Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system was examined in Fischer rats at 7, 11 and 14 days after Leydig cell tumour transplantation, and in age matched controls. Mean arterial blood pressure (MAP), active plasma renin and serum calcium were higher (P less than 0.01) in the tumour transplant rats than in the controls at 11 days after transplantation. There was a positive correlation of both active renin and MAP with serum calcium at this time. Although inactive renin levels were elevated in the tumour transplanted rats, the ratio of inactive to active renin was decreased in comparison to controls. Plasma norepinephrine, active renin and plasma angiotensin II were higher in tumour rats at 14 days. Nevertheless, basal levels of aldosterone and MAP as well as aldosterone responses to graded infusion of angiotensin II, ACTH and KCl were decreased in the tumour rats at 14 days. Moderate hypercalcaemia (day 7 and 11), induced by Leydig cell transplantation in the Fischer rat, is associated, therefore with elevated blood pressure which appears to be related, in part, to activation of the renin-angiotensin system. However, severe hypercalcaemia (day 14) was associated with hypotensive hyperreninaemic hypoaldosteronism state.
 ...
PMID:The renin-angiotensin system in association with hyperreninaemic hypoaldosteronism in neoplasia induced hypercalcaemia. 629 44

Two 8-yr-old children, a boy and girl, are described with Cushing's syndrome secondary to ectopic ACTH-secreting pancreatic islet cell carcinomas. The girl, seen 28 yr ago, had strong presumptive evidence of ectopic ACTH production and hypercalcemia. The boy, studied recently, had strikingly elevated concentrations of plasma ACTH (1,500 pg/ml) and beta-lipotropin (beta LPH; 2,500 pg/ml) and showed no suppression of urinary 17-hydroxycorticoids or cortisol with low and high dose dexamethasone. He had increased plasma calcitonin (257 pg/ml), glucagon (442 pg/ml), lactate dehydrogenase (497 IU/liter), and alpha-fetoprotein (5,144 pg/ml). He also had hypokalemic alkalosis with elevated plasma deoxycorticosterone (70 ng/ml) and PRA (6.9 ng/ml.h) but normal plasma aldosterone (8.2 ng/dl) and 18-hydroxycorticosterone (7.6 ng/dl). Preoperative localization of the tumor was accomplished by computed tomographic scan of the abdomen with concurrent barium enema. Cell-free translation of the tumor mRNA produced authentic proopiomelanocortin of 35,000 mol wt, indicating that the ACTH and beta LPH were produced by the tumor from a common precursor. After removal of a large amount of metastatic tissue from the boy, clinical progression of the remaining tumor was monitored by measuring plasma ACTH and beta LPH. Episodic secretion of ACTH and beta LPH was demonstrated by taking frequent plasma samples while suppressing pituitary ACTH with oral dexamethasone. Chemotherapy and radiation proved ineffective in controlling the growth of his tumor.
 ...
PMID:Endocrine, histological, and biochemical studies of adrenocorticotropin-producing islet cell carcinoma of the pancreas in childhood with characterization of proopiomelanocortin. 630 81

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.
 ...
PMID:Primary hyperparathyroidism associated with primary hyperaldosteronism. 634 7

The change of the pattern of clinical presentation of primary hyperparathyroidism in older patients is illustrated by a case history of a 61-year-old woman with multicystic kidney disease in whom a thiazide antihypertensive drug (clopamide) induced a very severe symptomatic hypercalcemia. Withdrawal of the drug was followed by a prolonged complete clinical remission, normocalcemia, normocalciuria, but consistently elevated parathormone levels. This "normocalcemic biochemical hyperparathyroidism" was complicated with hyperkalemia due to aldosterone suppression, a counterpart of the recently described association with hypokalemia due to primary hyperaldosteronism, necessitating further studies on the occurrence and significance of altered production of aldosterone in geriatric patients with primary hyperparathyroidism.
 ...
PMID:Simultaneous occurrence of hyperkalemia due to aldosterone suppression and hyperfunctioning parathyroid adenoma. 675 9

1. The effect of acute hypercalcaemia on blood pressure, blood volume, haemodynamic indices, plasma catecholamines, renin and aldosterone levels was investigated in 10 patients. 2. Calcium infusion (15 mg/kg over 3 h) increased (P < 0.05) plasma calcium and adrenaline levels, blood pressure, total peripheral resistance and packed cell volume. Plasma volume was decreased, and heart rate, cardiac output and plasma renin, aldosterone or dopamine levels were not significantly changed. Plasma noradrenaline was increased only minimally after 3 h of calcium infusion. 3. Mean blood pressure before and during calcium infusion correlated with concomitant serum calcium (r = 0.39; P < 0.02) or adrenaline levels (r = 0.57; P < 0.01); changes in blood pressure correlated with variations in plasma adrenaline (r = 0.68; P < 0.001). 4. Acute hypercalcaemic hypertension is mediated by an increase in peripheral vascular resistance and may be induced by a direct effect of calcium on blood vessels. The calcium-mediated increase in adrenaline release may play a contributory, and plasma volume contraction an inhibitory, role.
 ...
PMID:Role of haemodynamics, catecholamines and renin in acute hypercalcaemic hypertension in man. 700 29

