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)

Glucocorticosteroid hormones increase the level of rat plasma angiotensinogen by increasing its rate of synthesis. Two forms of plasma angiotensinogen have been purified differing with respect to molecular weight and affinity to concanavalin A. Immunochemical studies using antibodies raised against the separated forms of angiotensinogen revealed cross-reactivity with both antigens. Both antibodies were able to quantitatively precipitate the angiotensinogen activity present in rat serum samples. Cortisol increased the total amount of plasma renin substrate without changing the relative amounts of both angiotensinogen forms. mRNA coding for plasma angiotensinogen was determined by in vitro translation of poly(A)-containing RNA and immunochemical analysis of translation products. Angiotensinogen mRNA could be detected in total poly(A)-containing RNA isolated from rat liver, but not in mRNA isolated from brain, although angiotensinogen has been reported to be present in the latter organ. The level of hepatic mRNA coding for plasma angiotensinogen was high in rats treated with cortisol, but not detectable in animals depleted from endogenous glucocorticosteroids by bilateral adrenalectomy.
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PMID:Immunochemical studies on biosynthesis of rat plasma angiotensinogen and its regulation by cortisol. 404 81

Isolated adrenocortical cells from 6 patients with a 'normal' zona fasciculata, 4 patients with a 'normal' zona glomerulosa, and tumour cells from 1 adrenocortical adenoma and 1 carcinoma were incubated with and without increasing concentrations of ACTH 1-24 (10(-13) M to 10(-9) M) or Asp1-Ile5-angiotensin II (10(-11) M to 10(-7) M). In 4/5 'normal' cases, cortisol was clearly stimulated by 10(-13) M ACTH. The maximum of the dose-response curve (5-fold stimulation) was reached at 10(-10) M ACTH. Angiotensin II (AII) started to stimulate 'normal' cells at 10(-11) M with a maximum (2-fold stimulation) at 10(-9) M. Aldosterone production by 'normal' cells was less markedly stimulated by ACTH and AII, although the threshold doses for both peptides were similar to those of the cortisol response curves. The cells of the adrenocortical adenoma from a patient with Cushing's syndrome produced large amounts of cortisol and small amounts of aldosterone, both steroids being clearly stimulated by ACTH and AII. The adrenocortical carcinoma cells produced small amounts of cortisol and no aldosterone. Cortisol production responded to ACTH, but not to AII. The results suggest that an activated renin-angiotensin system may stimulate the zona fasciculata, since 10(-11) M AII (= 10 pg AII/ml) is a normal plasma AII concentration on an unrestricted diet. Clinical evidence supporting this thesis is reviewed. However, cortisol production itself will rarely be increased by AII in vivo, since a down-regulation of ACTH would occur.
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PMID:Effects of angiotensin II and ACTH on normal and tumourous human adrenocortical cells. 631 17

Twenty one patients with selective aldosterone deficiency due to type 2 corticosterone methyl-oxidase defect [hypoaldosteronism (HA)] and 7 with pseudohypoaldosteronism (PHA) were studied longitudinally for up to 18 yr. All individuals had spontaneous and progressive normalization of sodium and fluid balance with age. The severity of the clinical manifestations varied from acute salt-wasting crisis in infancy and unexplained short stature in childhood to an asymptomatic state in adults detectable only by biochemical studies. Infants with HA had extremely elevated plasma renin activity (PRA; 70-650 ng angiotensin 1/ml X h), which gradually decreased with age, and PRA was normal in adults. Cortisol followed a similar pattern, but marked elevations of plasma deoxycorticosterone (DOC; 28-553 ng/dl) and 18-hydroxycorticosterone (18-OHB; 650-6500 ng/dl) relative to aldosterone (3-29 ng/dl) persisted throughout life in all untreated patients. The plasma 18-OHB/aldosterone ratio, normally 6.2 +/- 3.5 (SD), ranged between 160-760. In contrast, patients with PHA had PRA (70-685 ng angiotensin 1/ml X h), DOC (56-1201 ng/dl), 18-OHB (650-6800 ng/dl), and aldosterone (150-2000 ng/dl) levels which all remained very elevated, but had normal 18-OHB/aldosterone ratios (6.9 +/- 5.1). Comparative studies in 14 untreated patients with 11 beta-hydroxylase deficiency, who had moderate to severe manifestations of mineralocorticoid excess, revealed DOC levels (38-1384 ng/dl) that were remarkably similar to those of patients with HA and PHA. PRA, DOC, and 18-OHB correlated significantly with each other during all variations in sodium balance (P less than 0.001). Sodium repletion partially suppressed these parameters in both disorders, but complete normalization was achieved only in HA when a mineralocorticoid was given. Although the degree of DOC and 18-OHB suppression was similar in all age groups, the changes in PRA were more marked in children than in adults since these were directly proportional to the initial elevations of PRA. Although angiotensin II and potassium increased plasma DOC and 18-OHB, dexamethasone failed to suppress them, indicating that these steroids originated predominantly from the zona glomerulosa. The spontaneous normalization of sodium balance is not due to quantitative differences in hormone secretion with age since the basic steroid abnormalities remain unchanged from infancy to adulthood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The natural history of salt-wasting disorders of adrenal and renal origin. 638 51

