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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations of calcium metabolism have been described in human essential hypertension and experimental hypertension. We investigated the interrelationship of parathyroid hormone (PTH) and 1,25(OH)2-vitamin D (1,25(OH)2D) in patients with untreated essential hypertension as compared to normotensive controls. The hypertensive subjects (n = 75; 43 men, 32 women) had a mean blood pressure of 138 +/- 8/95 +/- 5 mm Hg as compared with 120 +/- 11/80 +/- 8 in the normotensive group (n = 40; 22 men, 18 women). Serum PTH was measured with an intact molecule immunochemiluminometric assay and 1,25(OH)2D was measured with radioimmunoassay after HPLC separation. Hypertensive men had PTH levels that were 36% higher than normotensive men (5.3 +/- 2.9 v 3.9 +/- 0.8 pmol/L, P = .005). When blood pressure was analyzed as a continuous variable, there was a direct correlation between it and serum PTH in men (r = .31, P = .004). In women, by contrast, there was no difference in serum PTH between hypertensive and normotensive subjects and no relationship between blood pressure and the serum PTH concentration. Blood pressure was inversely correlated with serum phosphorus levels in both sexes (r = -0.20, P = .04). In men, the elevated serum PTH levels and depressed serum phosphorus levels would have predicted that serum 1,25(OH)2D would be higher in the hypertensive subjects. However, that was not observed, as serum 1,25(OH)2D was slightly lower in hypertensive (38.3 +/- 15.2 pg/mL) than normotensive men (42.7 +/- 11.3, P = .21).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium regulating hormones in essential hypertension. Importance of gender. 222 63

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl-induced hypertension in the Dahl salt-sensitive (S) rat. After a 5-day balance study, serum ionized calcium, parathyroid hormone (PTH), and 1,25-dihydroxy vitamin D concentrations were measured in Dahl-S and salt-resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than Dahl-R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5-day calcium balance was less positive in Dahl-S (P less than .05). Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.
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PMID:Calcium, parathyroid hormone, and vitamin D in the "prehypertensive" Dahl salt-sensitive rat. 222 64

Although altered cellular calcium handling plays a critical role in the pathophysiology of hypertension, little attention has been focused on the impact of calcium regulating hormones on this process. Recent research provides evidence that parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D, as well as newly described factors such as calcitonin gene-related peptide (CGRP), exert target-organ-specific actions in cardiac and peripheral vascular tissues, are linked to the renin-aldosterone system, and thus to the control of sodium metabolism, and may directly participate in the hypertensive process, especially in low renin and salt sensitive forms of hypertensive disease. The metabolic set-point of these linked renin and calcium hormone systems, which serve to transduce environmental dietary mineral signals at the cellular level, determines the blood pressure consequences of sodium and calcium loading and/or restriction, and helps to explain the heterogeneous and seemingly inconsistent effects of these dietary maneuvers on blood pressure. Measurement of renin and calcium factors in hypertension thus provides a physiological basis for individualized therapeutic recommendations in human hypertension.
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PMID:Calciotropic hormones in human and experimental hypertension. 222 65

Circulating substances that increase intracellular calcium, and other circulating substances that increase blood pressure, have been described in hypertensive animals and humans. In this study, we report the existence of a factor of the plasma of spontaneously hypertensive rats that does both. These effects were dose-dependent, and the time course for such effects was correlated with the time course for potentiation of pressor agents by the plasma. In addition, the plasma of spontaneously hypertensive rats was found to inhibit the depressor effects of parathyroid hormone. Our results confirm the presence of a circulating hypertensive factor in the plasma of spontaneously hypertensive rats, which may act by increasing calcium uptake in vascular smooth muscle. These findings may also help explain the secondary increase in parathyroid hormone noted in some forms of human and experimental hypertension.
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PMID:Vascular and calcemic effects of plasma of spontaneously hypertensive rats. 222 66

