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)

A 50-year old female with primary aldosteronism and masked hyperaldosteronemia is reported. Her blood pressure was 176/110 mmHg with no paralysis of hypokalemia. Serum potassium, aldosterone and renin activity were 4.3 mEq/L, 17 ng/dl and 0.6ng/ml/h, respectively. Following a stimulation test by sodium loading and furosemide plus standing, neither aldosterone nor renin activity responded. Adrenal computed tomographic scanning, ultrasonography and cortical scintiscanning failed to reveal the tumor mass. A definite diagnosis of aldosterone producing adenoma was made after adrenal venous sampling in which the concentration of aldosterone was 15-fold greater in the right adrenal vein than in the left. The diagnosis of right adrenal cortical adenoma was confirmed by surgery. Thus, this case indicates the usefulness of the sampling technique in making an accurate diagnosis for primary aldosteronism with normo-kalemia, normo-aldosteronemia and normo-reninemia.
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PMID:A case report of aldosterone producing adenoma with masked hyperaldosteronemia. 355 Nov 99

Previous experiments have shown that circulating epinephrine stimulates renin secretin and increases plasma renin activity (PRA) when it is infused intravenously, but not when it is infused directly into the renal artery at similar infusion rates. The present experiments were designed to test the hypothesis that the adrenal glands mediate the PRA response to intravenous epinephrine infusion. Accordingly, anesthetized dogs were prepared with either an acute bilateral adrenalectomy or a sham-adrenalectomy procedure. Epinephrine was then infused intravenously into each animal for 45 minutes at a rate of 25 ng X kg-1 X min-1. Time control experiments in which epinephrine was not infused were also conducted. In sham-adrenalectomized dogs, PRA (in nanograms per ml h-1) rose from 4.1 +/- 1.4 in the control period to 13.0 +/- 3.0 during intravenous epinephrine infusion (means +/- SE; p less than 0.01). In adrenalectomized dogs, PRA rose from 2.1 +/- 0.4 during the control period to 5.5 +/- 0.9 during intravenous epinephrine infusion (p less than 0.01). Neither the absolute increments in PRA nor the percent increases in PRA were significantly different between the two groups receiving epinephrine. PRA remained unchanged in time control experiments. These data demonstrate that the adrenal glands need not be present in order for intravenous epinephrine infusion to elicit an increase in PRA. The data do not support the hypothesis, therefore, that epinephrine-induced increases in PRA are initiated by receptors located within the adrenal glands.
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PMID:Effect of intravenous epinephrine infusion on plasma renin activity in adrenalectomized dogs. 389 14

Potassium is a major regulator of aldosterone production. It also increases adrenal renin. The causal relationship between potassium and adrenal renin is not known. To evaluate the role of the intraadrenal renin-angiotensin (ANG) system in potassium-stimulated aldosterone synthesis and release, specific adrenal renin activity, PRA, and plasma aldosterone were measured during potassium loading or captopril treatment in the rat. Adrenal ANGs were determined using a HPLC system combined with RIA to obtain quantitative information on the components of the adrenal renin-ANG system. In addition, the effect of pretreatment with captopril on aldosterone production by isolated adrenal glomerulosa cells was examined. In intact animals potassium loading markedly increased adrenal renin and plasma aldosterone, whereas PRA was suppressed. The administration of captopril to rats in normal potassium balance did not suppress plasma aldosterone. Captopril treatment during potassium loading inhibited the potassium-induced increase in aldosterone. Furthermore, pretreatment with captopril suppressed adrenal ANG II and reduced the response of aldosterone production to extracellular potassium concentration by isolated adrenal glomerulosa cells in vitro. These results suggest that the adrenal renin-ANG system plays a significant role in the control of aldosterone production under potassium stimulation.
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PMID:A role for the adrenal renin-angiotensin system in the regulation of potassium-stimulated aldosterone production. 389 15

The role of prostaglandins in the control of adrenal renin in vivo was evaluated in nephrectomized rats. Nephrectomy increased adrenal renin from 13.2 +/- 1.37 ng angiotensin I/mg protein/hr to 166.5 +/- 17.3 ng angiotensin I/mg protein/hr. Indomethacin treatment significantly suppressed the adrenal renin response to nephrectomy. (47.8 +/- 5.22 ng angiotensin I/mg protein/hr). Adrenal aldosterone was also suppressed by indomethacin. Adrenal prostaglandin E2 increased after nephrectomy and decreased after indomethacin. Plasma corticosterone and serum potassium did not change after indomethacin. These data indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the adrenal renin response to nephrectomy, suggesting that prostaglandins may play a role in the adrenal response to nephrectomy.
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PMID:Effect of indomethacin on the adrenal renin response to nephrectomy in the rat. 390 Nov 21