We have previously shown that ACTH administration (1 mg/day) for 5 days raises systolic blood pressure (BP) by some 20 mmHg in both normotensive and hypertensive subjects, accompanied by hypokalaemia, urinary Na retention, a rise in fasting blood glucose and a fall in plasma renin concentration (PRC). In the present study cortisol and deoxycorticosterone (DOC) were infused for 5 days in 7 and 6 subjects respectively at rates appropriate for conditions of ACTH stimulation to determine whether the effects of ACTH could be reproduced by either steroid. Cortisol infusion increased systolic BP from a control of 108 +/- 7 mmHg to 129 +/- 7 mmHg on day 5, p less than 0.001. Plasma [Na] increased from 137 +/- 1 to 139 +/- 1 mmol/l (p less than 0.01), plasma [K] fell from 3.8 +/- 0.1 to 3.6 +/- 0.1 mmol/l (p less than 0.05); blood glucose rose from 3.9 +/- 0.2 to 4.7 +/- 0.2 mmol/l (p less than 0.001); PRC fell from 26 +/- 7 to 12 +/- 3 mu iu /ml (p less than 0.05); renin substrate rose from 1629 +/- 140 to 2206 +/- 453 pmol AI/ml, (p less than 0.05); urine Na excretion fell from 93 +/- 19 to 41 +/- 10 mmol on day 2 (p less than 0.05) and rose to 209 +/- 31 mmol 48 hrs after infusion (p less than 0.001); urine output rose from 2.0 +/- 0.35 to 2.89 +/- 0.46 L on day 5, (p less than 0.01). Plasma cortisol levels were similar to those seen with ACTH treatment. DOC infusion was associated with a fall in diastolic BP (control 64.2 +/- 4.0 mmHg, day 5 57.0 +/- 4.2 mmHg, p less than 0.01). Urine Na excretion fell from 77 +/- 12 mmol/day to 49 +/- 8 mmol/day on day 1, (p = 0.06) and body weight rose from 76.0 +/- 5.8 kg to 76.8 +/- 5.9 kg day 5 (p less than 0.001). Thus in man, cortisol infusion (in contrast to DOC) at rates appropriate for conditions of ACTH stimulation reproduces both the BP and metabolic effects of ACTH. Whether cortisol acts to raise blood pressure by a classical glucocorticoid mechanism or by a hypertensinogenic mechanism is not known.
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PMID:Blood pressure and metabolic effects of cortisol and deoxycorticosterone in man. 672 88

Cortisol, insulin, somatotropin, thyreotropin, thyroxine, triiodothyronine, testosterone, aldosterone, c-AMP, c-GMP, prostaglandins (PGF1-x, PGF2-x, PGA + E), and renin concentrations in serum or plasma of the venous blood of the third international crew of the scientific orbital complex of "Soyuz 29 - Salyut 6 - Soyuz 31" were determined following the 7-day space flight. The increased activity of the renin-angiotensin-aldosterone system before the flight as well as variations in the pressor/depressor prostaglandin ratios indicate an increased strain during the pre-flight period. During the first stage of the post-flight period some parameters were changed due to the landing process and the returning to earth gravity. The associated physical load and the onset of reactions for enhancement of the orthostatic tolerance resulted in an increase of cyclic nucleotid and thyroxine concentrations. The relatively higher levels of the pressor PGs of group F in comparison with the prostaglandins A + E could be evaluated as a compensatory reaction for enhancement of the orthostatic tolerance. The cortisol and STH concentrations increased with growing motor activity. The variations seen after the 7-day space flight were essentially within the reference areas. It may be assumed that the readaptation was not yet totally accomplished by the 8th day after landing.
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PMID:[Results of endocrinolgic studies of the 3rd international crew of the scientific orbital station complex; Soyuz 29 - Salyut 6 - Soyuz 31 (joint space flight enterprise of the USSR - GDR). 2. Hormones and biologically active substances in blood]. 675

