Effects of Prostaglandin E2 and Prostaglandin F2α Upon Urinary Kallikrein Excretion in Rats

1978 ◽  
Vol 55 (s4) ◽  
pp. 187s-189s
Author(s):  
H. R. Croxatto ◽  
R. Arriagada ◽  
M. Rojas ◽  
J. Roblero ◽  
R. Rosas
Keyword(s):  
Prostaglandin E2 ◽  
Tap Water ◽  
Extracellular Fluid ◽  
Prostaglandin F2α ◽  
Urinary Kallikrein ◽  
Kinin System ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

1. In normally hydrated rats prostaglandin F2α (PGF2α) in doses of 5 μg/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, PGF2α 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 μg/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. PGF2α, 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 PGF2α may be part of a regulatory mechanism associated with the kallikrein—kinin system which contributes maintainance of extracellular fluid homeostasis.

scholarly journals Loss-of-Function Polymorphism of the Human Kallikrein Gene with Reduced Urinary Kallikrein Activity

2002 ◽  
Vol 13 (4) ◽  
pp. 968-976 ◽  
Author(s):  
Rola Slim ◽  
Florence Torremocha ◽  
Thierry Moreau ◽  
Anne Pizard ◽  
Steven C. Hunt ◽  
...  
Keyword(s):  
Vascular Diseases ◽  
Allelic Frequency ◽  
The Other ◽  
Nucleotide Polymorphisms ◽  
Urinary Kallikrein ◽  
Loss Of Function ◽  
Kinin System ◽  
Molecular Variants ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

ABSTRACT. Kallikrein is synthesized in the distal tubules and produces kinins, which are involved in the regulation of vascular tone in the kidney. Urinary kallikrein activity has been reported to be partly inherited and to be reduced in essential hypertension. In a systematic search for molecular variants of the human kallikrein gene, nine single-nucleotide polymorphisms were identified. Five of those polymorphisms, including two nonsynonymous substitutions in exon 3, i.e., Arg53His (allelic frequency in Caucasian subjects, 0.03) and Gln121Glu (allelic frequency, 0.33), were studied in a normotensive group and two independent hypertensive groups for which 24-h urinary kallikrein activity had been measured. A significant decrease in urinary kallikrein activity was observed for the subjects who were heterozygous for the Arg53His polymorphism, compared with the other subjects. This finding was consistent in the two hypertensive groups and was observed with several kallikrein enzymatic assays. The Gln121Glu polymorphism and the other polymorphisms were not associated with changes in urinary kallikrein activity. None of the polymorphisms was associated with hypertension. Recombinant kallikrein variants were synthesized and enzymatically characterized, using native kininogen and kininogen-derived synthetic peptide substrates. No important effect was observed after Gln121 mutation, but there was a major decrease in enzyme activity when Arg53 was replaced by histidine. A model of kallikrein derived from crystallographic data suggested that Arg53 can affect substrate binding. The identification of a subset of subjects with genetically reduced kallikrein activity as a result of an amino acid mutation could facilitate analysis of the role of the kallikrein-kinin system in renal and vascular diseases.

Increased Excretion of Kallikrein during Dexamethasone Administrationl in Normal Man on Low and Normal Salt Intake

1983 ◽  
Vol 65 (5) ◽  
pp. 487-490 ◽  
Author(s):  
José M. López ◽  
Eugenio Arteaga ◽  
José A. Rodriguez ◽  
Héctor Croxatto
Keyword(s):  
Salt Intake ◽  
Sodium Intake ◽  
Direct Action ◽  
Urinary Kallikrein ◽  
Kinin System ◽  
Sodium Potassium ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Normal Men ◽  
Kallikrein Kinin System

1. The effect of dexamethasone administration for 3 days on urinary kallikrein excretion was studied in 12 normal men with normal sodium intake (n=6) or low sodium intake (n=6). Urinary excretion of sodium, potassium, 17-hydroxycorticosteroids, aldosterone and water was also measured in all subjects. 2. Dexamethasone administration was associated with a significant increase in urinary kallikrein excretion (F3, 30 = 6.9; P < 0.001) regardless of sodium intake. No significant correlation could be established between the increase in urinary kallikrein excretion and changes in urinary sodium, potassium, 17-hydroxycorticosteroids, aldosterone or water. 3. These results suggest that dexamethasone can exert a direct action on the renal kallikrein-kinin system.

