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)

Dietary sodium modulates the aldosterone response to angiotensin, but available evidence does not indicate whether there is a gradual change in adrenal responsiveness with intermediate sodium intakes or a sharp shift from a low to a high responsive level at some threshold sodium intake. Nine normal subjects received angiotensin II infusions while in balance on five levels of sodium intake over two orders of magnitude, 3 to 300 mEq sodium per day. Basal plasma renin activity, plasma aldosterone and plasma angiotensin II concentrations gradually fell as dietary sodium intake increased. The adrenal was quite sensitive to the state of sodium balance since a shift in sodium intake of as little as 20 mEq (e.g. 10 to 30 mEq/day) induced a significant change in basal plasma aldosterone. Adrenal responsiveness to infused angiotensin varied inversely with the log of urinary sodium excretion over the entire range of sodium intake, indicating that there is a gradual modulation of adrenal responsiveness with changes in dietary sodium. In addition, despite a constant dietary potassium intake, serum potassium gradually fell from 4.55 +/- .06 to 3.98 +/- .07 mEq/l, (P less than 0.02), as sodium intake increased, partly due to increased urinary potassium excretion (mean cumulative potassium loss of 129 mEq). Thus, changes in potassium balance may be important in modulating the sodium-associated variation in aldosterone secretion.
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PMID:Changes in adrenal responsiveness and potassium balance with shifts in sodium intake. 332 91

It was demonstrated before that in addition to their typical changes in water-sodium-potassium balance Brattleboro rats, homozygous for hypothalamic diabetes insipidus (DI), revealed a discrepancy between aldosterone level and plasma renin activity (PRA). In the present study PRA was significantly increased (79%), and concomitantly juxtaglomerular (JG) index was increased, reflecting an increased secretory activity of renin-producing JG cells. Plasma concentration of aldosterone was significantly lower (-36%) in DI rats than in their Long Evans (LE) controls. Adrenal blood flow rates were not significantly different in both groups of rats but aldosterone concentrations in the adrenal venous effluents were significantly lower (-66%) in DI rats than in LE rats, suggesting that in vivo production rate of aldosterone was reduced in DI rats. This assumption was confirmed by morphometric data of zona glomerulosa. Our results demonstrated a significant reduction (50%) of angiotensin II receptors in the adrenal glands of DI rats, referring to the number of binding sites and to Kd. This finding threw light on the dissociation between a decreased aldosterone production and stimulated renin-angiotensin system in DI rats.
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PMID:Discrepancy between aldosterone production and renin-angiotensin system activity in Brattleboro rats. 332 44

Twenty-nine subjects with mild to moderate essential hypertension completed this 13 week randomized, double-blind, placebo-controlled study comparing the antihypertensive effects of nifedipine GITS (N) (30-60 mg/day), hydrochlorothiazide (H) (25-50 mg/day) and placebo (P). Nifedipine GITS is a new formulation designed for once daily administration. N lowered blood pressure 15/10 mmHg (p less than 0.0005/p less than 0.0001), H 15/8 mmHg (p less than 0.0005/p 0.05), and P 4/0 mmHg (p = NS). All patients required the larger dose of active drug to control BP. No drug affected the heart rate. For N, but not H, there was a positive correlation between age and the magnitude in reduction of SBP (r = 0.79; p less than 0.005), but not for DPB. N drug levels did not correlate with its antihypertensive effect. Epinephrine, norepinephrine, aldosterone, and plasma renin activity were not affected by N. No patients on N experienced immediate vasodilator side effects. N is a well tolerated and effective antihypertensive drug that can be given once daily. It does not cause reflex stimulation of the sympathetic nervous system.
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PMID:Nifedipine GITS and hydrochlorothiazide in essential hypertension. 333 Sep 92

Adrenal autoantibodies (AA) were found in 23 of 2571 (0.9%) patients with organ-specific autoimmune diseases, in one of 632 first-degree relatives of insulin-dependent diabetic patients, and in none of 375 normal controls. In AA-positive subjects the prevalence of human leucocyte antigens (HLA)-A1, -B8 and -DR3 was significantly higher with respect to the general population. Two groups were followed (15 subjects persistently positive for AA and 51 negative subjects) for a mean period of 3.2 years. Yearly tests were made for AA and adrenal function. Of the 15 subjects persistently positive for AA, six developed Addison's disease after a period varying from 6 months to 10 years. Of the 51 subjects initially negative, two became positive during follow-up, and one of these developed Addison's disease 15 months later. In contrast, all the remaining 49 persistently negative subjects maintained normal adrenal function tests. Overall, of the 17 positive subjects, seven (41%) developed Addison's disease, three (18%) showed various degrees of subclinical adrenocortical failure and the remaining seven maintained normal glandular function. In the positive patients the yearly incidence of detriment in adrenal function was 19%. Patients who developed Addison's disease showed significant association with HLA-B8 phenotype. The development from normal adrenocortical function to overt Addison's disease seemed to progress through four distinct stages of functional impairment: increased plasma renin activity with normal/low aldosterone (stage 1), low cortisol response after i.v. administration of ACTH (stage 2), increased ACTH (stage 3), and low basal cortisol (stage 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural history of adrenal function in autoimmune patients with adrenal autoantibodies. 339 2