The effect of acute hypercalcemia on blood pressure, blood volume, hemodynamic parameters, plasma norepinephrine, epinephrine, dopamine, renin, and aldosterone concentrations was investigated. After 1 hour of equilibration, 10 patients received an infusion of calcium gluconate in 5% dextrose (calcium 15 mg/kg of body wt in 3 hours). The calcium infusion increased the mean serum calcium from 8.7 to 13.0 mg/dl, the systolic blood pressure from 144 +/- 10 to 184 +/- (SEM) 12 mm Hg (P less than 0.001), the diastolic pressure from 78 +/- 4 to 93 +/- 5 mm Hg (P less than 0.01). The plasma volume was decreased by 9% (P less than 0.001), whereas the hematocrit was increased (P less than 0.05). Heart rate and cardiac output remained unchanged. Total peripheral resistance was increased from 1643 +/- 223 to 2256 +/- 387 dyne.sec/cm5 (P less than 0.05). The plasma epinephrine concentration rose from 4.5 +/- 0.7 to 6.9 +/- 1.2 ng/dl (P less than 0.01). The plasma norepinephrine concentration was unchanged after 2 hours and increased only slightly after 3 hours of calcium infusion. Plasma renin, aldosterone, and dopamine concentrations were not significantly changed. These findings demonstrate that acute hypercalcemic hypertension is mediated by an increase in peripheral vascular resistance. Hypercalcemic hypertension may be induced by a direct effect of calcium on blood vessels; calcium-mediated increase in adrenal epinephrine release may play a mild contributory role, and plasma volume contraction, an inhibitory role.
 ...
PMID:Acute hypercalcemic hypertension in man: role of hemodynamics, catecholamines, and renin. 702 19

Neoplasia-induced hypercalcemia in the Fischer rat results in hypertension 1 wk after Leydig cell tumor transplantation. Systolic blood pressure, plasma catecholamine, prolactin, plasma renin activity (PRA), and aldosterone responses to immobilization stress were evaluated in Fischer rats 10 days after tumor transplantation and in age-matched nontransplanted controls. Basal systolic blood pressure, norepinephrine, and PRA levels at 10 days after tumor transplantation were higher in association with elevated calcium levels in tumor-transplanted rats than in controls. Systolic pressure, norepinephrine, and epinephrine responses to immobilization stress were greater in the hypercalcemia 10-day transplanted rats. Although basal levels of prolactin and aldosterone were similar in the two groups. These observations suggest that elevated levels of the vasoactive hormones norepinephrine and angiotensin may play a pivotal role in development of hypertension in association with neoplasia-induced hypercalcemia. Further, neoplasia-induced hypercalcemia in the Fischer rat is associated with a relative hyperreninemic hypoaldosteronism state.
 ...
PMID:Hormonal changes associated with hypertension in neoplasia-induced hypercalcemia. 704 41

1. Angiotensin II was infused at stepwise increasing dose rates (2, 4 and 10 pmol min-1 kg-1) in 12 normal subjects. Infusions were performed in the presence of normocalcaemia, mild hypercalcemia induced by concomitant calcium gluconate infusion, and after 2 weeks of treatment with nifedipine. 2. Pre-infusion plasma levels of angiotensin II, renin or aldosterone were not altered by acute mild hypercalcaemia or administration of nifedipine. The angiotensin II-induced increases in plasma aldosterone were also similar under the three study conditions. 3. Variations in calcium metabolism occurring under clinical conditions appear to play a minor role in modulating the angiotensin II-dependent pathway of aldosterone regulation in normal man.
 ...
PMID:Studies on aldosterone responsiveness to angiotensin II during clinical variations in calcium metabolism in normal man. 709 40

Hyperparathyroidism and hyperaldosteronism coexisted in association with medullary sponge kidneys in a 27-year-old woman with severe hypertension. A modest fall in systolic and diastolic pressure followed removal of a parathyroid adenoma. Blood pressure was controlled with spironolactone therapy and restored to normal after removal of an aldosterone-secreting adrenal tumor. Elevated levels of aldosterone may have been responsible for the severe hypertension, while hypercalcemia may have had a synergistic effect on the arteriolar response to circulating vasoactive peptides.
 ...
PMID:Hyperaldosteronism, hyperparathyroidism, medullary sponge kidneys, and hypertension. 741 8

A 57-year-old man was admitted to our hospital because of dyspnea due to congestive heart failure caused by hypertensive heart disease in September, 1992. Twenty years ago, he was diagnosed to be hypertensive, and in 1980, he was diagnosed to at our hospital to have primary aldosteronism (PA) due to a right aldosterone-producing adrenocortical adenoma (APA). There were no hypertensive vascular complications at that time. He refused surgical removal, and anti-hypertensive drugs including spironolactone were administered. However, his drug compliance was very inaccurate. On this recent admission, left ventricular hypertrophy associated with impaired contractivity, hypertensive retinal change and mild protein uria were noted, but no hematuria was detected. His renal function was impaired (Ccr: 15.2ml/min). An abdominal CT scan showed a typical right APA, bilateral renal atrophy and fine granular calcification at renal medulla, even though he had no hypercalcemia and hypercalciuria. In addition, multiple cerebral infarction was demonstrated by a brain CT scan, along with coronary artery stenoses at the right coronary artery and left circumflex branch by coronary angiography and bilateral multiple renal artery stenoses by renal angiography. Right adrenalectomy and renal biopsy were performed. Histological examinations revealed a yellow tan-colored APA, many sclerotic glomerulus, and severely hyarinized renal arterioles. After adrenalectomy, blood pressure was not normalized but was controlled easily by hypotensive agents. Impaired renal function was not improved and deteriorated slightly but did not get worse there after. Since 1959, including ours, 22 cases of APAs complicated with chronic renal failure were reported in Japan. In conclusion, surgical removal should be recommended for APA, even if the patient's condition is complicated with chronic renal failure.
 ...
PMID:[A case report of aldosterone-producing adrenocortical adenoma complicated with chronic renal failure associated with nephrocalcinosis: review of APAs complicated with chronic renal failure]. 775 Jun 23


<< Previous 1 2 3 4 Next >>