The Relationship of Urinary Kallikrein Activity to Renal Salt and Water Excretion

1978 ◽  
Vol 54 (1) ◽  
pp. 39-45 ◽  
Author(s):  
S. B. Levy ◽  
R. P. Frigon ◽  
R. A. Stone
Keyword(s):  
Racial Differences ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Racial Groups ◽  
Urinary Kallikrein ◽  
Experimental Conditions ◽  
Water Excretion ◽  
Water Load ◽  
Black And White ◽  
Kallikrein Activity

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.

Steroid induced changes of the renal kallikrein-kinin system in rats

1984 ◽  
Vol 107 (1) ◽  
pp. 131-140 ◽  
Author(s):  
G. Bönner ◽  
R. Autenrieth ◽  
M. Marin-Grez ◽  
G. Speck ◽  
F. Gross
Keyword(s):  
Urinary Excretion ◽  
Time Course ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Sprague Dawley ◽  
Kinin System ◽  
Salt Loading ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

Abstract. In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 × 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 × 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralcorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.

Low-salt diet downregulates plasma but not tissue kallikrein-kinin system

1998 ◽  
Vol 275 (1) ◽  
pp. F88-F93 ◽  
Author(s):  
U. Hilgenfeldt ◽  
T. Puschner ◽  
U. Riester ◽  
J. Finsterle ◽  
J. Hilgenfeldt ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Plasma Levels ◽  
Plasma Kallikrein ◽  
Tissue Kallikrein ◽  
Kinin System ◽  
Water Excretion ◽  
Salt Diet ◽  
Active Peptide ◽  
Low Salt ◽  
Kallikrein Kinin System

The kallikrein-kinin system (KKS) is involved in the regulation of blood pressure and in the sodium and water excretion. In humans, the KKS is divided functionally into a plasma KKS (pKKS) generating the biologically active peptide bradykinin and into the tissue (glandular) KKS (tKKS) generating the active peptide kallidin. The objective of this study was to examine the effect of a low-NaCl diet on the concentration of both pKKS and tKKS in plasma and urine in 10 healthy volunteers. After a 4-day low-NaCl diet, the urinary sodium and chloride excretions had decreased from 234 to 21.2 mmol/24 h and from 198 to 14.6 mmol/24 h, respectively. The plasma levels of ANG I, aldosterone, and angiotensin converting enzyme (ACE) significantly increased from 50.4 to 82.8 pg/ml, from 129 to 315 pg/ml, and from 46.4 to 59.8 U/ml, respectively, demonstrating the physiological adjustment to the low-salt diet. In plasma, the levels of bradykinin and plasma kallikrein had significantly decreased from 13.7 to 7.57 pg/ml and 14.4 to 7.13 U/ml, respectively. However, the levels of high-molecular-weight kininogen (HMW kininogen) remain unchanged (101 vs. 112 μg/ml, not significant). Contrary to plasma kallikrein, the plasma levels of tissue kallikrein increased (0.345 vs. 0.500 U/ml; P < 0.01). The plasma kallidin levels, however, did not change (64.7 vs. 68.6 pg/ml, not significant). This can be explained by a simultaneous decrease in the plasma low-molecular-weight kininogen (LMW kininogen) levels (89.9 vs. 44.4 μg/ml; P < 0.05). As in plasma, we find increased urinary concentrations of renal (tissue) kallikrein (23.3 to 42.8 U/24 h; P < 0.05) that contrast with, and are presumably counterbalanced by, urinary LMW kininogen levels (77.0 vs. 51.8 μg/24 h; P < 0.05). Consequently, in urine low-NaCl diet caused no significant change in either bradykinin or kallidin (9.2 vs. 10.8 μg/24 h, and 10.9 vs. 10.3 μg/24 h). It is concluded that the stimulation of the renin-angiotensin system on a low-NaCl diet is associated with a decrease in pKKS (bradykinin and plasma kallikrein) but not in tissue and renal KKS. Although tissue kallikrein is increased, there is no change in kallidin, as LMW kininogen in plasma and urine is decreased. These data suggest a difference in the regulation of pKKS and tKKS by low-salt diet.

