Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A rapid increase in plasma renin activity occurred in dogs after intravenous administration of parathyroid extract. 2. This was not seen after injection of a purer parathormone preparation, or the solution used to dilute the parathyroid extract or calcitonin. 3. A vasoactive compound in parathyroid extract appears to provide the most likely explantation of this effect.
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PMID:Effect of parathyroid extract on renin release in the dog. 112 36

Changes in extra- and intracellular pH affect metabolic states and hormone responses. In general, alkalosis stimulates and acidosis inhibits glycolysis although the relationship is not a simple one. 6-phosphofructo-1-kinase, a rate limiting enzyme in glycolysis, seems to be activated directly by a rise in pH. Alkalosis stimulates the production of pyruvic acid and lactic acid. Citric acid cycle is stimulated in alkalosis and hexose monophosphate shunt pathway is facilitated in acidosis. Acid-base disorders affect the insulin secretion and insulin action. In acidosis, insulin action in the target tissues is reduced. Other hormones, including parathormone, renin-angiotensin-aldosterone system, and adrenocorticotropine, respond to the changes in pH.
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PMID:[Effects of pH on the endocrine system and metabolism]. 143 2

Given the significance of the calcium ion in the pathogenesis of essential arterial hypertension, blood levels of total and ionised calcium, phosphorus, parathormone, blood renin activity as well as urinary calcium and phosphorus were assayed in a group of hypertensives and a comparable control group with normal blood pressure. The results showed reduced ionised calcium in the blood of the hypertensives together with hyperparathyroidism and increased calciuria. In addition, the link between parathormone and mean blood pressure levels suggests that parathormone itself play a primary role in the genesis of high blood pressure. Finally the connection between renin activity in the plasma and ionised calcium in the serum suggests that the two hormone systems are closely linked and may interact via the calcium ion.
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PMID:[Serum ionized calcium, parathormone and plasma renin activity in essential arterial hypertension]. 266 59

Plasma levels of immunoreactive parathormone (iPTH), immunoreactive calcitonin (iCT) and prostaglandins (PGE2) were measured by RIA in 115 patients with bronchogenic carcinoma. In 37 of these cases the following hormones were also assayed: adrenocorticotropic hormone (ACTH), cortisol, plasma renin activity (PRA), aldosterone, prolactin, human growth hormone (HGH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), follicle stimulating hormone (FSH) human chorionic gonadotropin (HCG), progesterone (P), androstenedione (A), testosterone (T), estradiol (E2) and dehydroepiandrosterone sulphate (DHAS). High serum levels of many hormone-like substances and hormones were found and the levels of certain hormones varied in some cases according to the clinical evolution of the disease and the response to therapy.
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PMID:Circulating levels of immunoreactive peptides and steroid hormones in bronchogenic carcinoma. 342 45

Studies were undertaken to extend previous observations of the interaction between calcium and parathormone on renin synthesis by the kidney. Intact normovolemic mongrel dogs between 15 and 25 kg were used for all studies. Plasma renin activity (PRA) was measured by radioimmunoassay. Hypocalcemia produced by thyroparathyroidectomy or chelation with EDTA resulted in an elevated PRA of 3.76 +/- .86 ng/ml/hr in 17 dogs compared to 1.5 +/- .29 ng/ml/hr in 14 controls (p less than .05). In 5 renovascular dogs calcium-channel blockade with nifedipine resulted in a higher PRA of 31.8 +/- 0.5 compared to 11.9 +/- 1.1 ng/ml/hr in 23 renovascular controls, p less than .001. The reactive hyperreninemia following angiotensin blockade was greater in 22 hypocalcemic (10.94 +/- 2.03 ng/ml/hr) dogs compared to 14 controls (1.32 +/- .34 ng/ml/hr), p less than .001. Results with calcium antagonism on PRA levels in renovascular dogs were found similar to those described with angiotensin blockade. We conclude from these studies that calcium-channel blockade or calcium reduction independent of a rise in parathormone was associated with an elevation of PRA in normal and renovascular hypertensive dogs. The rise in PRA could occur without changes in blood pressure or volume, consistent with an interruption of the short feedback loop control of renin synthesis by calcium antagonism. Finally, hypocalcemia and calcium-channel blockade resulted in reactive hyperreninemia greater than or equal to that seen after angiotensin blockade in both groups of dogs, again suggesting interference with the short feedback loop control of renin synthesis.
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PMID:The effects of changes in serum calcium and parathormone on plasma renin activity in intact mongrel dogs. 643 11

Primary hyperparathyroidism (HPTH) is frequently associated with hypertension. To date, the relationship between these two conditions is still not clear. We have studied 34 consecutive patients with primary HPTH due to a parathyroid adenoma. The diagnosis was later surgically confirmed in 32 cases. Ten of thirty-four HPTH patients were hypertensive. Before adenomectomy (PTHX) and 1-2 months after PTHX, we measured the following parameters in all patients: circulating levels of total and ionized Ca, intact immunoreactive parathormone (iPTH) (1-84), plasma renin activity (PRA), aldosterone, and daily total urinary catecholamine excretion. Moreover, 10 hypertensive HPTH patients, 10 normotensive HPTH patients, compared to 10 to 10 sex- and age-matched healthy normotensive subjects, underwent an acute norepinephrine test to assess vascular reactivity to a pressor agent. Before PTHX, no significant difference was observed between normotensive and hypertensive patients in all the above-mentioned variables, except for PRA and plasma aldosterone levels which were higher in hypertensive patients. Furthermore, the pressor response to the norepinephrine test was significantly greater in hypertensive HPTH patients than in the other 2 groups. After PTXH, serum Ca and intact iPHT (1-84) levels were reduced to normal values in all patients, while blood pressure, PRA and plasma aldosterone levels became normal in 8 of 10 hypertensive patients. The pressor response to the norepinephrine test was similar in the 2 groups. These results are consistent with the hypothesis of a direct effect of PTH on renin secretion which could contribute to the pathogenesis of hypertension and to the vessels sensitization to pressor agents.
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PMID:Hypertension and primary hyperparathyroidism: the role of adrenergic and renin-angiotensin-aldosterone systems. 756 68

