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)

Changes in total and active renin concentrations (TRC and ARC) during pregnancy were studied; in addition, the changes in TRC and ARC in women taking oral contraceptives (OCs) were also investigated. 20 pregnant women aged 21-34 years were studied. TRC and ARC levels in normal subjects were 3.6 ng/ml/hour and 3.1 mg/ml/hour, respectively. Inactive renin concentration (IRC) was determined and its ratio was calculated from (TRC-ARC)/TRC. In normal subjects, IRC ratio was widely dispersed. TRC in women on OCs was slightly higher than normal, but ARC was not significantly different. Mean level of IRC/TRC (33%) in OC users was higher than that of normal subjects, but it was not significantly different. TRC and ARC showed an increasing tendency in term plasma. In contrast, the maximal value of the IRC ratio was in the second trymester. BY 3-4 weeks postdelivery, TRC and IRC were back to normal levels. When these measurements were related to cases of toxemia, 2 toxemic women showed values of TRC and IRC lower than those in normal pregnant women. It is concluded that development of the placenta or enlargement of the uterus does not affect the IRC ratio.
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PMID:Active and inactive renin in pregnancy and in women on estrogen-containing oral contraceptives. 39 34

mRNA levels for renin in the adrenal gland and kidney were measured by ribonuclease protection assay (RPA). Renin mRNA was not detected by RPA in aldosteronoma and kidney tissues obtained from two patients with primary aldosteronism (PA). In these patients, the PRA values, plasma concentrations of active renin (ARC), and total renin (TRC = ARC + prorenin) were below the assay limit (less than 0.03 ng/L.s, 2.5 ng/L, and 10 ng/L, respectively). On the other hand, renin mRNA was recognized by RPA in aldosteronoma and kidney tissues obtained from two other patients with PA treated with 50 mg/day spironolactone for more than 2 months. Their TRC values were 49.8 and 16.6 ng/L, but their PRA and ARC were undetectable. Renin mRNA content was greater in normal adrenocortical tissue and in the normal kidneys obtained from three hypertensive patients with renal cell carcinoma. In these patients, the mean values of PRA, ARC, and TRC were 0.28 +/- 0.03 (mean +/- SD) ng/L.s, 18.4 +/- 7.8 ng/L, and 110 +/- 15 ng/L, respectively. This is the first report of the lack of renin gene expression in aldosteronoma and kidney tissues obtained from untreated patients with PA. Furthermore, treatment with spironolactone resulted in an increase in the levels of renin mRNA in the aldosteronoma and kidney tissues of patients with PA.
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PMID:Renin gene expression in the adrenal and kidney of patients with primary aldosteronism. 172 6

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate). (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.
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PMID:Does heparin inhibit renin activity? 175 38

Plasma active renin (PARC) and plasma total renin (PTRC) were measured in 72 patients with childhood-onset IDDM and 37 control subjects in the supine posture. The diabetic patients were divided into three groups: group A, 55 patients with normoalbuminuria; group B, 11 patients with microalbuminuria; and group C, 6 patients with overt proteinuria. The levels of PTRC were 125 +/- 51, 240 +/- 124 and 580 +/- 285 ng/l in groups A, B and C, respectively; all of which were significantly higher than 114 +/- 33 ng/l in the control subjects. On the other hand, the ratios of plasma active to total renin, ARC/TRC, were 18.1 +/- 12.5, 10.7 +/- 6.7, and 2.9 +/- 1.4% in groups A, B and C, respectively; all of which were in turn significantly lower than 24.8 +/- 8.7% in the control subjects. Among the diabetic groups, PTRC became higher and ARC/TRC became lower in conjunction with the degree of albuminuria. The acute increments of PARC and PTRC during a standing load test were subsequently observed in 7 patients of group A, 5 of group B, 4 of group C, 13 patients with non-diabetic glomerulonephritis, and 6 control subjects. The ratios of increments of PARC to that of PTRC, delta ARC/delta TRC, were 48.3 +/- 22.3, 35.1 +/- 10.4 and 8.4 +/- 8.1% in groups A, B, C, respectively; all of which were significantly lower than 84.2 +/- 48.6% in the control subjects. Patients with non-diabetic glomerulonephritis showed, to a lesser degree, low ratio of delta ARC/delta TRC (60.4 +/- 37.9%) in conjunction with higher level of PTRC (249 +/- 89 ng/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered synthesis of renin in patients with insulin-dependent diabetes: plasma prorenin as a marker predicting the evolution of nephropathy. 226 47

Changes in plasma levels of active and inactive renin after the treatment with enalapril maleate (MK-421), a new angiotensin converting enzyme inhibitor, were studied in five patients with renovascular hypertension (RVH) due to unilateral renal artery stenosis. The dosage was increased when the blood pressure (BP) was not normalized for more than 3 days. Blood sampling was performed before, and 5 hours and 24 hours after the first administration, and on the 3rd day with each dosage. Active and inactive renin concentrations (ARC and IRC) showed a reciprocal change in 4 cases, 5 hours after the first dose. In the chronic treatment, ARC and IRC before the morning dose did not change apparently until the BP was normalized, when both ARC and IRC were evidently increased. It was suspected that a conversion from inactive to active renin may occur in the patients with RVH, when the active renin secretion is stimulated suddenly by the first dose of MK-421. The chronically diminished perfusion pressure in the kidney may stimulate the secretion of inactive renin, but the decrease in endogenous angiotensin II may not.
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PMID:Effects of enalapril maleate on plasma level of inactive renin in renovascular hypertension. 299 14

