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

Severe hypercalcemia with decreased renal function, hypertension, and renal calcifications developed in a 14-year-old boy who required prolonged immobilization for multiple fractures. Parathyroid hormone was not detectable in the serum. Urinary calcium excretion was high. Initially, mobilization was impossible and the patient was treated with a high fluid intake, low calcium intake, acidification of the urine, furosemide, and a passive exercise program. Renal function improved and renal calcifications resolved but hypercalcemia did not resolve. After mobilization the serum calcium concentration became normal rapidly. This treatment regimen is suggested for use in patients with immobilization hypercalcemia when mobilization is impossible.
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PMID:Severe immobilization hypercalcemia, renal insufficiency, and calcification. 44 Jul 90

We previously reported that preeclampsia is associated with hypocalciuria (N Engl J Med 1987; 316:715). The purpose of this study was to determine whether alterations in calcium regulatory hormones are present in preeclampsia and, if so, whether they are responsible for hypocalciuria. Thirty-two pregnant women were studied in the second and third trimesters of pregnancy (11 women with preeclampsia, nine with chronic hypertension, and 12 normotensive women). 1,25-Dihydroxyvitamin D, C-terminal parathyroid hormone, ionized calcium, and urinary calcium excretion were measured. 1,25-Dihydroxyvitamin D was significantly lower in the women with preeclampsia in the third trimester when the disease developed (37.8 +/- 15 pg/ml) than in women with chronic hypertension (75 +/- 15 pg/ml, p less than 0.05) and normal women (65 +/- 10 pg/ml, p less than 0.05). Parathyroid hormone was higher, but not significantly, in those with preeclampsia. Ionized calcium was not significantly different among the three groups. Urinary calcium excretion was abnormally low for pregnancy (less than 50 mg/24 hr) in all but one women with preeclampsia. We conclude that 1,25-dihydroxyvitamin D is reduced in preeclampsia and may lead to hypocalciuria by causing decreased intestinal absorption of calcium, stimulation of parathyroid hormone, and increased distal renal tubular resorption of calcium. The cause of reduced 1,25-dihydroxyvitamin D in preeclampsia is unknown and may be due to either diminished renal or placental production of the hormone.
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PMID:Abnormal 1,25-dihydroxyvitamin D metabolism in preeclampsia. 156 88

This review critically analyzes the available information on the relationship among calcium, parathyroid hormone, and blood pressure regulation. Both acute and chronic hypercalcemia increase blood pressure primarily via direct effects on vascular smooth muscle contractility. The evidence for indirect effects through activation of hormonal pressor systems is inconclusive. In apparent contrast with the notion that hypercalcemia can cause hypertension, more recently it has been proposed that calcium deficiency may be important in the genesis of hypertension both in humans and in spontaneously hypertensive animals. However, the evidence supporting this notion is still conflicting. Parathyroid hormone exerts complex actions on the cardiovascular system. On one hand, if injected in pharmacological doses, it is a vasodilator and antagonizes the pressor action of norepinephrine and angiotensin II; on the other hand, parathyroid hormone can potentiate the pressor effect of hypercalcemia.
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PMID:Calcium, parathyroid hormone, and blood pressure. 264 6

Parathyroid hormone (PTH) influences the calcium metabolism of many different mammalian cell types; indeed, hypertension due to changes in muscle tone is a frequent symptom of hypercalcemic hyperparathyroidism. In a blind study of 81 patients with various forms of heart disease undergoing coronary angiography, the plasma concentrations of the midcarboxyl regional PTH immunoreactivity were determined. PTH concentrations were elevated in 26 of the 56 patients exhibiting organic coronary artery disease (CAD). The plasma PTH levels were highest in those patients with CAD affecting three vessels and in patients with evidence of myocardial infarction. PTH levels were not influenced by previous drug treatments, and did not correlate to stress hormone levels. We propose that increased PTH levels may be a marker for initiation or potentiation of calcium-dependent changes in vascular smooth muscle behavior inducing coronary functional and anatomic lesions typical of CAD.
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PMID:Parathyroid hormone in coronary artery disease--results of a prospective study. 378 41

