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

Several reports suggested an involvement of parathyroid function in blood pressure regulation in animals and humans: hyperparathyroid subjects frequently display an elevated systolic blood pressure and young mild hypertensive patients show enhanced serum PTH levels. Moreover, removal of parathyroid glands (PTX) in young rats attenuates and delays the development of mineralocorticoid and genetic hypertension. In addition, in vivo cardiovascular reactivity to norepinephrine in PTX rats from both spontaneously the hypertensive rat (SHR) and Lyon hypertensive rat (LH) strains is decreased, as is calcium content in aortic and heart fragments. Moreover, parathyroid grafts from SHR, stroke-prone SHR (SHR-SP), LH, or Milan hypertensive rats (MHS) into previously parathyroidectomized normotensive recipient rats have been shown to induce an increase in blood pressure. Recently, in essential hypertensive patients and in SHR, a circulating hypertensive factor has also been described. Produced by the PTX in SHR, this factor is inversely related to the amount of dietary calcium. It appears, therefore, that the PTX plays a major role in experimental and probably also in human hypertension.
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PMID:Ions, parathyroids, and genetic hypertension. 814 Nov 51

Primary hyperparathyroidism (HPT) is characterised by a defective calcium sensitivity of the parathyroid glands. HPT is, furthermore, associated with a high prevalence of hypertension. In the present study BP was measured before operation, during surgery and after operation in 42 HPT patients and in 15 control subjects operated for non-toxic goitre. Parathyroid tissue was removed from all patients and the concentration of cytoplasmic calcium [Ca2+]i was determined in vitro in dispersed single cells by means of microfluometry at extracellular calcium concentrations of 0.5 mM and 3.0 mM. The SBP levels were found to be raised both before (158 +/- 23 (SD) mmHg vs. 144 +/- 24 mmHg in controls, P < 0.05), during surgery (maximal level 167 +/- 22 mmHg vs. 146 +/- 16 mmHg in controls, P < 0.01) and after operation (maximal level 180 +/- 26 mmHg vs. 148 +/- 20 mmHg in controls, P < 0.001) in the HPT subject when compared with controls. SBP during surgery was found to be related to the in vitro measured [Ca2+]i in the parathyroid cells at 3.0 mM extracellular calcium concentration or to the ratio of [Ca2+]i at 3.0 mM-0.5 mM (r = -0.25 and -0.27, respectively; P < 0.05). The degree of suppression of PTH release in vitro at 3.0 mM extracellular calcium was found to be related to both systolic and diastolic BP (r = 0.57 and r = 0.53, respectively; P < 0.05) before surgery. In conclusion, BP was found to be raised in HPT patients both before operation as well as during surgery and after operation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between abnormal regulation of cytoplasmic calcium and elevated blood pressure in patients with primary hyperparathyroidism. 820 37

The changes of erythrocyte deformability measured by the laser diffractometer in 25 cases of normal pregnancy and 37 cases of pregnancy induced hypertension (PTH) were studied. The results indicated that the erythrocyte deformability remained relatively stable over the course of normal gestation. There was no difference between controls and mild PIH cases (P > 0.05). However, in the moderate and severe PIH cases a significantly lower erythrocyte deformability (P < 0.01) was demonstrated. The relationship of low erythrocyte deformability with PIH needs further investigation.
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PMID:[Changes in erythrocyte deformability in patients with pregnancy induced hypertension and its significance]. 831 33

Dietary phosphorus restriction can prevent the progression of renal failure in subtotally nephrectomized rats or in rats with nephrotoxic serum nephritis, independent of protein and caloric intake. Conversely, diets high in phosphorus content result in a more rapid deterioration of renal function. The results are less compelling in indicating that phosphorus restriction can slow the progression of renal failure in the clinical setting. The toxicity of phosphate appears to be related to induction of calcium phosphate precipitation, resulting in tubulointerstitial disease. Most studies of prevention of renal calcification have addressed a single pathway in the development of nephrocalcinosis. These include inhibitors of calcium phosphate precipitation, calcium channel blockers, or an inhibitor of PTH secretion. All of these studies have shown a beneficial effect in preserving renal function. It is possible that a combination of these agents, started early in the course of CRF, may have an additive effect in preventing the progression to ESRD. The discussion of other factors associated with progression of renal failure is beyond the scope of this review. It is obvious that dietary protein restriction, treatment of systemic and intraglomerular hypertension and lipid abnormalities, and prevention of iron overload, all play roles in the preservation of renal function in CRF.
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PMID:Role of phosphate retention in the progression of renal failure. 832 Apr 87

