Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors evaluated the assay performances and clinical usefulness of a newly developed solid phase radioimmunoassay (RIA) for total renin concentration (TRC) in human plasma. The direct total renin RIA was performed by a sandwich technique with a pair of anti-human renin monoclonal antibodies. Renin activation with trypsin did not change TRC. The RIA showed satisfactory assay performances and demonstrated full compatibility with a direct RIA-kit for active renin concentration (ARC) in human plasma. The values of TRC were 105.3 +/- 8.6 pg/mL in normal subjects and 136.5 +/- 14.6 pg/mL in patients with essential hypertension. The values of TRC and the ratios of ARC to TRC were high in patients with renovascular hypertension and were low in patients with primary aldosteronism. Although the TRC value in diabetic patients was 134.4 +/- 14.8 pg/mL, the ratio of ARC to TRC was low. The RIA procedure was simple since prior purification or activation of renin was not required. These results suggest that the total renin RIA and its combined use with the active renin RIA may be helpful in understanding the renin-angiotensin system in human plasma.
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PMID:Measurement of plasma total renin by the anti-human renin monoclonal antibodies. 177 17

The physiological role of inactive renin, especially the question of whether and how a conversion to active renin takes place in vivo, remains controversial. In order to show the dynamic alterations from inactive to active renin following acute ACE-inhibition, both forms of renin were investigated in both renal veins and the peripheral circulation of 20 patients with essential hypertension and 20 patients with renovascular hypertension before and 1 h after 25 mg of captopril. Active and inactive renin were determined indirectly as plasma renin activity (PRA, unit: ng/ml x h). In vitro activation of inactive renin was achieved with trypsin (1 mg/ml plasma), followed by a further determination of PRA (= total renin). Subtraction of the active renin from the total renin yields the amount of inactive renin. In patients with essential hypertension, the mean values of active renin increase equally in both renal veins (1.4 and 1.3 before, 1.9 and 1.8 after captopril) and the peripheral circulation (0.9 and 1.3) (p less than 0.002), whereas the inactive renin decreases correspondingly. Renal veins: 7.6 and 8.2 before, 7.2 and 7.6 after captopril; peripheral circulation: 7.7 before and 7.0 after captopril (p less than 0.05). In all patients with renovascular hypertension, there is basally a marked lateralization of active renin (6.4 vs 3.5; p less than 0.01) and inactive renin (20.5 and 18.9, p less than 0.03) towards the side of the ischemic kidney. After captopril, the values for total renin and active renin increase (p less than 0.001), and the side difference for active renin becomes still more pronounced (33.0 vs 14.2; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conversion of inactive renin to active renin following acute angiotensin converting enzyme inhibition in essential hypertension and renovascular hypertension]. 265 7

The changes in active and inactive renin after captopril (n = 29) or furosemide administration (n = 10) were studied in hypertensive patients. Furthermore, after percutaneous transluminal angioplasty (PTA) in 3 cases of renovascular hypertension (RVH), and after nephrectomy in a case of juxtaglomerular cell tumor, the time course of the changes in these two types of renin was investigated. Inactive renin was activated by trypsin treatment. Plasma renin concentration was measured by using an excess of sheep substrate. In patients with essential hypertension or primary aldosteronism, inactive renin was unchanged, irrespective of response in active renin, after the administration of captopril and furosemide. In patients with RVH, inactive renin was markedly decreased by furosemide but unchanged by captopril, in spite of significant increase in active renin. After PTA and nephrectomy, inactive renin decreased slower than active renin. These data support the idea that in patients with RVH, the increase in active renin by furosemide is at least partly due to the activation of inactive renin. It is also suggested that the increase in active renin by captopril is mainly due to the promoted release of active renin from the kidney. Furthermore, it seems likely that the metabolic clearance of inactive renin is slower than that in active renin.
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PMID:The changes in active and inactive renin induced by various maneuvers in hypertensive patients. 294 48