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

Parathyroid hormone's cardiovascular effects were assessed in a model of experimental hypertension with known abnormalities of calcium metabolism. Mean arterial pressure (MAP) changes and serum ionized calcium responses were measured in the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto (WKY), following injections of synthetic human PTH 1-34. Six 22-wk-old SHR and six WKY were given intra-arterial serial injections (0.1-100 micrograms/kg) of hPTH 1-34. Both the SHR (P less than 0.001) and WKY (P less than 0.001) demonstrated log dose-dependent hypotensive responses that were maximal at 1 min, with recovery occurring between 15 and 30 min. The slopes, however, of the dose-response curves differed (P less than 0.01). The SHR experienced a greater maximal delta MAP [-93.7 +/- 2.4 (SHR) vs. -71.2 +/- 1.6 mmHg (WKY), P less than 0.01]. Furthermore, the duration of the hypotensive action of hPTH 1-34 was significantly longer (P less than 0.001) in the SHR. Even when corrected for base-line MAP the SHR demonstrated a significant (P = 0.025) enhancement of this vasodilator response at doses of 5 micrograms/kg and greater at time intervals between 3 and 9 min after injection. A transient decrease [2.25 +/- 0.10 (pre) vs. 2.17 +/- 0.11 meq/liter (1 min post), P less than 0.01] in serum ionized calcium occurred at 1 min. We conclude that hPTH 1-34 is a potent vasoactive peptide in both the normotensive WKY and the SHR. The greater maximal hypotensive response to hPTH 1-34 and the prolongation of this cardiovascular effect in the SHR may be an additional manifestation of this experimental animal's acknowledged abnormalities of cellular membrane calcium and phospholipid metabolism.
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PMID:Vasodilation mediated by human PTH 1-34 in the spontaneously hypertensive rat. 669 83

Parathyroid hormone (PTH) has been implicated in hypertension, but PTH infusion results in vasodilation. PTH activates adenylate cyclase in vascular smooth muscle, but little is known about the factors that regulate PTH receptor/adenylate cyclase coupling in vascular cells. To characterize hormone-receptor signaling, we measured cyclic AMP levels in rat arterial smooth muscle cells in culture exposed to PTH (bovine 1-34). PTH yielded time- and concentration-dependent increases in cyclic AMP levels. Compared with isoproterenol, PTH was more potent, with a threshold at 2 x 10(-9) versus 5 x 10(-8) mol/L and half maximal responses at 10(-8) versus 2.4 x 10(-7) mol/L. PTH-induced increases in cyclic AMP were independent of extracellular calcium, cyclooxygenase metabolites, phospholipase C, and protein kinase C because PTH-induced increases in cyclic AMP were not prevented by variations in extracellular calcium, indomethacin, angiotensin II, vasopressin, and protein kinase C activators or inhibitors. PTH/adenylate cyclase coupling was G protein-dependent because increases in cyclic AMP were prevented by preincubation with cholera toxin but not with pertussis toxin. Prolonged exposure to PTH resulted in time- and concentration-dependent homologous desensitization of cyclic AMP responses. Desensitization occurred proximal to G protein/adenylate cyclase because after prolonged PTH, responses to forskolin and cholera toxin remained intact. Desensitization was independent of protein kinase A and receptor sequestration because cyclic AMP responses remained after prolonged exposure to forskolin and pretreatment with phenylarsine oxide, colchicine, and cytochalasin D. We conclude that in vascular smooth muscle cells, PTH is coupled to adenylate cyclase through a cholera toxin-sensitive G protein.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Apr
PMID:Parathyroid hormone/adenylate cyclase coupling in vascular smooth muscle cells. 751 68