Three patients with primary aldosteronism were treated surgically between February and September 1984. All patients had suffered from hypertension with U waves in ECG and laboratory examinations revealed hypokalemia, hyperaldosteronemia and suppressed plasma renin activity. The localization of the adrenal tumor was diagnosed accurately in all 3 patients by adrenal vein sampling and in 2 of the patients by PRP, CT scan, adrenal scanning with 131I-iodo cholesterol and adrenal venography. Adrenal tumors were surgically removed by unilateral adrenalectomy through the flank approach in all cases. Histological examinations of removed specimens showed adrenocortical adenoma. Removal of the adenoma caused a prompt reversal of the laboratory serum abnormalities and hypertension was normalized within 2 weeks postoperatively in all cases. Severe ventricular tachycardia (Torsades de Pointes) was observed suddenly in one of the patients after about 5 hours postoperatively. Therapy including conventional antiarrhythmic drugs, such as lidocaine or procainamide, and potassium administration failed to prevent the arrhythmia. Ventricular tachycardia was successfully treated and disappeared with the use of magnesium sulfate (MgSO4) intravenously. The serum potassium concentration was normal during the episode and the serum magnesium concentration, which was not detected before or just after the operation, was under the limit of normal range (1.4 mEq/l) after the use of magnesium sulfate. Hypomagnesemia which is retrospectively thought to be the result of primary aldosteronism may be responsible for the episode of postoperative ventricular tachycardia.
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PMID:[Three cases of primary aldosteronism including one case with postoperative ventricular tachycardia]. 396 10

Angiotensin infusion evokes marked increases in aldosterone secretion in primary aldosteronism and little change in secondary aldosteronism. The low plasma renin activity of primary aldosteronism and the elevated plasma renin activity of secondary aldosteronism are thought to account for this differential response. The effect of angiotensin on aldosterone and 18-hydroxycorticosterone secretion was studied during adrenal vein catheterization in seven patients with primary aldosteronism (whose plasma renin activity had been elevated following spironolactone therapy), one hypertensive patient with normal plasma renin activity and normal aldosterone secretion, two patients with secondary aldosteronism who had elevated plasma renin activity, and one anephric patient whose plasma renin activity was 0. Adrenal venous aldosterone and 18-hydroxycorticosterone were measured before and after a ten min sub-pressor angiotensin infusion. The cells of the aldosterone-producing adenoma (APA) respond to small increases in plasma angiotensin with large increases in secretion of aldosterone and 18-hydroxycorticosterone. The dose of angiotensin capable of evoking this response from the aldosterone-producing adenoma produces little or no change in the secretion of the steroids from nontumorous glands. The augmentation of aldosterone secretion, induced by angiotensin, in primary aldosteronism is due solely to increased secretion by the adenoma and not by the contralateral zona glomerulosa. The increased sensitivity of the aldosterone-producing adenoma is characteristic of the tumor. This response is independent of fluctuations in endogenous plasma renin activity. This sensitivity is not blunted by high plasma renin activity, nor is it a function of tumor mass for the effect is observed in aldosterone-producing adenomas regardless of size. ACTH injection after angiotensin infusion resulted in a marked increase in aldosterone concentration in the effluent from the nontumorous adrenal, but was not capable of producing further increases in aldosterone concentration in the effluent from the APA. In view of this exquisite sensitivity to infused angiotensin, it may be that the small variations in endogenous plasma renin activity that have been observed in primary aldosteronism may be capable of evoking large changes in aldosterone secretion in patients with aldosterone-producing adenomas.
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PMID:Activation of aldosterone secretion in primary aldosteronism. 430 91

