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 relationship between urinary kallikrein, urinary aldosterone, and plasma renin activity (PRA) was studied in hypertensive patients and normal subjects. Kallikrein was measured by a radiochemical esterolytic assay. Nine white males with normal renin, mild essential hypertension (25 +/- 5 [SD] yr; blood pressure [BP] 143 +/- 7 / 95 +/- 5 mm Hg) and six white normal males (23 +/- 3 yr; BP 115 +/- 15 / 70 +/- 6 mm Hg) were placed on a one-week diet consisting of 400 mEq Na+, 80 mEq K+ diet and a one week diet of a 10 mEq Na+, 80 mEq K+ diet. During salt restriction, PRA, urinary aldosterone, and urinary kallikrein progressively rose. (Urinary kallikrein on day 7: normals 18.3 +/- 13.7 esterase units [EU] per 24 hr; hypertensives 22.7 +/- 12.5 EU/24 hrs). There were no significant differences between the normals and hypertensives in PRA, aldosterone, or kallikrein excretion. After sodium balance was achieved, during salt loading, the PRA, aldosterone and kallikrein values were similar in both normals and hypertensives. (Urinary kallikrein on day 7: normals 5.0 +/- 5.2; hypertensives 7.9 +/- 4.4 EU/24 hrs.) Abnormalities in urinary kallikrein in hypertensives were not found when young white males with normal renin essential hypertension were compared to age-matched white male normal subjects. PRA appears related to urinary kallikrein excretion in this type of patient.
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PMID:Urinary kallikrein in normal renin essential hypertension. 91 48

The possible effects of cimetidine on the pharmacokinetics and pharmacodynamics of enalapril, a pro-drug requiring hepatic de-esterification to an active angiotensin-converting enzyme (ACE) inhibitor enalaprilat, were assessed in a randomized, crossover study. Cimetidine (400 mg) or placebo was administered orally every 12 h for 3 days and on the day of a single oral administration of enalapril maleate (10 mg) to seven healthy male subjects. Serum ACE, plasma renin activity (PRA), plasma aldosterone concentration (PAC), and alpha-human atrial natriuretic peptide (alpha-hANP) were measured before and 4 h after the enalapril dosing. There were no significant differences in any serum- and urine-derived kinetic parameters of enalapril and enalaprilat, nor in hemodynamics, PAC, or alpha-hANP between the two treatment trials. ACE decreased and PRA increased to a similar extent in the two trials. Serum enalaprilat concentration correlated significantly (p less than 0.001) with percentage of inhibition of ACE activity. The results suggest that the pharmacokinetics and pharmacodynamics of enalapril are unaffected by preadministration of cimetidine. Thus, cimetidine does not appear to alter hepatic esterase activity toward enalapril.
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PMID:Effect of cimetidine on the pharmacokinetics and pharmacodynamics of enalapril in normal volunteers. 246 49

The level of tissue kallikrein in serum and urine, and of an erythrocyte kallikrein-like enzyme, were compared in 10 subjects without hypertension and in 10 patients with hypertension with normal renin levels. Each group consisted of five men and five women. All subjects were observed at a general clinical research center for consecutive 5- to 6-day periods of daily dietary sodium intake of 109, 9, and 259 mEq. Tissue kallikrein levels in serum and urine and levels of the erythrocyte kallikrein-like enzyme were measured with specific radioimmunoassays or with an activity assay, respectively. Mean active and total urinary kallikrein excretion rates were higher in women than in men (both with and without hypertension) when they were given all diets (p less than 0.05 to 0.025), and these rates varied inversely with sodium intake. The serum immunoreactive tissue kallikrein level was higher in men than in women when they were given all diets (p less than 0.05 to 0.001), but there was no difference between subjects with and without hypertension. There were no consistent changes in levels with altered sodium intake. Erythrocyte kallikrein-like esterase activity was greater in women without hypertension than in men without hypertension (p less than 0.05 to 0.001) when receiving the 9 and 109 mEq sodium diets, but values were similar in all groups receiving the 259 mEq sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gender differences of human tissue kallikrein and an erythrocyte kallikrein-like enzyme in essential hypertension. 318 93

1. The distribution of enzymatic activities was determined in subcellular fractions of rat kidney cortex homogenates after various homogenization procedures. The specific activities of kininogenase (KGA), BAEE esterase (pH 8.5), alkaline phosphatase and glucose-6-phosphatase were, on average, 3.4 times higher in the microsomal fraction than in the whole homogenate. The total amount of these activities in the microsomal fraction after gentle, ordinary and forced homogenization were about 15, 40 and 65% of total recovered activities, respectively. These results confirmed the localization of KGA in the microsomal fraction.2. Renin activity was primarily recovered in the heavy mitochondrial fraction. When the force of the homogenization was increased some renin activity was shifted to the soluble fraction.3. When a mixture of renin and purified urinary KGA was given intravenously to an anaesthetized rat, a hypotensive response due to the KGA was followed by a hypertensive renin response. Over a certain range of concentrations KGA and renin could be measured simultaneously. In fractions of kidney homogenates, however, KGA activity was too low to be measured by this method.
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PMID:Subcellular localization of renin and kininogenase in the rat kidney. 432 58

