Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The factors involved in the regulation and control of the human plasma fibrinolytic system at the cellular level are unknown at this time. The physiological regulation of plasmin formation in plasma depends primarily on the nature of the circulating zymogen, plasminogen, the physiological activators formed both in the blood and in the vascular endothelium, and the specific plasmin inhibitors found both in plasma and in certain of the cellular elements of the blood. The biosynthesis of the zymogen must be under genetic control, and the activators are probably released, after thrombus and clot formation, from components involved in the surface-mediated initiation of the coagulation system, and from the vascular endothelium. Activation of plasminogen can occur both in the fluid phase surrounding the thrombus and probably at thrombus surfaces, involving both the fibrin clot and the platelet membrane. The plasmin inhibitors act to control the system in order to prevent proteolytic degradation of important physiologic trace proteins of the coagulation, complement and kallikrein-kinin systems by the enzyme.
Mol Cell Biochem 1978 Aug 16
PMID:The human plasma fibrinolytic system: regulation and control. 15 4

1. Fractions highly enriched in plasma membrane, endoplasmic reticulum or brush border were prepared from rat kidney cortex. Kallikrein was concentrated in the plasma membrane fraction, but not in the brush border fraction. Angiotensin I-converting enzyme (kininase II) and angiotensinase were localized in the brush border membrane. 2. It is suggested that kallikrein in the urine may originate from plasma membrane distal to the brush border of proximal tubules and the conversion of angiotensin I and the inactivation of bradykinin and angiotensin II may occur on the lumen membrane of the proximal tubular cells.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Isolation of renal membranes that contain kallikrein, angiotensin I-converting enzyme (kininase II) and angiotensinase in the rat. 19 12

1. In normally hydrated rats prostaglandin F2alpha (PGF2alpha) in doses of 5 microgram/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2.5% of body wt. with 0.5% NaCl solution, PGF2alpha produced similar changes in kallikrein activity and electrolyte excretion. 2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion. 3. PGE2 in doses of 5, 12.5 and 25 microgram/100 g body wt. in overhydrated rats given 2.5% and 0.5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose. 4. PGF2alpha, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose. 5. The different actions of PGE2 and PGF2alpha may be part of a regulatory mechanism associated with the kallikrein-kinin system which contributes maintainance of extracellular fluid homeostasis.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Effects of prostaglandin E2 and prostaglandin F2alpha upon urinary kallikrein excretion in rats. 28 49

1. The values for kallikrein, amylase and protein were determined in samples of saliva obtained from 220 girls aged 14--18 years. 2. The concentrations of protein and amylase and kallikrein activities (per ml of saliva) were considerably more variable in samples taken in the morning than those in the afternnon. 3. The median amylase activity was about two and a half times greater in the morning than that in the afternoon. No such differences were seen in the median values for protein or kallikrein. 4. Examination of the vlues for salivary kallikrein during the menstrual cycle showed that there was significantly greater activity during days 29--32 and 1--4 than during the rest of the cycle. This pattern was most marked in the morning values of kallikrein but not apparent either in the morning or in the afternoon values of protein or amylase.
Clin Sci Mol Med Suppl 1978 Dec
PMID:A survey of salivary kallikrein and amylase in a population of schoolgirls, throughout the menstrual cycle. 28 47

1. We measured urinary kallikrein (kininogenin) excretion in black and white normotensive subjects during a variety of manipulations of salt and water balance. 2. A large intravenous saline load administered while the subjects were on an unrestricted sodium diet did not significantly change urinary kallikrein activity in either racial group. 3. After several days of dietary sodium restriction both racial groups increased their urinary kallikrein activity. An intravenous water load given then further increased urinary kallikrein activity. White subjects were studied for an additional 24 h period, and urinary kallikrein activity returned to pre-water load values, indicating that the excretion of a water load in sodium-depleted subjects is associated with an increase in kallikrein excretion. 4. Black subjects excreted less kallikrein in the urine than white subjects during the initial 24 h periods of unrestricted dietary sodium intake, but there were no other significant racial differences during the other experimental conditions.
Clin Sci Mol Med 1978 Jan
PMID:The relationship of urinary kallikrein activity to renal salt and water excretion. 62 Apr 92

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.
Clin Sci Mol Med 1978 Jul
PMID:Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism. 66 67

1. Urinary kallikrein excreted by normal rats is significantly increased (P less than 0-001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0-27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion (P less than 0-01) but considerably increased sodium excretion (P less than 0-001). 2. Renal kallikrein, measured by its kininogenase activity within 2 h of water loading, was significantly increased (P less than 0-05); after water loading and frusemide it was 40% decreased (P less than 0-001) and after salt loading it was reduced by approximately 50% (P less than 0-02). Renin did not change renal kallikrein. 3. Severely hypertensive (one-kidney) rats (blood pressure greater than 150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis, in moderately hypertensive rats (blood pressure less than 150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Renal urinary kallikrein in normotensive and hypertensive rats during enhanced excretion of water and electrolytes. 107 23

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Urinary kallikrein and plasma renin during the reversal of renovascular hypertension in rats. 107 24

1. A technique has been developed for the measurement of kallikrein 'production' in rat renal cortical cells in suspension. 2. After preparative steps, column chromatography on DEAE-cellulose yielded a peak of alpha-N-tosyl-L-arginine methyl ester (Tos-Arg-OMe) esterase activity identical with kallikrein isolated from rat urine in respect of pH optimum, effects of inhibitors, biological activity and immunological properties. 3. The nutrient medium surrounding incubated cells contained measurable kallikrein activity, which was increased by aldosterone and decreased by spironolactone. 4. The results raised the possibility that kallikrein could be an aldosterone-induced protein.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The effects of aldosterone and spironolactone on renal kallikrein in the rat. 107 27

1. Urinary kallikrein excretion was measured in rats by an enzyme kinetic method employing radioimmunoassay of generated bradykinin. 2. Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin. 3. Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin. 4. A close and significant direct relation between plasma renin activity and urinary kallikrein excretion was demonstrated. 5. The diuresis and natriuresis induced by frusemide in rats was associated with increased urinary kallikrein excretion and acute rises in plasma renin. 6. In chronic renal hypertensive rats urinary kallikrein excretion was increased only in the animals with two-kidney Goldblatt hypertension. This group was also the only group that demonstrated a significant rise in plasma renin activity.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Renin-angiotensin and kallikrein-kinin systems in sodium homeostasis and hypertension in rats. 107 28


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