Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We found that a few patients with urolithiasis had normal parathyroid hormone levels but high cyclic AMP excretion. The purpose of this paper was to study the endocrinological mechanism. Male rats were given intraperitoneally dibutyryl cyclic AMP (DBcAMP), a derivative of cyclic AMP, per 100 gm of body weight for 50 days. Feed and water were supplied ad libitum. Crystal formation or calcification in mainly the dystal tubules and collecting system were found in 3 out of 10 rats, and renal calcium stones in 2 rats. The cyclic AMP of the renal parenchyma, especially the renal medulla, was elevated by more than 100 times after DBcAMP administration. Serum calcium levels, urinary calcium and phosphate excretion, and the adrenaline levels of the renal parenchyma were significantly increased. Serum parathyroid hormone was slightly enhanced, but vitamin D and the noradrenaline levels of the renal parenchyma were not changed. Based on these findings, it is suspected that stone formation in rats injected DBcAMP occurs through the action of DBcAMP on the renal tubules to increase urinary calcium excretion and to make renal stones as a form of primary hyperparathyroidism.
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PMID:[Studies on the endocrinological metabolism of the parathyroid. I. The production of renal calcinosis by cyclic AMP injection in rat]. 300 37

To elucidate the pathophysiology of elevated blood pressure in hypercalcemic patients, we studied the plasma concentration of catecholamines and their major metabolites (as an index of sympathetic function) and the blood pressure response to norepinephrine infusion (vascular reactivity) in patients with primary hyperparathyroidism, in patients with primary hypertension, and in normal controls. In addition, we evaluated the hemodynamic response to calcium infusion in normotensive and hypertensive subjects. Plasma levels of both norepinephrine and epinephrine and the metabolites normetanephrine and dihydroxyphenyl-glycol were significantly higher in the hypercalcemic group than in the other two groups. Norepinephrine infusion increased blood pressure by 8.5 +/- 1.4 mm Hg in the control group, by 19 +/- 2 mm Hg in the hypercalcemic group and by 29 +/- 3 mm Hg in the primary hypertensive group. Infusion of calcium produced a significant rise in both systolic and diastolic blood pressures and in peripheral resistance in the hypertensives, whereas in the normotensive group only systolic blood pressure increased, associated with a rise in cardiac output. We conclude that the observed increased activity of the sympathetic nervous system in hypercalcemia could account for the elevation in blood pressure and the enhanced vascular reactivity could explain the hypertension in some patients with primary hyperparathyroidism.
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PMID:Sympathetic system function and vascular reactivity in hypercalcemic patients. 706 99

In order to elucidate a participation of intact parathyroid hormone (PTH(1-84)) in blood pressure (BP) and body fluid homeostasis, we studied fluctuations of PTH(1-84) during manipulations of BP in hyperparathyroid and healthy subjects, and during manipulations of blood volume in patients with glomerulonephritis or liver cirrhosis and in controls. Angiotensin II induced BP elevation was associated with increased values of PTH(1-84) both in healthy subjects (12-25 ng l-1, medians, p < 0.01), in patients with primary hyperparathyroidism (94-125 ng l-1, p < 0.01), in patients with low calcium due to end stage renal disease before requirement of dialysis (95-151 ng l-1, p < 0.02), and in patients with tertiary hyperparathyroidism (221-264 ng l-1, p < 0.05), but not in dialysis patients without hypercalcaemia (126-174 ng l-1, NS). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was positively correlated to the increase of serum PTH(1-84) in the healthy subjects (p = 0.619, n = 15, p < 0.05) and in the patients with primary hyperparathyroidism (p = 0.549, n = 18, p < 0.05). Noradrenaline induced BP elevation did not have a similar effect on PTH(1-84), and changes of PTH(1-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of angiotensin II, resulted in elevation of PTH(1-84) in controls, cirrhotics, patients with glomerulonephritis without the nephrotic syndrome, but not in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH(1-84) in healthy subjects (20-18 ng l-1, p < 0.02), but not in patients with nephrotic syndrome and liver cirrhosis. Volume expansion induced by albumin infusion caused increased plasma levels of ANP, but PTH(1-84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(1-84), and PTH(1-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or changes in blood volume per se do not seem to influence PTH(1-84) levels.
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PMID:Parathyroid hormone in blood pressure and volume homeostasis in healthy subjects, hyperparathyroidism, liver cirrhosis and glomerulonephritis. A possible interaction with angiotensin II and atrial natriuretic peptide. 786 30

In order to evaluate the role of the hyperparathyroid state for blood pressure and volume homeostasis, eight patients with primary hyperparathyroidism were studied before and after corrective surgery. Neither noradrenaline induced blood pressure changes nor basal blood pressure were affected by the operation, and the values were the same as in an age- and sex-matched control group. Noradrenaline infusion induced an increase in PTH(1-84) values before (72-86 ng l-1, medians, p < 0.02), in contrast to a decrease after (28 to 19 ng l-1, p < 0.05) operation for primary hyperparathyroidism. Basal plasma atrial natriuretic peptide was lower before than after removal of adenomata (3.2 vs. 4.8 pmol l-1, medians, p < 0.02). Cyclic 3'-5'-guanosine monophosphate was not significantly changed (4.7 vs. 5.5 nmol l-1). Aldosterone was higher before than after surgery (139 vs. 71 pmol l-1, p < 0.02), whereas angiotensin II was unaltered (20 vs. 9 pmol l-1). Arginine vasopressin was higher before than after the operation (0.9 vs. 0.7 pmol l-1, p < 0.05), but urinary excretion of prostaglandin E2 was unchanged. In conclusion primary hyperparathyroidism was not associated with changes in noradrenaline reactivity or basal blood pressure despite derangements of hormones adjusting sodium and water homeostasis. It is suggested that the hormonal changes may be secondary to a relative volume depletion.
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PMID:Unchanged noradrenaline reactivity and blood pressure after corrective surgery in primary hyperparathyroidism. 821 Sep 70