We present an unusual case of primary aldosteronism in childhood. A 9-year-old boy had hypertension, hypokalemia, hyporeninemia and hyperaldosteronism. Dexamethasone administration decreased plasma aldosterone transiently but failed to correct the hyperaldosteronism, excluding dexamethasone-suppressible hyperaldosteronism. Plasma aldosterone decreased with upright posture and showed a circadian rhythm. Spironolactone treatment normalized blood pressure and serum potassium and lowered aldosterone secretion. During the studies, plasma aldosterone correlated with serum cortisol but not with plasma renin. Preoperative results indicated that this patient presented the functional features of aldosteronoma. Adrenal computed tomography, scintigraphy and left venography were not diagnostic of adrenal lesions. The left adrenal venous sampling showed hypersecretion of aldosterone from the left adrenal gland. The left adrenalectomy revealed micronodular hyperplasia but resulted in a prompt and sustained reversal of hypertension and hyperaldosteronism. These findings suggest that primary aldosteronism in this patient resulted from primary adrenal hyperplasia. Thus, adrenal hyperplasia is a heterogenous group of disorders and carefully selected studies allow prospective selection of appropriate treatment.
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PMID:Primary aldosteronism in childhood due to primary adrenal hyperplasia. 341 79

Recently, it has been showed that Epinephrine (E) plays an important role in the pathogenesis of essential hypertension in rats. Furthermore, some literature data demonstrated the existence of high E plasma levels at rest and after stress in essential hypertension. To evaluate the sympatho-adrenal activity, both in basal condition and after stress, and its relationship with the renin-angiotensin-aldosterone (RAA) system, 31 borderline hypertensives (BH), 30 essential hypertensives (EH), and 15 healthy subjects were studied. After a wash-out period and electrolyte evaluation, all subjects were studied at rest, during dynamic exercise, and after 30 minutes of recovery; at the same time blood pressure and heart rate were automatically recorded and blood samples were collected for plasma renin activity (PRA), E, Norepinephrine (NE) and aldosterone plasma concentrations assay. BH showed a percentage increase of mean blood pressure greater than EH (p less than 0.01) during dynamic exercise. PRA showed no significant differences between the 3 groups examined at rest; on the contrary, PRA levels and the percentage increases were significantly higher in BH than in EH (p less than 0.05 respectively). E plasma levels and its percentage increases were significantly greater in BH than both in EH (p less than 0.05) and in controls after exercise. Furthermore, raised E plasma levels lasted significantly throughout the recovery period (p less than 0.05) only in BH. A significant correlation between both E plasma levels and percentage increases with NE percentage increases was observed after exercise in BH. Our results demonstrate a sympatho-adrenal overactivity in borderline hypertension, which is characterized by a prolonged E hyper-responsiveness, a renin hyper-secretion and a high hemodynamic response to stress. In borderline hypertension, E, excessively released from the adrenal gland, may act as a sympathetic cotransmitter inducing functional adrenoceptors hyperactivity.
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PMID:Role of epinephrine in the development of essential hypertension. 345 96

To determine whether the increase in renin secretion rate (RSR) produced by the beta 2-adrenoceptor agonist epinephrine was dependent on intact renal innervation, epinephrine (10 ng X kg-1 X min-1) was infused bilaterally into an innervated and a denervated kidney (ira) of the same anesthetized dog at spontaneous and reduced renal arterial pressure (decreases RAP, 100 mmHg). Epinephrine ira did not affect mean arterial pressure, renal hemodynamics, or urinary sodium excretion of either kidney. At spontaneous RAP epinephrine ira increased RSR from 633 +/- 134 to 926 +/- 137 ng/min in innervated kidneys but did not change RSR in denervated kidneys. decreases RAP in the presence of epinephrine ira resulted in an increase in RSR from 969 +/- 248 to 2,564 +/- 630 ng/min in innervated kidneys, which was greater than that produced in the absence of epinephrine, from 741 +/- 244 to 1,606 +/- 431 ng/min. In denervated kidneys decreases RAP resulted in similar increases in RSR in the absence and presence of epinephrine ira from 41 +/- 15 to 166 +/- 60 ng/min and from 59 +/- 210 to 235 +/- 78 ng/min, respectively. These results demonstrate that the increase in RSR produced by epinephrine is dependent on intact renal innervation at spontaneous and decreases RAP and suggest that epinephrine increases RSR by a prejunctional mechanism. The beta 1-adrenoceptor antagonist metoprolol (0.3-0.5 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine ira. Similarly, the beta 2-adrenoceptor antagonist ICI 118551 (0.005-0.25 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction between epinephrine and renal nerves in control of renin secretion rate. 352 29

