded that daily administration of 6 g of calcium lactate produces a slight antihypertensive effect in EEH, and that this might be useful as a supplementary treatment for essential hypertension, especially in the aged.
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PMID:Effect of calcium supplementation on blood pressure in essential hypertensive subjects. 362 59

Relations between indices of mineral metabolism and blood pressure were examined in 182 subjects, comprising 58 patients with essential hypertension (EHT) and 124 healthy subjects attending a general health survey. Multivariate techniques of statistical analysis were employed to test the hypothesis of different relationships between blood pressure and calcium metabolism within the subpopulations and to eliminate confounding effects of age, sex and obesity. Plasma ionized calcium was inversely related and the urinary calcium excretion positively related to blood pressure in the total group. This was not significantly different between the groups. Serum parathyroid hormone (PTH) was, however, related to diastolic blood pressure only in the EHT group. The EHT patients had significantly lower plasma levels of ionized calcium, significantly higher levels of PTH and significantly greater excretion of calcium in the urine than the healthy subjects. The results of this investigation support the hypothesis that among patients with EHT the renal tubular reabsorption of calcium is impaired resulting in a reduction of plasma ionized calcium and thereby stimulation of PTH. The findings of linear relationships suggests the possibility of a direct association between calcium metabolism and the regulation of blood pressure.
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PMID:Relationships between calcium metabolic indices and blood pressure in patients with essential hypertension as compared with a healthy population. 366 47

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. 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. 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. 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. 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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PMID:Abnormalities of calcium metabolism in essential hypertension. 630 48

Calcium metabolism in otherwise uncomplicated term pregnancies associated with essential hypertension is characterized by significantly reduced levels of parathyroid hormone and ionized calcium, as well as significantly increased levels of phosphorus in both the mother and fetus. It is not possible at this time to delineate with certainty the precise pathophysiology of these changes.
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PMID:Calcium metabolism in the hypertensive mother, fetus, and newborn infant. 665 May 97

Disorders of calcium metabolism are not generally considered important either clinically or pathophysiologically in essential hypertension. Recent reports, though, suggest that increased parathyroid gland function may be one of the more common endocrine disturbances associated with hypertension. We measured serum parathyroid hormone (PTH) concentrations as well as routine blood and urine chemistries in 34 hypertensives. Their mean PTH, 79.1 +/- 3.1 muliter Eq/muliter, was significantly higher (p less than 0.025) than the mean PTH, 66.9 +/- 3.3, of an age- and sex-matched normotensive control population. The mean serum calcium, 9.5 +/- 0.1 mg%, was identical in the two populations. Compared to a second age- and sex-matched normotensive population, the hypertensives demonstrated a significant (p less than 0.005) relative hypercalciuria. For any level of urinary sodium, hypertensives excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland activity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalciuria, or renal calcium leak, associated with essential hypertension. We conclude that the increased prevalence of hypertension in subjects with hyperparathyroidism probably represents the final event in a continuum that begins with obligatory urinary calcium losses in hypertensives, but whose pathological presentation is hyperparathyroidism. The results of this pilot study indicate a need for derivative experiments directed at defining the importance of our preliminary findings in the pathogenesis of human and experimental hypertension.
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PMID:Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak. 738 May 20

To investigate the possible relationships between blood pressure, parathyroid hormone (PTH) and platelet cytosolic Ca2+ concentration ([Ca2+]i) in patients with essential hypertension, we studied 17 patients with this disease aged 48 +/- 2 years and 17 normotensive controls aged 44 +/- 3 years. Platelet [Ca2+]i was measured by spectrofluorimetry using the dye Fura-2 acetoxymethylester. Patients with essential hypertension displayed lower levels of serum ionized Ca2+ (0.99 +/- 0.03 versus 1.1 +/- 0.01 mmol/l, P < 0.05) and higher serum intact PTH levels (37 +/- 3 versus 26 +/- pg/ml, (P < 0.01) than the normotensive controls. Although serum levels of intact PTH were significantly correlated with mean arterial pressure (MAP) in the combined group of subjects (r = 0.42, P < 0.05), there was no correlation when each group was considered separately. Resting platelet [Ca2+]i was also higher in patients than in controls (57 +/- 3 versus 48 +/- 2 nmol/l, P < 0.005). When platelets were stimulated in vitro with thrombin, the increment in [Ca2+]i was also greater in patients than in controls in the presence of extracellular Ca2+ (264 +/- 24 versus 194 +/- 19 nmol/l, P < 0.05) but not in its absence (123 +/- 12 versus 112 +/- 10 nmol/l). The thrombin-induced increment in [Ca2+]i was correlated with MAP in the hypertensive patients (r = 0.64, P < 0.01) and in the combined group of subjects (r = 0.42, P < 0.05). There was no relationship between resting or thrombin-induced [Ca2+]i and serum PTH in either group of patients or in the combined group of subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone and platelet cytosolic calcium concentration in essential hypertension. 779 32