Parathyroid hormone (PTH) is hypotensive in mammals and is a potent coronary vasodilator. Parathyroid hormone-related peptide (PTHrp) has been reported to have similar vascular activity. In the present study, the effects of human PTH (hPTH) and human PTHrp (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive rats. Isolated rat tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, PTHrp was several times more potent than PTH. PTHrp was also significantly more potent than PTH in relaxing tail artery precontracted with arginine vasopressin (AVP). PTHrp and PTH both inhibited the spontaneously contracting portal vein, but again PTHrp was significantly more potent. PTHrp (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of PTH. These data suggest that PTHrp is more potent than PTH in its cardiovascular actions. It is possible that PTHrp is the endogenous vasodilating ligand, and the structural similarity between PTH and PTHrp may explain the pharmacological action of PTH. It is therefore unlikely that PTH or PTHrp may be involved in the genesis or maintenance of hypertension. Because the parathyroid gland seems to be involved in some forms of essential hypertension, factor(s) other than PTH or PTHrp may be responsible.
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PMID:Cardiovascular effects of human parathyroid hormone and parathyroid hormone-related peptide. 751 45

Although calcium (Ca) is pivotal for the prevention of osteoporosis, its role in the prevention of other unrelated diseases such as arterial hypertension, cancer of the colon and nephrolithiasis is perplexing. No unitarian hypothesis explaining these unrelated effects of Ca has been postulated. Cytosolic Ca concentration is 10,000-fold lower than in the extracellular space, and this gradient is tightly maintained. Abnormal elevation of cytosolic Ca causes cell damage and death. Parathyroid hormone is a Ca agonist and the suppression of its secretion by Ca could explain the beneficial role of Ca intake in multiple diseases. Thus, parathyroid ablation improves hypertension in rats and cardiomyopathy in hamsters. Since anthropologic data suggests a higher Ca intake, of approximately 1,600 1,600 mg/day, in preneolithic than in modern diets, it is likely that our levels of PTH on genetically predisposed subjects with a loose cellular Ca control may aggravate frequent modern diseases and the process of aging. A higher Ca intake in both sexes should be one of the goals of preventive medicine of our time.
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PMID:Calcium, why and how much? 756 57

Parathyroid hormone and parathyroid hormone-related protein lower blood pressure and relax contracted arteries. Parathyroid hormone also attenuates angiotensin II-induced vasoconstriction. To determine the cellular mechanism or mechanisms by which parathyroid hormone analogues antagonize pressor effects, we examined the effect of these peptides on angiotensin II-induced calcium mobilization in fura 2-AM-loaded cultured rat vascular smooth muscle cells. Either 100 nmol/L parathyroid hormone or parathyroid hormone-related protein significantly reduced the amount of calcium mobilized by 100 nmol/L angiotensin II. The attenuating effect of these peptides was mimicked by 10 mmol/L forskolin and 10 mmol/L isobutylmethylxanthine and was not dependent on the presence of extracellular calcium. This effect of the parathyroid hormone analogues was reduced when cells were pretreated with 100 mmol/L 2',5'-dideoxyadenosine, an adenylate cyclase inhibitor. Combined inhibition of cyclic nucleotide-dependent protein kinases eliminated the inhibitory effect of parathyroid hormone, whereas protein kinase C inhibition had no effect. Parathyroid hormone analogues decreased the amount of calcium released by inositol 1,4,5-trisphosphate in digitonin-permeabilized vascular smooth muscle cells. This effect was inhibited by treatment with 2',5'-dideoxyadenosine. These results suggest that these peptides attenuate inositol 1,4,5-trisphosphate-sensitive calcium mobilized by angiotensin II via an adenylate cyclase-dependent mechanism. This may be a mechanism by which acute administration of parathyroid hormone or parathyroid hormone-related peptide antagonizes vasoconstriction.
Hypertension 1994 Mar
PMID:Parathyroid hormone analogues inhibit calcium mobilization in cultured vascular cells. 812 68


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