Dissociation of urinary kallikrein activity and salt and water excretion in the rat

1986 ◽  
Vol 250 (6) ◽  
pp. F1082-F1089 ◽  
Author(s):  
D. M. Pollock ◽  
M. I. Butterfield ◽  
J. L. Ader ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Linear Regression Analysis ◽  
Urine Flow ◽  
Urinary Kallikrein ◽  
Water Excretion ◽  
Time Control ◽  
Dose Dependent Decrease ◽  
State Group ◽  
Kallikrein Activity ◽  
The Relationship

Experiments were designed to examine the relationship, if any, between urinary kallikrein activity (amidolytic assay) and sodium and water excretion in 12-wk-old Munich-Wistar rats. Five groups of animals were studied: euvolemic, saline-expanded and water-loaded anesthetized rats, and euvolemic and saline-expanded conscious restrained rats. Following surgery, animals were allowed to stabilize (60-180 min) and reach a steady-state urine flow. By design, basal sodium and/or water excretion varied markedly among groups as a function of hydration state. Group means for sodium excretion and urine flow ranged from 0.8 to 12.4 mu eq/min and 6 to 112 microliter/min, respectively. In contrast, neither active nor total urinary kallikrein activity differed significantly among the five groups. In anesthetized euvolemic rats, intravenous administration of aprotinin produced a dose-dependent decrease in urinary kallikrein activity. The greatest inhibition of 93 +/- 3% (active) and 72 +/- 10% (total) was observed with a dose of 5,000 kallikrein inhibiting units (KIU)/kg and 1,000 KIU X kg-1 X min-1. This dose produced a significant decrease in active and total kallikrein activity in each group (P less than 0.001). However, sodium and water excretion were unchanged in aprotinin-treated rats and similar to values in vehicle-treated time-control groups. Linear regression analysis revealed no significant correlations between urinary kallikrein activity and sodium excretion or urine flow either among or within groups. These results indicate that urinary kallikrein activity is not related to acute sodium and water homeostasis in anesthetized or conscious rats.

Enzymes of the kallikrein-kinin system in rainbow trout

1990 ◽  
Vol 258 (2) ◽  
pp. R501-R506 ◽  
Author(s):  
D. W. Lipke ◽  
K. R. Olson
Keyword(s):  
Rainbow Trout ◽  
Kinin System ◽  
Alpha Adrenergic Receptors ◽  
Plasma Injection ◽  
Pressor Responses ◽  
Vascular Sensitivity ◽  
Esterolytic Activity ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

Evidence for a kallikrein-kinin system (KKS) in fish is incomplete. In the present study, components of the KKS were identified in rainbow trout. Tissues were assayed for kallikrein-like esterolytic activity using three synthetic kallikrein substrates (TAME, VGAN, and PPAN), and the presence of kallikrein substrate (kininogen) in trout plasma was estimated by bradykinin (BK) radioimmunoassay of plasma activated with trypsin (T). Formation of pressor-depressor substances in vivo by porcine glandular kallikrein (GK) and T was measured after intra-arterial injection into unanesthetized trout. Gill and kidney contained kallikrein activity (TAME and VGAN assays); little activity was observed with PPAN. Aprotinin inhibited gill activity (TAME assay). T liberated 42 +/- 3 (SE) ng (n = 10) of immunoreactive BK per milliliter of plasma. Injection of GK in vivo reduced plasma kininogen levels for over 24 h. GK produced pressor responses only in fish pretreated with the angiotensin-converting enzyme (ACE) inhibitor captopril. This effect was mediated partly through stimulation of alpha-adrenergic receptors. T produced slight pressor responses that were captopril insensitive. These results show that trout possess elements of the KKS system including kallikrein-like enzymatic activity, kininogen, receptor-mediated vascular sensitivity to kallikrein products, and kininolytic activity consistent with ACE (kininase II).

Effect of vasopressin on renal kallikrein excretion

1980 ◽  
Vol 239 (4) ◽  
pp. F388-F392 ◽  
Author(s):  
Géza Fejes-TÓth ◽  
Tibor Zahajszky ◽  
János Filep
Keyword(s):  
Technical Assistance ◽  
Free Water ◽  
Urinary Kallikrein ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Kinin System ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Induced Changes

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU·kg-1·h-1 in the dog and 3 mU·kg-1·h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion. Note: With the Technical Assistance of Klára Peres and Edit Spitzár water diuresis; antidiuresis; natriuresis; kinins; dog; rat Submitted on October 8, 1979 Accepted on May 21, 1980

Urinary Kallikrein and Plasma Renin during the Reversal of Renovascular Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Experimental Hypertension ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Water Excretion

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.

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