The influence of 11 days at moderate altitude (2,000 m) combined with exercise on plasma concentration of testosterone, FSH (follicle-stimulating hormone), LH (luteinizing hormone), cortisol, aldosterone, and renin activity was studied in ten healthy subjects. Within 48 h of arrival at moderate altitude a significant increase in testosterone was found whereas FSH had decreased significantly and LH showed a tendency to decrease. Cortisol increased significantly at the beginning and reached a maximum at the end of altitude exposure. The plasma aldosterone level rose continuously and on the last day of altitude was significantly elevated. Plasma renin activity showed a tendency to decrease. On return to low land all measured parameters returned to base line values within 2 days. The findings of increases in plasma levels of aldosterone and testosterone (and serum T3 and T4, as reported by others) are in contrast to the previously found decrease of urinary excretion of all these hormones. This appears to be a distinct dissociation of serum levels of adrenal (and thyroid) hormones from their urinary excretion. The observed increase in plasma aldosterone is probably mediated through ACTH and the rise in plasma potassium, since plasma renin activity showed an opposite trend. The rise in plasma testosterone is probably of adrenal origin since plasma gonadotropins declined simultaneously. The increase of plasma levels of glucocorticoids, mineralocorticoids, and androgens after an ascent from 600 m to 2,000 m above sea level is compatible with an ACTH-mediated stimulation of the entire adrenal cortex and/or a diminished elimination of adrenal steroids: The concomitant fall of FSH, LH, and plasma renin would then be a consequence of a direct negative feedback inhibition of these hormones.
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PMID:Influence of exposure to moderate altitude on the plasma concentraton of cortisol, aldosterone, renin, testosterone, and gonadotropins. 678 Mar 38

In a randomized trial of pulsatile vs nonpulsatile cardiopulmonary bypass for coronary artery surgery, we studied hemodynamic and hormonal responses. Anesthesia did not produce a response but, from the time of the incision, cortisol and antidiuretic hormone levels and plasma renin activity all increased. Cortisol levels continued to rise after surgery, whereas the other began to fall. Systemic vascular resistance fell dramatically during cardiopulmonary bypass but rapidly rose after bypass with a reciprocal change in cardiac index. We did not see the changes ascribed to nonpulsatile bypass by others. There ws no difference between our pulsatile and nonpulsatile cases. High-flow cardiopulmonary bypass, vasodilating inhalation anesthesia and continuation of Inderal therapy may account for our results.
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PMID:Pulsatile cardiopulmonary bypass: failure to influence hemodynamics or hormones. 699 24

To establish the frequency and clinical and biochemical characteristics of hyporeninemic hypoaldosteronism (HH), we reviewed 100 consecutive cases of hyperkalemia (potassium content > 5.3 mEq/L). The most common cause was end-stage renal failure (34%). Other causes included overzealous potassium replacement, spironolactone therapy, hemolysis, acute renal failure, acidosis, thrombocytosis, and Addison's disease. Ten of 19 patients with unexplained hyperkalemia showed suppressed renin (0.12 to 1.3 ng/mL/hr) and aldosterone (5.4 to 21.6 ng/dL) responses to furosemide-posture challenge. Cortisol reserve was normal in HH. Fludrocortisone acetate therapy corrected the hyperkalemia. Other features of HH include low serum bicarbonate content, mild renal insufficiency, diabetes, and advanced age. The use of indomethacin and ibuprofen was associated with one case of HH each. Results suggest that HH is an overlooked cause of hyperkalemia, especially in patients whose hyperkalemia is unexplained.
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PMID:Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia. 700 70

Evidence for a role of dopamine and endogenous opioids in the control of the secretion of renin and adrenal steroids was sought in man. The effects of L-dopa, L-dopa plus carbidopa, dopamine, domperidone and naloxone were studied on the renin and aldosterone responses to head-up tilt. L-dopa diminished the rise in renin following tilt and this effect of L-dopa was abolished by carbidopa. Aldosterone was not significantly affected by any of the compounds. Cortisol secretion was stimulated by carbidopa plus L-dopa more than L-dopa alone, and was also increased by both dopamine and naloxone. The significance of these findings is discussed.
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PMID:Studies on the responses of plasma renin activity and aldosterone and cortisol levels to dopaminergic and opiate stimuli in man. 703 May 27

The behaviour of plasma renin, aldosterone, cortisol and prolactin after administration of a drug with antidopaminergic action, metoclopramide, was evaluated in 6 normal subjects, 8 patients affected by primary aldosteronism and in 5 patients affected by anterior hypopituitarism. In the first two groups, besides the predictable increase of prolactin under metoclopramide, a significant aldosterone increase was noted. Cortisol remained unchanged, and PRA was not significantly increased. A similar pattern of aldosterone, cortisol and PRA was also found in patients with hypopituitarism. However, the plasma prolactin did not increase in this group. The comparative examination of three groups of patients leads us to conclude that aldosterone increase is not imputable to ACTH, renin or to prolactin. This may be explained by a possible direct effect of the antidopaminergic drug at the adrenal level, which is more likely than an effect through some yet undetermined factor.
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PMID:Effect of metoclopramide on plasma aldosterone in normal subjects, primary aldosteronism and hypopituitarism. 703 23


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