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)

We have reported tissue distribution studies in rats and dogs with a new adrenal imaging agent. 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59). This agent concentrated five times higher in the adrenal cortex than 131I-19-iodocholesterol without increased concentration in non-adrenal tissues. We now report in 34 patients, the findings on scintigraphy with NP-59 compared with angiograms and/or adrenal vein hormone levels and histopathology, including 13 patients with hypercortisolism, 12 with primary aldosteronism, 2 with low renin hypertension, 5 with catecholamine excess, 1 with a liver metastasis from an aldosterone producing adrenal cortical carcinoma, and 1 with anaplastic adrenal cortical carcinoma. NP-59 adrenal cortical uptake was more rapid and intense and background activity was less prominent, allowing earlier and more definite interpretation of images than was possible with 131I-19-iodocholesterol.
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PMID:A new and superior adrenal imaging agent, 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59): evaluation in humans. 88 97

A system for discriminating between adrenal adenoma and hyperplasia based on the levels of aldosterone production, plasma renin concentration, severity of electrolyte disturbances, plasma aldosterone patterns during recumbency and after assuming erect posture, and 131I-19-iodocholesterol scan has been developed. Indicated for operation are patients with adenomas whose elevated blood pressure cannot be continuously controlled with usual doses of medication and patients with documented deterioration of target organ function. Adrenalectomy has been performed 83 times in 81 patients with a diagnosis of primary hyperaldosteronism. Results of excision of adrenal adenomas have been excellent with significant lowering of blood pressure in all cases and cure of hypertension in over 60%. Results of total or subtotal adrenalectomy for hyperplasia have been poor with almost all patients still requiring medication for hypertension. Adenomas have always been unilateral, and usually can be localized so that unilateral exploration is curative. Therefore, we have tried to distinguish preoperatively between adenoma and hyperplasia. Anterior transperitoneal adrenalectomy has been effective with few complications, and no postoperative hypercortisolism after unilateral adrenalectomy for adenoma. The unilateral extraperitoneal approach gives shorter morbidity and potentially fewer serious complications.
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PMID:Selection of patients and operative approach in primary aldosteronism. 118 May 75

In vitro studies have shown that glucocorticoids may increase atrial natriuretic-hormone (ANH) synthesis and/or release. This action of glucocorticoids has also been suggested in vivo in patients with Cushing's syndrome. However, in this circumstance, plasma AH elevation might be due to humoral disturbances associated with cortisol overproduction. We studied 16 patients with endogenous hypercorticism and 11 of them after successful treatment. Plasma levels of ANH, plasma renin activity (PRA), aldosterone, desoxycorticosterone (DOC), angiotensin II (AII), cortisol, osmolarity, sodium and potassium, urinary free cortisol (UFC), and blood pressure were measured. Before treatment the mean plasma ANH concentration in patients with Cushing's syndrome was significantly higher than in controls (11.3 +/- 2.6 vs. 4.9 +/- 2.3 pmol/l; p less than 0.001). ANH was correlated with cortisol and UFC (r = 0.715, r = 0.700; p less than 0.05). There was no significant correlation between plasma ANH, PRA, aldosterone, DOC, AII, osmolarity, sodium or blood pressure. After recovery, ANH concentration decreased in all patients and was not different from that of normal subjects (4.9 +/- 2.3 vs. 4.3 +/- 2.6 pmol/l). These results suggest that in Cushing's syndrome, ANH secretion is mainly dependent on the severity of hypercortisolism and independent of the other associated disturbances that we studied.
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PMID:Plasma concentration of atrial natriuretic hormone during endogenous glucocorticoid hypercorticism. 215 15

