Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
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PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5

A 30-year-old female was admitted to our hospital complaining of hematuria and right flank pain in September, 1987. She had been diagnosed idiopathic thrombocytopenic purpura in 1980, and had similar symptoms before. Hematoma in the right ureter was demonstrated by retrograde pyelography and CT-scanning, and these symptoms improved within one month. Each activity of plasma clotting factors was within normal limits. Enzymatic studies of the urine revealed low values of plasmin-, urokinase-, and kallikrein-like activities in both excerbation and remission. These hemorrhagic tendencies might have been the result of marked thrombocytopenia: After bleeding into the urinary tracts began, the bleeding would tend to form hematoma because of elevated clotting activity; then hematoma would grow due to decreased urine fibrinolytic activities. This suggested that a decline of fibrinolysis in urine might have a promoting effect on the process of hematoma formation.
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PMID:[Possible mechanisms of hematoma formation in the urinary tracts in a patient with idiopathic thrombocytopenic purpura]. 224 28

An antibody against rat kallikrein was produced in rabbits and its localization was studied in various organs of the rat to confirm its specificity. The distribution of immunoreactive kallikrein was studied in rat ureter by use of immunochemical techniques. Ureteral tissue was fixed in Zamboni's-glutaraldehyde fixative and immunostained with indirect immunofluorescence and the peroxidase-antiperoxidase (PAP) method for light and electron microscopy. Preabsorption of the primary polyclonal antiserum with purified rat urinary kallikrein and substitution with normal serum were used as controls. By light microscopy, kallikrein was localized in the lamina propria and in the adventitial connective tissue surrounding the entire ureter. Immunoelectron microscopy confirmed this immunolocalization. Immunoreactive kallikrein was concentrated in fibroblasts of connective tissue and was not present in collagen fibers. Immunoreactivity was associated with the Golgi complex, free polyribosomes, and rough endoplasmic reticulum. No immunostaining was observed in other subcellular components of fibroblasts.
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PMID:Localization of a renal kallikrein immunoreactive-like substance in rat ureter. 305 70

Purified urinary kallikrein induces contractions of the rat ureter in vitro. Antibodies against kallikrein block the contractile response of the isolated ureter to rat urine.
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PMID:Inhibition of the ureteral contractions induced by rat urine with kallikrein antibodies. 655 May 34

The luminal membrane of collecting duct cells, especially the intercalated cells, is normally exposed to active kallikrein. This is the consequence of the specific localization of this renal enzyme in the connecting tubule cells and its principal route of secretion being into the tubular lumen. It is conceivable that kallikrein acts downstream on a transporter involved in distal bicarbonate handling. To investigate this possibility, we estimated bicarbonate concentration and measured kallikrein amidolytic activity in urine fractions collected after a classical stop-flow experiment in rabbits. A highly significant inverse correlation was found between these parameters (r = -0.94, p < 0.001) in the peak kallikrein fractions. Neither sodium nor potassium concentration were correlated to kallikrein. This suggests that the physiological role of renal kallikrein may be to regulate extracellular fluid pH by inhibiting collecting duct bicarbonate secretion. To test the hypothesis that tubular fluid kallikrein activity and bicarbonate secretion are causally related, we developed a novel in vivo stop-flow injection model ('orthograde stop-flow'). A hog-kallikrein containing solution (0.5 microgram/ml) was injected through the abdominal aorta into the renal tubular system of one kidney of barbiturate-anesthetized rats, while the renal blood supply was interrupted. The ureter was then occluded and renal blood perfusion reinitiated. After a 2-min contact time five 125-microliters urine fractions were collected. Bicarbonate secretion was clearly detected in the second and third fractions (i.e. those coming from the collecting ducts) of the control animals, which had received only the vehicle. There was no bicarbonate secretion peak in the corresponding urine fractions collected from kallikrein-injected animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for an inhibitory effect of kallikrein on collecting duct bicarbonate secretion in rats and rabbits. 753 9

