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)

The antigen-antibody complex formation in the angiotensin I radioimmunoassay appears to be influenced by the pH of the radioimmunoassay incubation mixture. This may lead to erroneous results in the determination of the plasma renin activity, when an aliquot of a plasma sample, buffered at pH 6 for optimum renin activity is brought into a radioimmunoassay mixture of another pH, while the radioimmunoassay standards are not corrected for this pH shift. In our experiments we studied this general pH effect, and evaluated the effect on the New England Nuclear Angiotensin I radioimmunoassay procedure. We propose a slight modification of this radioimmunoassay kit.
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PMID:Influence of the pH on the antigen-antibody coupling in angiotensin I radioimmunoassay. Its consequences for the determination of the plasma renin activity. 1 99

Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.
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PMID:[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)]. 1 16

Although the role of renin in hypertension continues to be incompletely defined, recent progress in the chemistry of renin has been considerable. Extensive purifications of hog kidney renin and the renin-like mouse submaxillary gland enzyme have been achieved. Various inhibitory peptides based on tetradecapeptide renin substrate have been useful in renin kinetic studies and in renin affinity chromatography. Classification of renin as an acid protease results from its marked inhibition by pepstatin and from the discovery that free carboxyl at the active site is essential for activity in human and hog kidney and mouse submaxillary gland enzymes. The presence of pseudorenin in all tissues has limited the use of model peptides as renin substrates in plasma and crude tissue extracts, since the proteolytic properties of the two enzymes are nearly identical. The existence of renin in multiple, chromatographically separable forms has been known. More recently inactive forms have been found in plasma, amniotic fluid, and hog and rabbit kidneys. Prolonged storage or treatment with acid, trypsin, or pepsin causes activation; in some instances the conversion is from a higher than normal molecular weight. The implications of these findings with respect to the renin-angiotensin system need much further investigation.
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PMID:New developments in our knowledge of the chemistry of renin. 1 50

Changes in blood pressure, plasma renin activity, and hemodynamic components were studied in 23 patients with essential hypertension treated with oral pindolol or propranolol. These beta-adrenergic blocking agents effectively lowered the blood pressure in the majority of the patients. Although plasma renin activity was not significantly changed, the higher was the pretreatment level, the more it tended to be decreased. Systemic vascular resistence was significantly decreased, while changes in cardiac index and circulating blood volume were variable. Pindolol showed less effect in reducing the heart rate than propranolol. The antihypertensive effect of these drugs had no correlation with the change in plasma renin activity or in any one of hemodynamic components.
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PMID:Effects of beta-adrenergic blocking agents on the blood pressure, plasma renin activity and hemodynamics of hypertensive patients. 1 42

Administration of androgen to female mice is known to increase the level of several proteins in the submaxillary gland, including nerve growth factor, epidermal growth factor, esteroproteolytic activity, and renin. In the present study, renin activity has been assessed in extracts of submaxillary gland of female mice from two inbred strains (SWR/J and C57BL/10J), from F1 and F2 hybrids, and from backcrosses between F1 and parental strains. In both uninduced and induced mice, renin activity of submaxillary gland was more than 100-fold greater in SWR/J than in C57BL/10J mice as measured by either an enzymatic assay or an immunodiffusion method. This difference was not due to differences in plasma testosterone levels between the strains, and the enzymes from the two strains had similar pH optima, substrate specificities, heat stabilities, and apparent Michaelis constants. In the submaxillary gland the difference was relatively specific for renin because increases in esteroproteolytic activity, nerve growth factor, and epidermal growth factor after androgen treatment appeared to be similar in both strains. Studies with the various hybrids indicate that the difference in renin activity between the two strains is apparently due to a single regulatory gene.
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PMID:Genetic control of renin activity in the submaxillary gland of the mouse. 1 53