Urinary kallikrein has been reported to activate human plasma inactive renin. Our previous report suggests that rat urinary kallikrein releases active renin from rat renal cortical slices. Recently, McPartland et al. were able to separate the A esterase activity of male rat urine into two components: A1 and A2. To evaluate whether these other urine arginine esterases release renin from the kidney, esterases A1 and A2 were isolated from male rat urine using DEAE-Sephadex chromatography and superfused to rat renal cortical slices. The renin-stimulating action of these enzymes was compared to that of rat urinary kallikrein. Rat urinary kallikrein stimulated renin release in a dose-dependent fashion between 70--140 milliesterase units (mEU)/ml. Esterase A2 dose stimulated renin release significantly between 120--140 mEU/ml. However, esterase A1 did not stimulate renin release at concentrations between 70--140 mEU/ml. Although Trasylol completely abolished kallikrein and esterase A2 stimulated renin release, soybean trypsin inhibitor blocked only esterase A2-stimulated renin release. The physiological role and site of origin of the A1 and A2 esterases is unknown. However, similar to kallikrein, esterase A2 is a potent stimulator of renin release and may be physiologically important for the release and activation of renin in the kidney.
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PMID:Effects of rat urinary arginine esterases on rat kidney to release renin. 616 23

One of the esteroproteinases present in the submandibular glands of female mice was purified and characterized. The enzyme, designated proteinase F in this report, had a pI value of 4.6 and a molecular weight of 27600, being comprised of two subunits of 10000 and 18000 daltons. The amino acid composition of proteinase F resembled that of the epidermal growth factor-binding protein, but antiserum against proteinase F only reacted weakly against the binding protein. Proteinase F had an optimum pH at around 9.0 and was strongly inhibited by Cu2+ and Hg2+ (42 and 76% inhibition, respectively, at a concentration of 4 x 10(-6) M). It was also inhibited by aprotinin, phenylmethylsulfonylfluoride, iodoacetamide, leupeptin, antipain, and benzamidine but neither by trypsin inhibitors from pancrease, soybean, or ovomucoid, nor by TLCK, TPCK, and epsilon-amino-n-caproic acid. Although its actual physiological function has yet to be determined, these properties indicate that proteinase F is a new enzyme, being distinguished from known proteinases, kallikrein, plasmin, trypsin, chymotrypsin, tonin, angiotensin-converting enzyme, proteinase A (beta-nerve growth factor endopeptidase), proteinase D (epidermal growth factor-binding protein), P-esterase, renin A, and renin C. Proteinase F was present in the submandibular glands of female mice more abundantly than in those of males, but it increased in males following castration. Thus, proteinase F appears to be affected by male hormones in vivo.
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PMID:A new esteroproteinase (proteinase F) from the submandibular glands of female mice. 633 33

The plasma renin activity (PRA), plasma volume (PV), urinary excretion of Kallikrein (UK) and PGE2, PGF2 alpha, 6-keto PGF1 alpha and TXB2 were measured in 24 ambulant patients without treatment on normal sodium diets with pregnancy-induced hypertension (HT) (diastolic BP greater than or equal to 90 mmHg, appearing after 20 weeks' pregnancy and absent 2 months after delivery). The UK was measured by an esterase technique, prostaglandins by radioimmunological assay and PV by dye dilution (Evans blue). Two subgroups of patients were identified according to the evolution of their blood pressure at rest at home; the first (7 patients) with labile HT, and the second (14 patients) with permanent HT. The PRA was significantly lower (p less than 0,001) in patients with permanent compared to labile hypertension (4,7 +/- 0,3 compared to 12,2 +/- 0,8 ng/ml/h) and compared to a control group of normotensive pregnant women (6,5 +/- 0,5). The PV, expressed as a percentage of the theoretical volume with respect to the stage of pregnancy and body surface area was low in both groups. In permanent HT: 1) there was no correlation between PV and PRA, 2) a positive correlation between UK and urinary 6-keto PGF1 alpha (r = 0,62; p less than 0,001) and PGE2 (r = -0,51, p less than 0,05). Discriminative linear analysis showed that urinary 6-keto PGF1 alpha was mainly related to PRA and to a lesser degree to UK.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renin-angiotensin-aldosterone system, blood volume, serum uric acid and urinary excretion of prostaglandins and kallikrein in the arterial hypertension induced by pregnancy]. 644 41