Many physiological abnormalities have been described in essential hypertension, yet the cause of this condition remains unknown. Included among the reported abnormalities are alterations in serum and tissue calcium levels, abnormalities in calcium regulating hormones, and the involvement of the parathyroid gland in some forms of hypertension. In the current study, the authors review evidence suggesting that a newly described hypertensive factor may explain a number of these abnormalities. This factor was first described in spontaneously hypertensive rat (SHR) plasma and is characterized by its ability to raise blood pressure in a delayed manner in normotensive rats, as well as by its ability to increase calcium uptake in vascular smooth muscle. The factor seems to be produced by the parathyroid gland, yet it is distinct from parathyroid hormone. Histological studies suggest that the factor may be produced by a specific cell type in the parathyroid glands. Given the parathyroid gland dependency of this factor, the authors have tentatively named it "parathyroid hypertensive factor," or "PHF."
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PMID:Parathyroid origin of a new hypertensive factor. 222 61

Plasma ionized calcium, platelet cytosolic calcium (using the fura-2 method in gel-filtered platelets), parathyroid hormone (both the intact hormone and a midmolecule portion), calcitriol, and calcidiol were measured in 19 untreated male patients with essential hypertension and 19 age-matched normotensive male research subjects. Mean levels of platelet cytosolic calcium, parathyroid hormone, calcitriol, and calcidiol were all significantly higher, whereas plasma ionized calcium was significantly lower, in the hypertensive group compared with the normotensive group. Both platelet cytosolic calcium and intact parathyroid hormone were positively correlated with mean arterial pressure (r = 0.58, p less than 0.001; r = 0.54, p less than 0.001, respectively), whereas plasma ionized calcium was inversely correlated with mean arterial pressure (r = -0.60, p less than 0.001) in the combined group of all study subjects. All three of these correlations were significant in the hypertensive group alone but not in the normotensive group alone. When analyzed with plasma ionized calcium, body mass index, serum calcitriol, and calcidiol in a multivariable regression model, the significance of the partial regressions of platelet cytosolic calcium and parathyroid hormone with mean arterial pressure persisted. Intact parathyroid hormone was positively correlated to platelet cytosolic calcium (r = 0.43, p less than 0.01) and plasma ionized calcium was inversely correlated to platelet cytosolic calcium (r = -0.44, p less than 0.01). These results confirm previous reports of disturbances of calcium metabolism in essential hypertension and suggest that the elevated platelet cytosolic calcium observed in essential hypertension may be linked to one or more of these alterations of calcium metabolism.
Hypertension 1990 Nov
PMID:Calcitropic hormones, platelet calcium, and blood pressure in essential hypertension. 222 52

In rats, verapamil decreases intestinal absorption of calcium, increases serum parathyroid hormone (PTH), and induces osteopenia. In this prospective study, verapamil 80-120 mg three times daily was given for 2 months to 20 patients with hypertension, and the effects on calcium homeostasis were recorded. This dose of verapamil significantly reduced supine systolic and diastolic blood pressure (+/- SD) from 158/100 +/- 9/8 mmHg to 146/89 +/- 14/8 mmHg (P = 0.001). Serum alkaline phosphatase (ALP) increased significantly from 2.77 +/- 1.06 mu kat l-1 to 3.19 +/- 1.22 mu kat l-1 (P = 0.004), and isoenzymes of ALP of skeletal origin appeared after verapamil treatment. The excretion of sodium in the urine increased (Na/creatinine ratio 8.95 +/- 6.01 before and 13.16 +/- 8.26 after verapamil; P = 0.04), while the excretion of calcium, phosphate and potassium was not changed. PTH was slightly increased at the end of verapamil treatment (1.09 +/- 0.54 vs. 0.98 +/- 0.74 microgram l-1; P = 0.07), and s-1,25(OH)2D3 was also somewhat increased (22.3 +/- 14.4 vs. 17.6 +/- 4.9 ng l-1; P = 0.26). Serum Ca was not affected by verapamil (before verapamil 2.43 +/- 0.11 mmol l-1, after verapamil 2.40 +/- 0.12 mmol l-1; P = 0.28). The increase in serum ALP demonstrates that verapamil affects bone cell metabolism in man. This effect could be secondary to the enhancement of PTH secretion.
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PMID:Verapamil increases serum alkaline phosphatase in hypertensive patients. 226 42