In order to know if abnormalities of calcium metabolism may be involved in the pathophysiology of pregnancy-induced hypertension (PIH), as it has been incriminated in essential hypertension, we measured plasma and urinary calcium and phosphate as well as plasma PTH and free calcitriol index (ratio of total calcitriol on the D binding protein) in normotensive pregnant women (n = 25), in women with PIH after the same duration of amenorrhea (> 28 wk, n = 21:preeclampsia and 20 transient hypertensions), and in age-matched nonpregnant women (n = 15). The severity of PIH was mild since blood uric acid was not increased and plasma volume, measured with the Evans blue technique, was found only moderately decreased (-10.5 +/- 3.1% of normal value). The results show that normotensive pregnant women showed the expected increase of the vitamin D parameters in comparison to nonpregnant controls. Hypertensive pregnant women were not different from the normotensive ones regarding plasma corrected calcium and phosphate and urinary excretion of calcium and phosphate, but had higher plasma PTH (13 +/- 1 v 8.8 +/- 1.6 pg/mL) and lower total and free calcitriol index (86 +/- 7 v 110 +/- 6 pg/mL and 1.72 +/- 0.10 v 2.25 +/- 0.13 x 10(-5)). Correlative studies showed PIH having a negative correlation between blood pressure and plasma corrected calcium (r = -0.43, P < .05), which is in agreement with epidemiological studies of essential hypertension. In conclusion, disturbances of calcium regulating hormones do exist in transient forms of pregnancy-induced hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium metabolism, plasma parathyroid hormone, and calcitriol in transient hypertension of pregnancy. 834 36

Free intracellular calcium is increased in primary hyperparathyroidism (HPT) and may be related to the higher incidence of hypertension in this disease. This elevation returns to normal when primary HPT is corrected. In essential hypertension, an alteration in calcium channels allows a intracellular accumulation of calcium. Aiming to asses if a similar mechanism operates in primary HPT, we measured intracellular calcium concentrations using QUIN-2-AM, before and after a 10 mg sublingual dose of nifedipine, in 9 subjects with primary HPT, 12 subjects with essential hypertension and 17 normal controls. Intracellular calcium was higher in subjects with primary HPT and with essential hypertension than in normal controls (276 +/- 56, 343 +/- 50 and 113 +/- 12 nM respectively). Among patient with primary HPT, intracellular calcium correlated with plasma PTH (r = 0.82). Nifedipine reduced intracellular calcium to 173 +/- 36 nM in subjects with primary HPT and to 188 +/- 35 nM in those with essential hypertension. In the latter, the decreased in intracellular calcium and blood pressure correlated significantly (r = 0.65 p < 0.03). We conclude that increased intracellular calcium in primary HPT and essential hypertension seems to depend on an increased inflow through specific channels. However in primary HPT, this alteration is related to PTH levels.
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PMID:[Nifedipine reduces the increase of free intracellular calcium in primary hyperparathyroidism: role of calcium channels and PTH]. 852 65

Calcium homeostasis is an important aspect of maternal and fetal physiology during gestation, and recent evidence implicates alterations in calcium metabolism in the pathogenesis of hypertension during pregnancy. Deficiencies in calcium intake have been linked to preeclampsia/eclampsia, and hypocalciuria and deviations in both 1,25(OH)2D3 and PTH have been shown in women with preeclampsia. Preliminary studies also suggest that calcium supplementation may lower blood pressure and prevent preeclampsia in pregnant women.
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PMID:Calcium metabolism in normal and hypertensive pregnancy. 858 10