The effect of acute volume expansion by saline (1 L/40 min) on serum parathyroid hormone (PTH) concentration was studied in 28 subjects with mild essential hypertension. At the zenith volume expansion there was a significant increase in systolic pressure (7 +/- 2 mm Hg, P < .01) while diastolic pressure and heart rate showed minor (NS) variations. The rise in systolic pressure was accompanied by a significant (P = .02) decrease in plasma ionized calcium (from 1.12 +/- 0.03 to 1.08 +/- 0.03 mmol/L) and by a marked PTH increase (from 36 +/- 3 to 60 +/- 4 pg/mL, P < .01). The arterial pressure variations were independent of changes in serum PTH. In a second experiment (n = 11), aimed at preventing the changes in calcium concentration brought about by hemodilution, we infused the same volume of saline with the addition of 1.25 mmol of elemental calcium. In this study PTH showed a small, nonsignificant, decrease while systolic pressure changes were similar to those of the first study (ie, an isolated 9 +/- 4 mm Hg increase in systolic pressure). In a third experiment (n = 7), aimed at studying the effect of raised plasma PTH concentration in isocalcemic conditions, PTH1-38 was continuously infused (1 ng/kg/min) during the volume expansion phase performed with the same solution as used in the second experiment. The hemodynamic changes were again identical to those of the other studies (an isolated 9 +/- 3 mm Hg increase in systolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of extracellular volume expansion on circulating PTH1-84 in subjects with mild essential hypertension. 784 22

Alteration of calcium metabolism and changes in the levels of calcium-regulating hormones have been described in essential hypertension. In the majority of the reported clinical trials, calcium supplementation has resulted in a decrease in blood pressure. However, the mechanisms by which such a response would be mediated are entirely unknown. The present study confirmed that daily supplementation with 1.4 g of elemental calcium led to a significant decrease in both systolic and diastolic blood pressures (P < .01). Decrease in blood pressure was negatively correlated with increase in plasma calcitonin gene-related peptide (CGRP), measured with radioimmunoassay and by radioreceptor assay (P < .001), and positively correlated with decrease in intact parathyroid hormone (PHT) (P < .05). Following cessation of calcium supplementation, plasma CGRP levels and the blood pressure both reverted back to the base-line values, suggesting a direct effect of supplemented calcium on these two parameters.
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PMID:Antihypertensive effects of oral calcium supplementation may be mediated through the potent vasodilator CGRP. 813

Elevated levels of serum parathyroid hormone (PTH) and platelet cytosolic free calcium ([Ca2+]i) have been reported in subjects with essential hypertension. In addition, there is a positive correlation between serum PTH and platelet [Ca2+]i in white subjects with essential hypertension. Black normotensive subjects have relatively higher levels of serum PTH when compared to white normotensive subjects. To investigate the possibility that elevated serum PTH levels in black normotensives may contribute to elevated platelet [Ca2+]i, calcitropic hormone profiles and platelet [Ca2+]i were determined in 31 black normotensive subjects and 34 age-matched white normotensive subjects. There was no difference between the two groups in total serum calcium, plasma ionized calcium, or creatinine clearance. However, serum PTH was significantly elevated (P < .02) in the black normotensive group. Serum 1,25(OH)2 vitamin D levels were similar between the two groups whereas serum 25(OH) vitamin D levels were significantly lower (P < .001) in the blacks. The 24 h urinary excretion of Ca was also lower (P < .05) in the black normotensive group. Basal platelet [Ca2+]i was significantly lower (P < .05) in black normotensive than in white normotensive subjects. Serum PTH levels did not correlate with platelet [Ca2+]i in either group, or in the groups combined. These results demonstrate that the higher serum PTH concentrations in black normotensives is not associated with higher platelet [Ca2+]i, as is the case in white hypertensive patients.
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PMID:Racial differences in platelet cytosolic calcium and calcitropic hormones in normotensive subjects. 842 61


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