To evaluate the relationship between the elevation of blood pressure and altered bone metabolism, the changes of systolic blood pressure in six experimental models for bone disorders were investigated. Rats used were either parathyroidectomized, ovariectomized, fed with a calcium-deficient diet, fed with a vitamin D-deficient diet, treated with HEBP (1-Hydroxyethylidene-1, 1-bisphosphonate) or treated with streptozotocin. Hypertension developed in 5-week-old male rats fed with a calcium-deficient diet for 2 weeks, which evoked hypocalcemia and nutritional hyperparathyroidism. The blood pressure returned to normal when fed with a normal calcium diet. In parathyroidectomized rats receiving a normal calcium diet, the blood pressure did not rise, though the plasma calcium level decreased to an extent similar to the rats fed with the calcium-deficient diet. These findings seem to indicate that hyperparathyroidism, but not hypocalcemia, was involved in the elevation of blood pressure in rats fed with a calcium-deficient diet. Hypertension was not observed in rats fed with a vitamin D-deficient diet or treated with streptozotocin. These rats showed not only an increase in parathyroid hormone (PTH) but also a decrease in 1,25 (OH)2 D3. These results may suggest that the presence of 1,25 (OH)2D3 as well as the enhanced parathyroid function is necessary for the development of hypertension. The elevated blood pressure was reduced by a calcium antagonist, nifedipine, or by calcium supplementation, but not by an inhibitor of angiotensin-converting enzyme, captopril, or by calcitonin. This may indicate that hypertension due to nutritional hyperparathyroidism responds to the calcium antagonist nifedipine and to calcium supplementation, but does not depend on renin or salt. Furthermore, an acute hypotensive effect by human PTH (1-34) was not observed in the hypertension of calcium-deficient rats, suggesting the difference between acute and chronic effects of PTH. The hypertension developed in the present experiment may be a useful model for pharmacological evaluation of antihypertensive drugs, such as calcium and calcium antagonists.
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PMID:[Pharmacological study on blood pressure in rats with bone disorders]. 253 55

Abnormalities of calcium metabolism and of its two principal regulating hormones, parathyroid hormone and 1,25-dihydroxyvitamin D3 (calcitriol), have been reported in the spontaneously hypertensive rat (SHR). Reports of abnormal calcitriol metabolism in the SHR by several groups have not provided measurements of tissue calcitriol receptors. Similarly, few data are available as to the parathyroid status of the SHR. In the present study, circulating calcitriol levels and intestinal and parathyroid gland calcitriol receptor status were determined in male SHR and in Wistar-Kyoto (WKY) rats. Parathyroid status was investigated by determination of parathyroid gland mass together with tissue micromorphometry and by quantitative histology of bone as a measure of the biological action of parathyroid hormone. Circulating calcitriol levels were reduced in the 11-week-old SHR compared with the WKY rat (165 +/- 23 vs. 194 +/- 28 pmol/l, p less than 0.01, mean +/- SD). Calcitriol-free ratio was diminished and maximal specific binding capacity for calcitriol was increased in the SHR in parathyroid tissue (172 +/- 4.9 vs. 123 +/- 6.6 fmol/mg protein, p less than 0.01) and in intestinal mucosa with no change of receptor affinity. Plasma ionized calcium (1.29 +/- 0.05 vs. 1.45 +/- 0.35 mmol/l, p less than 0.05) and phosphate (1.5 +/- 0.26 vs. 2.4 +/- 0.03 mmol/l, p less than 0.05) were significantly lower in the SHR. Parathyroid gland mass was increased in the SHR (59 +/- 12 vs. 17 +/- 7 micrograms/100 g body wt, p less than 0.001) as a result of hyperplasia and not hypertrophy. Higher osteoclast numbers were observed in SHR bone (27.6 +/- 0.79 vs. 23.9 +/- 0.66 osteoclasts/mm2, p less than 0.01), suggesting increased parathyroid hormone activity. In summary, in the 11-week-old SHR we observed reduced circulating calcitriol levels together with increased tissue calcitriol receptor numbers, increased parathyroid gland mass, and histological evidence of hyperparathyroidism. It is possible that these abnormalities influence the development of hypertension in the SHR.
Hypertension 1989 Mar
PMID:Hyperparathyroidism and abnormal calcitriol metabolism in the spontaneously hypertensive rat. 253 97

Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium metabolism and hypertension. 254 Mar 74


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