There is circumstantial evidence that disturbances of calcium metabolism are implicated in primary hypertension. From a large number of observational epidemiological studies, data have shown that a low dietary calcium intake increases the risk for high blood pressure. There is no general sensitivity for the effects of inadequate calcium intake, but subgroups of hypertensive patients have been described characterized by reduced serum ionized calcium levels, increased urinary excretion of calcium, raised intracellular calcium levels, reduced cellular membrane calcium binding, and other indicators of a relative calcium need. Some of these changes, however, may be secondary to blood pressure elevation. The family history approach enables to study the pathophysiology of early primary hypertension, at a stage at which blood pressure differences between future hypertensive subjects and normotensive subjects are still limited. In the Dutch Hypertension and Offspring Study, young normotensive subjects were studied selected on the basis of presence or absence of familial predisposition for hypertension. The findings show that disturbances in calcium metabolism are present in the early phase of primary hypertension and may precede the development of high blood pressure. Moreover, they suggest that changes in calcium metabolism may be a characteristic of familial hypertension and could reflect a genetic basis for calcium sensitive hypertension. The presence of a relatively reduced serum calcium and increased plasma PTH [1-84] level in the offspring of hypertensive parents indicates that calcium balance in prehypertensive subjects is maintained at a higher level of circulating PTH. The implications of these findings in relation to other available data are discussed.
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PMID:Calcium metabolism and familial risk of hypertension. 858 11

Intracellular calcium has been reported to be increased in essential hypertension, and thought to play a role in its genesis through facilitation of vascular smooth muscle contraction. Since hypertension is more prevalent in primary hyperparathyroidism, intracellular calcium may also be increased in this condition. To investigate whether the hyperparathyroid condition, i.e., hypercalcemia and increased PTH per se, could be associated with high intracellular calcium, we measured intracellular calcium in platelets with the Quin-2 AM fluorometric method in 11 normotensive patients with primary hyperparathyroidism, 15 patients with essential hypertension, and 18 normal controls, all matched for age and sex. We repeated the measurements in 9 of the hyperparathyroid patients after successful surgery. We found that intracellular calcium was higher in normotensive patients with primary hyperparathyroidism than in normal controls (198 +/- 24 vs 113 +/- 11 nM, p < 0.05), but lower than in patients with essential hypertension (198 +/- 24 vs 286 +/- 38 nM, p < 0.05). Successful removal of a parathyroid adenoma decreased intracellular calcium from 215 +/- 22 to 116 +/- 19 nM, (p < 0.01). In the patients with primary hyperparathyroidism, intracellular calcium was strongly correlated with the levels of PTH (r = 0.87, p < 0.01), but not with the total serum calcium levels (r = 0.04, NS). The decrease in intracellular calcium after parathyroidectomy was also strongly correlated with the decrease in PTH (r = 0.84, P < 0.01), but not with the decrease in total serum calcium (r = 0.16, NS). In the patients with essential hypertension, intracellular calcium correlated well with systolic (r = 0.69, p < 0.01), diastolic (r = 0.76, p < 0.01) and especially mean arterial pressure (r = 0.86, P < 0.01). There was no correlation between blood pressure and intracellular calcium in the patients with primary hyperparathyroidism. We conclude that normotensive patients with primary hyperparathyroidism, as well as patients with essential hypertension, can have increased concentrations of intracellular calcium in platelets. The correction of the hyperparathyroid condition normalizes intracellular calcium concentration. The close correlation between PTH and intracellular calcium suggests that PTH may act as a ionophore for calcium entry into cells. Whether the increased levels of intracellular calcium may reflect a pre-hypertensive condition in normotensive patients with primary hyperparathyroidism remains to be determined.
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PMID:Intracellular calcium and blood pressure: comparison between primary hyperparathyroidism and essential hypertension. 877 53

This paper presents a 59-year-old man who was admitted to our hospital because of abdominal pains in 1973. He had pancreatic calcification and showed high levels of serum amylase, Ca, and PTH. He was diagnosed as primary hyperparathyroidism with chronic pancreatitis. After excision of an ectopic parathyroid adenoma, serum Ca levels were decreased and normalized by dihydrotachysterol p.o. At the same time his symptoms disappeared. The exocrine and endocrine pancreatic functions, however, decreased gradually. Diabetes mellitus appeared in 1975 and he required insulin injection since 1983. In spite of the treatment, his diabetic control was poor. Seventeen years later in 1992, he showed hypertension and edema (nephrotic syndrome). Because of renal failure, he underwent hemodialysis and passed away due to myocardial infarction in 1993. Autopsy findings showed existence of diabetic nephropathy as the cause of renal failure. Clinical course of this patient suggests that severe complications occur even in pancreatic diabetes and that we have to control diabetes strictly in pancreatic diabetes as well as in primary diabetes.
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PMID:[An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis]. 894 Aug 1


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