1. Plasma renin (measured in the presence of additional substrate) was significantly higher (10.7 +/- 1.1 S.E. of mean ng/ml.hr) in foetal lambs of 111-144 days gestation age (full term 147 days) than in their mothers (1.5 +/- 0.2 ng/ml.hr S.E. of mean, P < 0.001) but plasma angiotensin II concentrations were in the same range (ewe 47.3 +/- 6.6 S.E. of mean, foetus 47.4 +/- 14.1 S.E. of mean pg/ml.). The endogenous velocity of renin production by foetal plasma was also greater than that of maternal plasma.2. Foetal plasma [Na(+)] (137 +/- 0.8 S.E. of mean m-equiv/l.), was lower than that in the ewe (142 +/- 1.5 m-equiv/l. S.E. of mean, P < 0.01).3. Foetal plasma renin in lambs of less than 120 days gestation was lower (9.2 +/- 2.7 S.E. of mean ng/ml.hr) than that in lambs of over 130 days gestation (12.6 +/- 2.6 ng/ml.hr S.E. of mean, P < 0.01). Foetal plasma [K(+)] (3.8 +/- 0.1 S.E. of mean m-equiv/l.) was also lower in lambs of less than 120 days gestation than in those over 130 days (4.1 +/- 0.1 S.E. of mean m-equiv/l., P < 0.001).4. When small volumes of blood (</= 3% of blood volume) were withdrawn from foetal lambs, plasma renin increased. The% increase of plasma renin in hypoxaemic foetal lambs was significantly less (P < 0.05) than in control lambs. At the end of 60 min hypoxaemia, arterial pressure and plasma [K(+)] were significantly higher in hypoxaemic than in control foetal lambs.5. During foetal hypoxaemia, plasma angiotensin II concentration increased concurrently with plasma renin.6. Bilateral nephrectomy was performed in two foetal lambs. Plasma renin fell to very low levels and angiotensin II became undetectable.7. Adrenaline ( approximately .0.42 mug/min.kg I.V.) infused into the foetus did not alter foetal plasma renin. When adrenaline was infused into the ewe ( approximately 0.26 mug/min.kg) maternal plasma renin increased. Maternal infusion of adrenaline raised foetal plasma renin significantly more (P < 0.05) than foetal infusion.8. It is concluded that the foetal kidney is the major source of foetal renin in the last quarter of gestation and that renin release is stimulated by very small reductions of blood volume. Hypoxaemia does not augment renin release and cannot be responsible for high levels of renin and angiotensin associated with vaginal delivery.
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PMID:Factors influencing plasma renin and angiotensin II in the conscious pregnant ewe and its foetus. 437 85

To determine if alpha 1-or alpha 2-adrenergic receptors mediate the inhibition of ACTH stimulation of growth hormone secretion, decrease in blood pressure and inhibition of renin secretion produced by release of catecholamines in the brain, drugs with varying amounts of alpha 1- and alpha 2-adrenergic activity were injected directly into the third ventricle in pentobarbital anesthetized dogs. To determine whether the receptors mediating the responses to clonidine were pre- or postsynaptic, the effect of intravenous clonidine was determined 2 weeks after intraventricular 6-hydroxydopamine, and 24 h after intravenous alpha-metyl-p-tyrosine. Norepinephrine, epinephrine and clonidine, but not methoxamine and phenylephrine inhibited ACTH secretion. None of these alpha-agonists affected growth hormone secretion. Epinephrine and clonidine lowered blood pressure. Clonidine decreased plasma renin activity, but the other agonists increased it. In dogs treated with 6-hydroxydopamine, the decrease in blood pressure and ACTH and renin secretion produced by clonidine was not altered but the growth hormone response was reduced. alpha-methyl-p-tyrosine had no effect on the ACTH and growth hormone responses to clonidine. The data suggest that postsynaptic alpha-adrenergic receptors mediate inhibition of ACTH secretion and stimulation of growth hormone secretion, although in the case of growth hormone secretion, a presynaptic receptor is also involved. In addition, postsynaptic alpha 2-adrenergic receptors mediate a decrease in blood pressure, and they may mediate decreased renin secretion.
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PMID:Further characterization of putative alpha--adrenergic receptors in brain that affect blood pressure and the secretion of ACTH, GH and renin in dogs. 612 26

The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.
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PMID:Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat. 615 22

The existence of renin in the adrenal gland of the mouse was determined by its enzymatic activity and by immunohistochemical techniques using monospecific antibodies to mouse submandibular gland renin. The adrenal gland of mouse was found to contain a very high level of renin significantly greater than other mouse tissues except for the kidney and submandibular gland. Also, the renin level in mouse adrenal was significantly higher than that in adrenals of other species. This renin activity was distinct from the nonspecific renin-like activity of acid proteases in that its activity was optimal at neutral pH and specifically inhibited by antirenin antibody. Adrenal renin increased upon nephrectomy indicating that it is not derived from the kidney. Immunohistochemical studies localized the renin-immunoreactive substance to cells in the inner region of the cortex. The intensity of staining was highest in the innermost region and decreased in cells in outer layers.
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PMID:Immunoreactive renin in mouse adrenal gland. Localization in the inner cortical region. 620 34


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