The effects of strain, sex, hypophysectomy and hormone treatment on mouse submandibular gland renin, kallikrein, S2266 hydrolase, and BAEe esterase activities have been examined. Renin activity is determined by the Rnr locus on mouse Chromosome 1. Female SWR/J mice (Rnrs/Rnrs) have 1000-fold higher submandibular gland renin activity than C57BL/6J mice (Rnrb/Rnrb). Both strains have similar kallikrein activity. Renin, BAEe esterase, and S2266 hydrolase are substantially higher in male mice compared to females of the same strain whereas kallikrein is not. Dihydrotestosterone and/or thyroxine treatment induces renin, BAEe esterase, and S2266 hydrolase in female mice with little effect on kallikrein. All four enzyme activities are profoundly reduced by hypophysectomy. Dihydrotestosterone and thyroxine are both required to restore renin, BAEe esterase, and S2266 hydrolase to induce levels. Dihydrotestosterone and/or thyroxine restores kallikrein to control levels. We conclude that renin and kallikrein in the mouse submandibular gland are under different genetic and endocrine control. In addition, the synthetic substrate S2266 is not a specific substrate for kallikrein activity in mouse submandibular gland cytosol.
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PMID:Comparison of genetic and endocrine control of renin and kallikrein in mouse submandibular gland. 675 23

The relationships between urinary kallikrein (Ukal), and plasma renin activity (PRA), urinary aldosterone (Ualdo), Na+ balance, SK+, and renal function were studied in essential hypertensives (EHT) and normals. Ukal was measured by a radiochemical esterolytic assay. We studied 18 white patients with EHT (15 men, 3 women) ages 31.6 to +/- 2.1 (SEM) yrs, BP 138 +/- 2/95 +/- 2 mm Hg. and 12 white normals (NLS) (7 men, 5 women) ages 30.2 +/- 2.3 yrs, BP 112 +/- 4/71 +/- 2 mm Hg. All received a 5-day diet of 400 mEq Na+, 80 mEq K+/day, and 5 days of 10 mEq Na+, 80 mEq K+/day. All achieved Na+ balance by Day 5. On Day 5 of the low Na+ diet, 24 hr. Ukal in EHT was 15.8 +/- 2.4 (esterase units/24 hr) vs NLS, 17.0 +/- 2.8 PRA was the same in EHT and NLS, but Ualdo was higher in NLS. (Day 5, low Na+, EHT, Ualdo = 29.4 +/0 3.3 microgram/24h. vs NLS 41.8 +/- 4.7, p less than 0.02). Analysis of individuals showed that all NLS increased Ukal after salt restriction, while 3 EHT decreased Ukal after salt restriction. This abnormal response in EHT was not related to abnormalities in Ualdo, PRA, Na+ balance, SK+, or creatinine clearance. In 3 EHT with low-renin EHT, the Ukal response was normal. In two of four patients with primary aldosteronism, Ukal was normal despite increased Ualdo. The Ukal response to salt restriction is abnormal in some EHT, unrelated to Ualdo or PRA, suggesting either a primary defect in Ukal and/or the presence of other factors modulating Ukal in EHT.
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PMID:Abnormal urinary kallikrein in hypertension is not related to aldosterone or plasma renin activity. 700 36

Acid activation of plasma prorenin occurs during dialysis to pH 3.3. and also during subsequent dialysis to pH 7.4. The latter, alkaline phase, involves Hageman factor-dependent formation of kallikrein, which in turn activates prorenin. The present study evaluates whether prorenin activation always occurs whenever kallikrein is activated in plasma. TAME esterase activity was used as a measure of plasma kallikrein activity an increase was observed during the alkaline phase of acid activation of prorenin. TAME esterase activity was absent when Hageman factor- or prekallikrein-deficient plasmas were similarly assayed and prorenin was not activated. Kaolin treatment of normal plasma rapidly increased TAME esterase activity at both 25 degrees and -4 degrees C, but no prorenin activation occurred. Similar changes in TAME esterase activity were observed in acid-treated plasma, in which setting prorenin was activated. No change in TAME esterase or renin activity occurred after addition of kaolin to acid-treated plasma deficient in Hageman factor; however, both enzymatic activities increased slightly in acidified prekallikrein-deficient plasma. Mixtures of these deficient plasmas exhibited normal kaolin activation of both TAME esterase and prorenin after acidification. Thus both Hageman factor and prekallikrein are needed for optimal contact activation of prorenin. These results demonstrate that prorenin activation does not always occur when active kallikrein is present in plasma. Prior acidification appears to be a prerequisite. Acidified prorenin may be more susceptible to cleavage; alternatively, competing substrates and/or inhibitors of kallikrein may be destroyed at acid pH, thereby permitting kallikrein to activate prorenin. Under normal conditions, activation of the plasma kallikrein-kinin system appears unlikely to result in activation of prorenin in vivo.
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PMID:Contact activation of human plasma prorenin in vitro. 701 41


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