The renal origin of kallikrein is now clearly established. However, the presence of kallikrein in urine raises questions about a possible physiological role of this enzyme at the urinary level. We have already demonstrated the presence of kallikrein-like substance in rat ureter. For establishing the continuity of the presence of kallikrein-like substance along the urinary tract we have studied the localization of immunoreactive kallikrein-like substance in urinary bladder of the normal rat by immunohistochemical methods for light- and electron-microscopy, using an antibody against rat urinary kallikrein. By light microscopy, kallikrein-like substance was found to be associated with the lamina propria, which is the connective tissue component which constitutes one layer of the bladder wall. Weak staining was present in the smooth-muscle layer. By immuno-electron microscopy, kallikrein-like substance was localized in fibroblasts which were present in the connective tissue and which penetrated into the layer of smooth muscle; immunoreactivity was observed in endoplasmic reticulum, Golgi apparatus and free polyribosomes. Immunolabelling was demonstrated in no other part of the wall bladder and in no other cellular component. The continuity of the presence of kallikrein-like substance from the kidney to the urinary bladder gives new indications concerning the significance of this system in renal physiology.
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PMID:Immunolocalization of renal kallikrein-like substance in rat urinary bladder. 769 24

The origin of urinary bradykinin was defined by use of plasma kininogen-deficient B/N-Katholiek rats, whose ureter urine contains very low amount of urinary kinin. The kinin level increased after the rats received an infusion of normal plasma. Furthermore, the bradykinin content in the ureter urine of these kininogen-deficient rats increased more by infusion of partially purified rat- low-molecular-weight kininogen than by that of high-molecular-weight kininogen. Urinary kallikrein activity of B/N-Katholiek rats was enzymatically identical with that of normal B/N-Kitasato rats. These results indicate that urinary bradykinin found in the ureter urine of normal rats is derived from plasma low-molecular-weight kininogen by cleavage by urinary kallikrein.
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PMID:Demonstration of derivation of rat urinary bradykinin from plasma low-molecular-weight kininogen: a study using kininogen-deficient rats. 798 May 99

1. The experiments reported here were performed to test the hypothesis that renal kallikrein is involved in the regulation of acid-base balance. 2. The bicarbonate concentration and the kallikrein activity in the spontaneously voided urine of conscious rats (experiment 1) were inversely correlated (correlation coefficient (r) = -0.63, P < 0.0001). The correlation was even greater when the urinary bicarbonate concentration was expressed per milligram excreted creatinine (r = -0.74, P < 0.00002). 3. Intravenous injection of the kallikrein inhibitor aprotinin in barbiturate-anaesthetized rats (experiment 2) reduced urinary kallikrein activity (P < 0.05) and increased bicarbonate excretion rate (P < 0.012). 4. Renal arterial infusion of aprotinin in barbiturate-anaesthetized rats (experiment 3) reduced urinary kallikrein activity (120 min, P < 0.01), and increased bicarbonate excretion rate (120 min, P < 0.01). Animals infused with the inhibitor developed a moderate metabolic acidosis (base excess: control, 2.9 +/- 0.7 mM (mean +/- S.E.M.); experimental, -8.1 +/- 0.7 mM; P < 0.05). 5. The bicarbonate concentration of urine fractions obtained after retrograde injection of kallikrein through the ureter into the collecting duct system of barbiturate-anaesthetized rats was lower than that from kidneys administered the vehicle (experiment 4; P < 0.001). A retrograde injection of bradykinin was without effect (experiment 5). 6. We conclude that renal kallikrein is involved in the regulation of urinary bicarbonate excretion. Increased intraluminal activity of the enzyme reduces, and decreased kallikrein activity increases, bicarbonate excretion. The enzyme may be a component of a negative feedback loop controlling the hydrogen ion activity of the extracellular space.
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PMID:Involvement of renal kallikrein in the regulation of bicarbonate excretion in rats. 856 52