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comprehensive studies on the renal kallikrein-kinin system in essential hypertension. 302 78

Possible differences in structure-function relationship of urinary kallikrein between normotensive and hypertensive individuals were analysed using two different assay systems which detect two distinct entities of the enzyme. A monospecific goat anti-human urinary kallikrein antibody was characterized by inhibition studies with the purified active enzyme and by trypsin activation of endogenous urinary prokallikrein. Analysis of the data revealed that the antibody is directed against active kallikrein by recognizing an epitope which is different from the catalytic site of the enzyme but which is being exposed together with the active site during trypsin activation of the proenzyme. A direct radioimmunoassay for urinary kallikrein was developed and correlated with the kinin generating activity of the enzyme by assessing endogenous active and trypsin activated kallikrein in the urine of normotensive and hypertensive subjects. Significant positive correlations were found between the two assays for both active and total kallikrein in normotensive and hypertensive subjects and the slopes of the respective regression lines were identical. These data do not provide evidence for a defective enzyme, a defective activation of the proenzyme or for the presence of an inhibitor of urinary kallikrein in essential hypertension.
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PMID:Correlation of two different assays for urinary kallikrein in normotensive and hypertensive subjects. 324 81

In 36 patients with unilateral renal artery stenosis and in 24 with essential hypertension the plasma levels of total immunoreactive renin, and enzymatically active renin were measured in both renal veins (V) and in the aorta (A) by direct RIA by using monoclonal renin antibodies. Active renin and trypsin-activatable inactive renin were also measured by indirect RIA with angiotensin-I antibodies. The V/A ratio for the different forms of renin calculated from the results of direct and indirect RIA were not different. The V/A ratio of active renin for the kidney with the stenotic artery was 3.04 +/- 0.28 (mean +/- sem) with direct and 3.02 +/- 0.25 with indirect RIA. The contralateral ratio was 1.04 +/- 0.02 with the direct and 1.05 +/- 0.02 with the indirect RIA. In essential hypertension it was 1.28 +/- 0.04 with direct RIA and 1.28 +/- 0.04 with indirect RIA. Chronic treatment with captopril had no influence on this ratio in both patients groups. The V/A ratio of total immunoreactive renin was lower than that of active renin and this ratio had lost discriminative power for lateralization. This ratio was significantly greater than one on the affected side in renal artery stenosis but not contralaterally and in essential hypertension. This study shows that renin activity after trypsin-activation of plasma is an accurate measure of the total renin concentration, i.e. active renin plus prorenin. It also shows that a kidney with a stenotic artery secretes inactive renin, which is immunologically related to active renin and is likely to be prorenin. Direct RIA for measuring active renin is technically more simple than indirect RIA. Direct RIA however is somewhat less sensitive. For measuring the V/A ratio for active renin in patients with renal artery stenosis this can be overcome by stimulating the renin-angiotensin system for instance by captopril.
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PMID:Renal vein immunoreactive renin in patients with renal artery stenosis and essential hypertension. 330 95

We compared the effectiveness of two techniques involving the use of the enzyme trypsin to activate inactive renin in human plasma. Both these methods were developed to optimize activation with trypsin by preventing the possible destruction of activated renin by trypsin itself. In one method, an antitryptic agent such as benzamidine is added to plasma, concomitantly with trypsin (liquid phase). In the other a low concentration of Sepharose-bound (immobilized) trypsin is used. In six plasma samples we have found that trypsin (1.5 mg/ml) activation, with or without benzamidine (0.8 mg/ml), yielded similar values of activated renin (11.0 +/- 2.7 vs. 11.3 +/- 2.3 ng/ml/hr). However, the addition of immobilized trypsin to pool plasma pretreated with trypsin plus benzamidine caused a further increase in plasma renin activity (PRA); in contrast, the addition of trypsin and benzamidine to pool plasma pretreated with immobilized trypsin caused a decrease in PRA. In 17 plasma samples from patients with essential hypertension we found that the inactive renin values were always higher after treatment with immobilized trypsin than with trypsin plus benzamidine (9.0 +/- 0.7 vs. 6.1 +/- 0.5 ng/ml/hr, P less than 0.01); moreover, there was a positive correlation between the differences in the values of inactive renin measured with the two methods and the values obtained with immobilized trypsin (r = 0.64, P less than 0.01). Therefore, the activation with immobilized trypsin is more effective than that with liquid-phase trypsin, alone or in combination with benzamidine, in converting inactive renin in human plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effectiveness of Sepharose-bound trypsin versus liquid-phase trypsin plus benzamidine for activation of inactive renin in human plasma. 354 Jan 63

