Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Blood kinin concentration and plasma renin activity (PRA) were determined in the renal veins and in the inferior caval vein (ICV) below the level of the renal veins in 9 normal individuals (5 men and 4 women) and 7 patients with primary aldosteronism (3 men and 4 women). PRA in the renal veins and ICV was significantly lower and plasma aldosterone concentration in ICV significantly higher in the patients as compared to the normals. Kinin concentration in the renal veins and ICV did not differ significantly between the patients and the normals (0.31 +/- 0.04 (mean +/- SEM) vs 0.45 +/- 0.03 and 0.27 +/- 0.05 vs 0.45 +/- 0.06 microgram/l, respectively). In the normal individuals kinin concentration and PRA were inversely related in the left renal vein (r = -0.80; P less than 0.02), whereas this relation did not reach statistical significance in the right renal vein (r = -0.60; P less than 0.10). Kinin concentration in both renal veins was positively correlated to kinin concentration in ICV (r = 0.73; P less than 0.05 and r = 0.83; P less than 0.02 for the right and left renal vein, respectively). These results indicate that intrarenal kinin formation and renin release are inversely related in normal subjects. Furthermore, they suggest that one and the same enzyme, possibly renal kallikrein, may be implicated in the kinin formation in the systemic as well as in the renal circulation. Intrarenal kinin formation seems not to be increased in primary aldosteronism.
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PMID:Kinins in relation to renin activity in renal and inferior caval veins in normal individuals and patients with primary aldosteronism. 700 81

Urinary kallikrein, as a reflection of the intrarenal kallikrein, is distinct from plasma kallikrein. The kallikrein-kinin system, activated via antigen-antibody complexes, has been implicated in the pathophysiology of acute transplant rejection. We studied urinary excretion of sodium, potassium, protein, and kallikrein following renal transplantation in nine patients, In four patients who took steroids daily and were followed from the time of transplantation (without rejection episodes), urinary kallikrein remained stable (3.7 +/- 0.5 EU/24 hr, x +/- SEM). Since sodium-retaining steroids influence urinary kallikrein excretion, two patients were studied 2 and 3 months post-transplantation while receiving alternate-day prednisone. Values from urinary kallikrein in these patients did not differ from those in patients taking steroids daily (3.7 +/- 0.5 versus 2.7 +/- 0.3 EU/24 hr). In three patients experiencing acute rejection episodes, urinary kallikrein excretion rose markedly (24 to 260 EU/24 hr) and remained elevated until the patients became oliguric. Furthermore, this rise occurred 1-3 days before the clinical diagnosis of rejection was made. For the group as a whole there was no significant correlation between urinary kallikrein excretion, the excretion of sodium or potassium, or urine volume. Although the number of patients studied is small, the increases observed in urinary kallikrein suggest that activation of the intrarenal kallikrein-kinin system is associated with acute transplant rejection.
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PMID:Urinary kallikrein excretion in renal transplant patients. 704 34

Uterine homogenates of cycling and early pregnant Sprague Dawley rats and purified rat urinary kallikrein showed similar curves of displacement of 125I-kallikrein binding to a polyclonal antibody. Uterine kallikrein concentration measured by RIA was 8.7 +/- 2 SEM ng/g wet weight during the cycle (n = 6 in diestrus and metestrus) and 20.8 +/- 2 SEM (n = 7) ng/g wet weight on Day 7 of pregnancy (P7) (p < 0.001). On P7, kallikrein concentration was increased 12.4-fold in the implantation nodes, as compared to the interimplantation segments. Uterine homogenates of rats on P7, submitted to DEAE-cellulose chromatography and Sephadex gel filtration, yielded two fractions containing kallikrein immunoreactivity and kininogenase activity, with molecular masses that ranged from 120-125 kDa and 39-43 kDa, respectively. In the RIA, both fractions displayed parallelism with purified kallikrein. Enzymatic activity was expressed after activation by trypsin. It was inhibited by aprotinin, PMSF, p-amino-benzamidine, and leupeptin, but not by soybean or ovomucoid trypsin inhibitors. Kallikrein mRNA was demonstrated by reverse transcriptase/polymerase chain reaction in uteri of nonpregnant and P7 rats. These results show that rat uterus synthesizes one or more serine proteases that are immunologically and enzymatically related to tissue kallikrein in the implantation node on P7--determined both by an increment of whole uterus kallikrein content and a depletion of the interimplantation segments--suggests that kallikrein may play a role in the vasoactive changes of implantation.
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PMID:Uterine kallikrein in the early pregnant rat. 821 45


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