Severe hypertension discovered incidentally in a 10 year-old boy was associated with persistent hypokalaemia and metabolic alkalosis. Primary hyperaldosteronism was diagnosed by demonstrating elevated plasma aldosterone levels and increased urinary aldosterone excretion with concomitant depressed plasma renin activity. Adrenal sonography identified a left adrenal adenoma which was removed surgically; normotension and normalization of plasma renin and aldosterone values ensued. This appeared to be the first use in children of sonography to identify adrenal adenoma and it is suggested to be the first step in the differential diagnosis of primary hyperaldosteronism.
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PMID:Severe hypertension in a ten-year-old boy secondary to an aldosterone-producing tumour identified by adrenal sonography. 353 37

We previously showed that adrenal renin is highest in the rat zona glomerulosa (ZG) and that low sodium or high potassium and nephrectomy increase adrenal ZG renin and aldosterone. Dahl salt-sensitive rats (S) have been shown to have lower plasma renin activity and plasma aldosterone and higher plasma 18-hydroxy-11-deoxycorticosterone than Dahl salt-resistant rats (R). In this study we assess the possible role of adrenal ZG renin in the suppression of aldosterone in S rats. Adrenal ZG renin was significantly decreased in S as compared with R rats even at 6 weeks of age, when both S and R rats are still normotensive (S = 7.2 +/- 0.2, R = 18.0 +/- 1.6 ng angiotensin I/mg protein/hr). Adrenal ZG aldosterone was also significantly lower in S than in R rats (S = 21.1 +/- 4.3, R = 39.5 +/- 3.6 ng/mg protein). Furthermore, the rise in adrenal ZG renin and aldosterone after nephrectomy in S rats was significantly less than that in R rats. To determine if the suppressed adrenal ZG renin of S rats is due to volume expansion, we studied the effect of a sodium-deficient diet on adrenal ZG renin in S and R rats. After 2 weeks of a sodium-deficient diet S rats had significantly lower basal adrenal ZG renin than did R rats (S = 7.6 +/- 0.4, R = 21.7 +/- 1.9 ng angiotensin I/mg protein/hr) and a marked blunting of the adrenal ZG renin response to nephrectomy (S = 13.6 +/- 1.1, DR = 167 +/- 16.1 ng angiotensin I/mg protein/hr).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppression of adrenal renin in Dahl salt-sensitive rats. 353 95

Evidence has accumulated that aldosterone secretion is under endogenous dopaminergic inhibition. To examine potential sources of the dopamine thus inhibitorily acting in the adrenal zona glomerulosa, the responsiveness of aldosterone, plasma renin activity, prolactin, and plasma catecholamines to haloperidol, a dopaminergic antagonist, was studied in rats 6 weeks after unilateral adrenalectomy (Group B), 6 weeks after unilateral adrenal demedullation followed by contralateral adrenalectomy 5 days later (Group C), and in controls without any pretreatment (Group A). In Group C, there were increases in basal levels of norepinephrine (P less than 0.01), prolactin (P less than 0.02), and aldosterone (P less than 0.01). Basal plasma renin activity was also increased (P less than 0.05), epinephrine concentrations were decreased. Two hours after haloperidol 1 mg/kg b.wt. i.p., aldosterone levels were increased in Groups A + B (P less than 0.01) but unresponsive in Group C. Haloperidol-induced stimulation of prolactin and norepinephrine was not impaired by the surgical procedures. Epinephrine levels were increased by haloperidol only in groups A + B (P less than 0.002). In none of the groups were plasma renin activity or dopamine levels influenced by haloperidol. It is concluded that dopaminergic inhibition of aldosterone production is brought about neither by circulating dopamine nor by potential dopaminergic nerves accompanying arterial blood supply of the adrenal cortex but by dopamine originating directly in adrenal medulla.
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PMID:The role of adrenal medulla in endogenous dopaminergic inhibition of aldosterone secretion. 354 25


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