The method of measurement for urinary total kallikrein (KAL) and preKAL in human was developed, and daily excretions of urinary total KAL, KAL and preKAL were investigated in patients with essential hypertension. Forty microliter of urine samples were incubated with or without 120 micrograms of chymotrypsin-free trypsin for total KAL or KAL, respectively. KAL was measured with direct radioimmunoassay and kininogenase assay. PreKAL was calculated by the subtraction of KAL from total KAL. The subjects of this study included 7 normotensives (NT) and 8 essential hypertensives (EHT). Daily excretions of total KAL, KAL and preKAL were significantly lower in EHT than those in NT. KAL/total KAL ratio, which reflects the conversion rate from preKAL to KAL in the kidney, was not significantly different between EHT and NT. From these results, it is suggested that decreased urinary KAL excretion in EHT is mainly caused by reduced preKAL production rather than the impaired conversion from preKAL to KAL in the kidney. It is emphasized that this method of measurement for urinary total KAL and preKAL may be a very useful tool for research of the renal kallikrein-kinin system.
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PMID:The method of urinary total kallikrein and prekallikrein measurement, and their urinary excretions in the patients with essential hypertension. 364 31

Most previous studies have not significantly correlated urinary kallikrein to urinary kinins. We investigated whether urinary kininogen might influence kinin formation within the urine. On an ad-lib diet the 24 hour excretion of total and intact kininogen, kinins and kallikrein was determined in 24 control subjects, 20 untreated essential hypertensives, 12 with end-stage renal disease and 8 subjects with liver disease. Kallikrein and kinins were measured by a direct radioimmunoassay. Total kininogen was determined from the sum of preformed kinins and kinins generated after trypsin (intact kininogen). Cross reactivity between purified human low molecular weight kininogen and bradykinin antiserum was 3%. Total and intact kininogen were significantly correlated with kinins in controls, essential hypertension and liver disease. In essential hypertension, end-stage renal and liver diseases kinins were significantly decreased. This was associated with a reduction in kininogen but not kallikrein in essential hypertension and liver disease, and a reduction in kallikrein but not kininogen in end-stage renal disease. Thus, renal kinin generation in various states may be affected by either or both kininogen and kallikrein.
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PMID:Urinary kininogen: a possible regulator of kinin formation in normal individuals and subjects with essential hypertension, end-stage renal and liver disease. 381 87

The total renin activity (TRP) and inactive renin levels (IR) in the blood plasma were examined with the help of cryo- and trypsin activation in 9 normal subjects, in 40 patients with essential hypertension and in 18 patients with primary aldosteronism (PA). The cryoactivation method was shown to detect 40-80% of IR determined by the method of trypsin activation. Both methods revealed analogous ratios of the two renin forms in its total production in the presence of essential hypertension (in different "renin" subgroups) and arterial hypertension secondary to PA and may be used as the methods of choice when examining essential hypertension patients with the normal and subnormal plasma renin activity. The method of trypsin activation is more preferable for a more accurate quantification of small amounts of IR found in essential hypertension patients with a high plasma renin activity. With a high level of the TRP (over 8 ng/ml/h) activation should be performed in diluted plasma.
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PMID:[Comparative evaluation of the efficacy of methods of cryo- and trypsin activation of inactive renin in vitro]. 388 76


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