After administration of the cytokines interleukin 1 (IL1), tumor necrosis factor (TNF), interleukin 2 and interleukin 6 to laboratory animals or humans, plasma levels of glucocorticoids are elevated. This effect is mediated by activation of the hypothalamic-pituitary unit. IL1 and TNF inhibit aldosterone production by rat adrenocortical cells in vitro and stimulate renin release by rat renal cortical cells. Administration of IL1 or TNF in rats suppresses hypothalamic-pituitary-thyroid function, whereas IL1 acts at the level of the brain and the gonads to interfere with gonadotropin and sex steroid secretion. During stimulation of the immune system (e.g. during infectious diseases), peculiar alterations in hormone secretion occur (hypercortisolism, hyperreninemic hypoaldosteronism, euthyroid sick syndrome, hypogonadism). The role of cytokines in these alterations remains to be established.
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PMID:Cytokines and the hypothalamic-pituitary-adrenal axis. 228 99

A 62-year-old man arrived at our hospital with recurrence of Cushing's syndrome 14 years after successful surgery for adrenocortical carcinoma. Investigations demonstrated recurrence of a large tumor above the right adrenal area; it was found to be inoperable. The patient was treated initially with a new glucocorticoid antagonist, RU 486, and later with the adrenolytic agent mitotane (o,p'DDD). The latter achieved hypoadrenocorticism and a substantial reduction of tumor size. During the initial period, worsening hyperadrenocorticism resulted in a rise of atrial natriuretic factor and an inhibition of renin activity, consistent with an increase of cortisol and plasma volume. Changes in opposite direction were observed after treatment with mitotane.
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PMID:Late recurrence of operated adrenocortical carcinoma: atrial natriuretic factor before and after treatment with mitotane. 252 92

We studied the hormonal background of the fluid derangements and arterial hypertension associated with adrenocorticotrophic hormone (ACTH) treatment for infantile spasms in ten infants aged 5-22 months. They received a 6 week course of (carboxymethyl-cellulose-)ACTH: 80 IU at 0800 hours daily in weeks 1-3, then tapering, and termination at the end of week 6. The infants showed large, variable increases in 24 h urine cortisol during treatment. The mean plasma cortisol concentration (24 h after ACTH injection) was not significantly increased, but was correlated with the relative dose of ACTH. The mean plasma aldosterone concentration decreased. No significant change occurred in plasma renin activity (PRA), or in the concentrations of renin substrate (RS) or arginine vasopressin (AVP). Seven infants developed arterial hypertension, which was severe in three. This severe hypertension was associated with the highest relative ACTH doses and the highest plasma RS and cortisol concentrations. In the group as a whole, systolic blood pressure correlated with plasma RS and cortisol concentrations, but not with the other parameters. At the end of treatment urine and plasma cortisol dropped below the pretreatment levels and stayed low for greater than 2 weeks. There was a sharp peak in PRA and plasma aldosterone concentration, and a decrease in plasma RS. Plasma AVP levels dropped markedly. The mean body weight increased sharply and urine flow decreased. Mean plasma electrolyte levels remained unaltered. The danger at termination of ACTH treatment appears to be associated with a sudden transition from hypercortisolism to hypocortisolism, activation of the renin-angiotensin-aldosterone axis, and suppression of AVP secretion.
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PMID:Hormonal background of the hypertension and fluid derangements associated with adrenocorticotrophic hormone treatment of infants. 255 92