To investigate the effect of aging on the renin-angiotensin-aldosterone system, plasma renin substrate concentrations (PRSC); plasma total, active, and inactive renin concentrations (TRC, ARC, and IRC); PRA; and plasma aldosterone concentrations (PAC) were measured simultaneously in 60 normal subjects, 18-84 yr old. PRSC was measured by the addition of excess human renal renin. ARC and TRC after trypsin activation were measured by adding sheep renin substrate; IRC was calculated by subtracting ARC from TRC. The active renin ratio was calculated as follows: ARC/TRC X 100%. PRA and PAC were measured by RIA. There were no significant changes in PRSC, TRC, IRC, and PRA to PAC ratio with aging. Both ARC and active renin ratio fell significantly with aging (r = 0.46 and P less than 0.01; and r = 0.54 and P less than 0.01, respectively). PRA and PAC also tended to decrease with aging (r = 0.35 and P less than 0.01; and r = 0.59 and P less than 0.01, respectively). A significant positive correlation was found between PRA and ARC (r = 0.72; P less than 0.001). PRA was also correlated with PAC. In conclusion, the age-related decrease in PRA is not due to the change in PRSC, but is mainly due to the fall in ARC. Decreased conversion of inactive to active renin might be responsible in part for the reduced ARC in the elderly.
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PMID:Effect of age on the renin-angiotensin-aldosterone system in normal subjects: simultaneous measurement of active and inactive renin, renin substrate, and aldosterone in plasma. 351 Feb 26

Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome. A single oral dose of captopril (8-25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.
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PMID:Dynamic changes in plasma inactive renin levels in Bartter's syndrome after administration of captopril and angiotensin II. 351 17

To assess the role of inactive renin in hypertensive patients, active, inactive and total renin concentrations (ARC, IRC and TRC) were measured in 37 patients with hypertension of various etiologies. Inactive renin was activated by trypsin and renin concentration was measured using an excess of sheep substrate. Mean values of ARC, IRC, TRC and active renin ratio (AR ratio = ARC/TRC) were higher in 6 cases of renovascular hypertension, and lower in 6 cases of primary aldosteronism and 1 case of idiopathic hyperaldosteronism, when compared with 59 cases of normal subjects. Between ARC and IRC, a slightly positive correlation was observed. Moreover, between ARC and TRC as well as between ARC and AR ratio, close positive correlations were observed. Exceptionally, in a case of juxtaglomerular cell tumor, AR ratio was low in spite of the extremely high value of ARC. Our data suggest that the increase in circulating active renin is due to both the enhancement of the release of renin from the kidney and the increase in the activation of inactive renin, and vice versa.
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PMID:Active, inactive and total renin concentrations in plasma of hypertensive patients. 389 74

Changes in plasma active and inactive renin concentrations (ARC and IRC) were measured in 10 patients with primary aldosteronism (PA) due to adrenal adenomas. Before the resection of adrenal adenomas, venous blood samples were taken at supine resting state, after 1-hour standing and 30 min. after furosemide injection and these samplings were repeated after surgical treatment. Plasma inactive renin was measured after activation with trypsin. Before the treatment ARC and IRC did not change by standing or furosemide. After the treatment, however, ARC was increased clearly by standing or furosemide, and IRC was also increased by furosemide injection. Both ARC and IRC at supine resting state were increased after the surgery. When the renin-angiotensin system is suppressed chronically by the over-produced aldosterone in patients with PA, not only active but also inactive renin secretions are suppressed, and fail to respond to orthostasis or furosemide. The secretion of IR could be stimulated after the removal of aldosteronoma.
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PMID:Synchronous changes in active and inactive renin secretion after furosemide in patients with primary aldosteronism. 638 13

Active and inactive plasma renin concentrations (ARC and IRC) from both renal veins and the femoral artery, and the molecular weight (MW) of active and inactive renin (AR and IR) from both renal veins were measured in 6 patients with renovascular hypertension due to unilateral renal artery stenosis. Venous ARC on the affected side was higher than that on the unaffected side and arterial ARC. In 4 patients ARC increased and IRC decreased after circulating through the stenotic kidney, while in the other 2 cases venous IRC on the stenotic side was higher than arterial IRC. The MW of AR on the stenotic and non-stenotic sides were 40000-48000 and 45000-48000, respectively, and those of IR varied from 45000-53000 and 48000-55000, respectively. These values seem to be smaller than those of normal subjects. The renin molecule may be small immediately after the release from the kidney and become larger in the circulation. In 3 cases, whose ARC increased and IRC decreased after passing through the stenotic kidney, AR and IR from the stenotic kidney were smaller than those from the non-stenotic kidney. Some mechanism of AR and IR molecule reduction may work in the stenotic kidney to activate IR.
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PMID:Studies on the active and inactive renin in renovascular hypertension. 639 48


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