This case report describes a patient with malignant hypertension and phaeochromocytoma in whom blockade of angiotensin II receptors by the competitive antagonist 1-sar-8-ala-angiotensin II (Saralasin) resulted in a partial correction of the elevated BP. Plasma renin activity was high and rose further during the blockade. Competitive inhibition of angiotensin II by Saralasin does not abolish the pressor effect of catecholamines. It was therefore interesting to observe that in this patient with phaeochromocytoma, independently, both alpha-adrenergic receptor blockade and angiotensin II receptor blockade were effective in lowering BP.
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PMID:Partial correction of hypertension by angiotensin II blockade in a patient with phaeochromocytoma. 1 5

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.
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PMID:Effects of calcium on renin and aldosterone in the rat. 1 57

To examine extrarenal sources of "renin-like" activity plasma was obtained from 19 anephric males. Plasma renin activity (PRA), concentration (PRC) (obtained after addition of exogenous renin substrate) and total renin concentration (TRC) (obtained after acid-activation of plasma and subsequent incubation with exogenous renin substrate) demonstrated values for several anephric patients comparable or above those seen in plasma from 10 normal subjects. Incubation of untreated plasma (PRA and PRC) and acid-dialyzed plasma (TRC) for angiotensin I generation was performed at pH 7.5, at 37 degrees C with EDTA, dimercaprol, and 8-OH-quinoline as angiotensinase and converting enzyme inhibitors. The pH optimum for acid-activation of TRC in anephric plasma was the same as that in normal plasma (pH 3.3). Molecular weight determinations following Sephadex gel chromatography demonstrated that the renin-like enzyme in normal plasma had a molecular weight of about 42,000 before and after acid-activation, while that in anephric plasma had a molecular weight of approximately 61,000. A saliva sample from one anephric subject with the highest levels of PRA, PRC, and TRC in plasma also demonstrated measurable amounts of PRA, PRC, and TRC. The molecular weight of this salivary "renin-like" activity also was 61,000. These observations suggest a possible extrarenal source of "renin-like" activity in anephric man. The physiological significance of these studies remains to be clarified.
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PMID:An extrarenal source of "renin-like" activity in anephric man. 1 33

Normal human plasma contains an active form of renin that is activated by acidification to pH 3.0 and comprises 56% of the total renin. In our study, inactive renin was also present in plasma from five anephric persons, and the proportion of active to inactive renin in these subjects was similar to normal. Plasma from normal pregnant women contained increased concentrations of inactive renin and the proportion of inactive renin was raised to around 66%. Plasma from persons with renal hypertension contained varying amounts of inactive renin but the mean percentage (35%) was lower than normal. An infusion of saralasin sufficient to lower the blood pressure in five subjects with renal hypertension resulted in a rise in active renin concentration but no change in the concentration of inactive renin. Plasma angiotensin II correlated with active renin but not with inactive renin, suggesting that the inactive renin does not produce angiotensin II in vivo.
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PMID:An inactive renin in human plasma. 1 36

1. The morphology of the juxtaglomerular apparatus, plasma renin activity, plasma renin substrate and renal renin have been studied in rats after maximal stimulation by bilateral adrenalectomy and salt depletion, and also after blocking this stimulation by deoxycorticosterone and salt load. 2. After stimulation the juxtaglomerular apparatus showed a well-developed granular endoplasmic reticulum and a low secretory granule content. Plasma renin activity was markedly elevated and plasma renin substrate was low. After blockade numerous specific granules with crystalline structures were seen and the granular endoplasmic reticulum was less developed. Plasma renin activity was now low and plasma renin substrate elevated. 3. After prior acidification of the kidney extract a significant increase of renal renin was observed in both conditions but was greater in the second group at the time when large numbers of young granules containing crystalline material were seen. 4. Kidney slices from the adrenalectomized salt-depleted rats released more renin than control slices. Vincristine did not affect this release, but inhibited release from slices stimulated by isoprenaline.
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PMID:Control of renin secretion in vivo and in vitro in rats: arguments in favour of a precursor form of renin and of a role of a microtubular system. 1 63


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