The effects of Ketoconazole (600 mg/day) were evaluated in 10 patients with Cushing's syndrome during a mean period of 4.5 weeks (range 1-12). The urinary free cortisol excretion (UFC) decreased by 21 +/- 15% (mean +/- SEM) (p less than 0.01) on day 1; 54 +/- 8% (p less than 0.0001) on day 2; 60 +/- 15% (p less than 0.0001) on day 3 and 87 +/- 3% (p less than 0.0001) on day 8 compared to baseline. Salivary cortisol at 0800 h decreased similarly. On day 3, 7 patients showed normal UFC values and on day 8, only 1 patient, with the ectopic ACTH syndrome, had persistent hypercortisolism. The cortisol decrease was associated with an increase in desoxycorticosterone values (p less than 0.01) and a decrease in dehydroepiandrosterone sulfate (p less than 0.001), delta 4 androstenedione (p less than 0.05) and testosterone (p less than 0.05). No significant variations were observed in ACTH, 11 desoxycortisol, aldosterone, plasma renin activity, corticosteroid-binding globulin and sex hormone-binding globulin. Side effects were few: mild clinical adrenal insufficiency (n = 5), oedema (n = 3) and reversible hepatic toxicity (n = 1). We conclude that Ketoconazole is an effective inhibitor of cortisol and androgens synthesis. It is well tolerated, rapidly effective and its efficacy persists unchanged for at least one month in all forms of Cushing's syndromes. For these reasons Ketoconazole may be a valuable drug for preoperative treatment of Cushing's syndrome.
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PMID:[Short term effects of ketoconazole in Cushing's syndrome]. 269 87

Exercise stimulates the hypothalamic-pituitary-adrenal and renin-angiotensin-aldosterone axes and causes growth hormone and prolactin release in an intensity-dependent fashion. Activation of the different endocrine responses examined occur at different exercise intensities. Subjects of differing training status respond similarly to matched exercise intensities. Highly trained subjects have elevated basal concentrations of ACTH and cortisol and a blunted response to exogenous corticotropin releasing hormone. These data are compatible with mild sustained hypercortisolism in highly trained runners.
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PMID:Hormonal responses to the stress of exercise. 285 59

Among the many potential causes of secondary hypertension are renal parenchymal disease, occlusive renal arterial disease, adrenocortical abnormalities, and pheochromocytoma. Renovascular hypertension can result from either renal parenchymal or occlusive renal arterial disease. Laboratory testing can help in identification and differentiation. Parenchymal diseases usually modify the urine substantially without producing urographic abnormalities, while occlusive arterial lesions produce urographic abnormalities but the urine remains normal. The diagnosis of renal occlusive arterial disease is best defined by arteriography. The only definite criterion for the existence of hypertension of renal origin is cure by either nephrectomy or renal revascularization. Adrenocortical causes of hypertension include enzymatic deficiencies, Cushing's syndrome, and primary aldosteronism. In enzymatic deficiencies, the physical findings provide the most important clues to the type of enzyme deficiency involved. In Cushing's syndrome, accurate determination of the cause of the hypercortisolism is important in terms of choice and success of treatment. The diagnosis of primary aldosteronism rests primarily on the demonstration of nonsuppressible aldosterone excretion rate during salt loading; the presence of inappropriate kaliuresis and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Pheochromocytoma, although rare, is a serious and potentially fatal cause of hypertension. Definitive diagnosis depends on laboratory test results, and the tumor is usually localized by computed tomography.
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PMID:Secondary hypertension. A streamlined approach to diagnosis. 372 9

Over two thirds of patients with Cushing's disease suffer from hypertension. An analysis of 155 patients with Cushing's syndrome was undertaken to study its incidence and effects, and the biological profile and prognosis of the patients. The renin-angiotensin-aldosterone system was given particular attention in 5 patients. Serum angiotensin was raised and a positive correlation was observed with the serum cortisol. Serum aldosterone did not respond as normal to the usual stimuli and the normal plasma renin activity did not vary during the 24 hour period. The physiopathogenesis of hypertension in Cushing's disease is still not fully understood, especially with regard to the mode of action of the hypercortisolism, the essential factor. A mineralocorticoid type of behaviour, especially in the severe forms, may be associated with that of the ACTH-dependent precursors, a permissive action on certain pressor substances, the increase in secretion of angiotensin in parallel to that of the cortisol and finally, the increase in the risk factors probably play a role. The outcome of the hypertension after specific treatment of Cushing's disease is usually favourable. However, hypertension persists in a third of cases.
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PMID:[Hypertension and Cushing's disease]. 662 11


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