The plasma renin activity and its changes after parathyroidectomy indicate a preserved internal secretory renal function in dialyzed patients. The PRA values before parathyroidectomy are not unequivocally related to the blood pressure reading. After parathyroidectomy during the initial months the renin and aldosterone plasma levels decline in patients with secondary and primary HPT (p < 0.001), the urinary Na/K quotient rises in primary HPT (p < 0.05) and the systemic blood pressure declines in dialyzed patients with secondary HPT (p < 0.001). The findings suggest relations between the two hormonal systems during hyperparathyroidism and in the early stage after parathyroidectomy. Parathormone probably stimulates renin secretion. After a prolonged time interval following operation the parathormone levels in the blood steam reach normal levels and the same probably applies to intracellular calcium in cells of the iuxtaglomerular apparatus along with PRA.
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PMID:[Changes in plasma renin and aldosterone after parathyroidectomy in patients with hyperparathyroidism]. 845 49

A high prevalence of hypercalciuria has been reported in patients with essential hypertension. Nevertheless, the clinical and therapeutic implications of this finding have scarcely been studied. This study was designed to determine the prevalence of hypercalciuria in an unselected population with essential hypertension and to analyze the relationship between the urinary calcium and the clinical and therapeutic status of these patients. This article presents a prospective study of 112 patients with essential hypertension and 49 healthy normotensive control subjects. Urinary excretion rates of calcium, sodium, chloride, potassium, urinary calcium/creatinine index, the fractional excretion of sodium, potassium and uric acid, the creatinine clearance and serum values of creatinine, urea, uric acid, electrolytes, total proteins, parathormone (intact molecule), plasma renin activity, aldosterone, glucose, and insulin (fasting and after an oral glucose load) were performed in every patient and control subject. Untreated hypertensive patients had a higher prevalence of hypercalciuria (35% had a urinary calcium/creatinine ratio > 0.20 versus 20% of treated hypertensives and 2% of control subjects; P < 0.001). Patients on thiazide or beta-blocker monotherapy had lower urinary excretion rates of calcium and urate than patients on calcium-antagonist monotherapy or untreated patients. Urinary calcium, sodium, and urate correlated positively both in treated and untreated essential hypertension patients. Patients with the higher urinary calcium levels also had higher excretion rates of sodium and urate, higher creatinine clearance rates, and lower serum creatinine and serum uric acid levels. It was concluded that hypercalciuria is a frequent finding of untreated essential hypertension. The association of high urinary calcium levels with high urinary urate excretion rates in the same patient may predispose to development of lithiasis in patients with essential hypertension. Antihypertensive drugs have a variable effect on calciuria-uricosuria, which may constitute an additional criterion in the selection and individualization of therapy. Thiazides and beta-blockers can decrease calciuria and uricosuria and, therefore, the lithogenic risk in these patients.
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PMID:Urinary calcium excretion in treated and untreated essential hypertension. 882 22

A double blind, placebo-controlled, parallel study was conducted on the effect of a high daily oral calcium supplementation of 1 g elemental calcium, given twice daily for 16 weeks in normal male subjects, on plasma renin, aldosterone, kallikrein, cGMP, cAMP, and calciotropic hormones, intracellular calcium concentrations, and plasma total and ionized calcium. After a 1-month run-in period on a limited use of dairy products, the subjects (n = 32) were allocated to a placebo or a calcium group. Placebo or 1 g elemental calcium was administered twice daily in the morning and evening for 16 weeks. All subjects were investigated at baseline and after 1, 2, 4, 8, and 16 weeks of placebo or calcium administration. A decreased intraerythrocyte and intraplatelet Ca2+ concentration was observed in the calcium-treated subjects. Compared with the placebo group, an increase in the plasma renin activity (PRA) in the calcium group was observed after 4, 8, and 16 weeks of oral calcium administration. However, plasma aldosterone and urinary excretion of aldosterone, kallikrein, cGMP, and cAMP were not changed during calcium administration. Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of intact parathyroid hormone and 1,25-dihydroxyvitamin D3, and an increase in 24-h urinary calcium excretion, but no change in the plasma total Ca2+ concentration, serum ionized Ca2+ level, and plasma phosphate or 25-hydroxyvitamin D3. Our data show that the increase in PRA observed in men during oral calcium supplementation is accompanied by a reduction in the intracellular free and total Ca2+ concentration in platelets and erythrocytes and by a decrease in the plasma concentration of intact parathormone and 1,25-dihydroxyvitamin D3.
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PMID:Modification of intracellular calcium and plasma renin by dietary calcium in men. 1061 85

Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.
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PMID:Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome. 1194 55


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