Changes in Renal and Urinary Kallikrein Activity by Mannitol-Induced Osmotic Diuresis

1981 ◽  
Vol 61 (1) ◽  
pp. 47-51 ◽  
Author(s):  
G. Bönner ◽  
M. Marin-Grez ◽  
D. Beck ◽  
M. Deeg ◽  
F. Gross
Keyword(s):  
Renal Cortex ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Plasma Aldosterone Concentration ◽  
Urinary Kallikrein Excretion ◽  
Short Period ◽  
Urinary Potassium ◽  
Renal Kallikrein ◽  
Kallikrein Activity

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

Effects of thyroid hormones on urinary and renal kallikreins

1992 ◽  
Vol 263 (3) ◽  
pp. E430-E434
Author(s):  
S. Avigdor ◽  
F. Alhenc-Gelas ◽  
J. Bouhnik
Keyword(s):  
Thyroid Hormones ◽  
Urinary Excretion ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Single Measurement ◽  
Kidney Weight ◽  
Plasma Aldosterone Concentration ◽  
Renal Kallikrein ◽  
Enzyme Changes ◽  
Intact Rats

The effects of thyroid hormones on the urinary excretion of kallikrein and on renal kallikrein were studied in rats. Total and active urinary kallikrein was decreased after thyroidectomy, but renal kallikrein content remained unchanged. Diuresis increased, and kidney weight and plasma aldosterone concentration decreased. Treatment with 3,5,3'-triiodo-L-thyronine restored the urinary kallikrein in thyroidectomized rats to normal and increased it in intact rats. It also produced increases in kidney weight and plasma aldosterone and a decrease in diuresis. The effect of thyroid hormones on the urinary kallikrein response to mineralocorticoids was also tested. Deoxycorticosterone acetate increased urinary kallikrein more in normal than in thyroidectomized rats. These results suggest that thyroidectomy decreases renal kallikrein synthesis and lowers the turnover rate of the enzyme, changes not detectable by a single measurement of the renal kallikrein content but reflected by an alteration in the urinary excretion of the enzyme. Thyroid hormones participate in the control of urinary kallikrein. This effect, however, is probably indirect and may be mediated by mineralocorticoids since thyroid function affects both the plasma level of aldosterone, which is known to influence renal kallikrein, and the kallikrein response to exogenous mineralocorticoids.

Renal Kallikrein Activity and Urinary Kallikrein Excretion in Rats with Experimental Renal Hypertension

1982 ◽  
Vol 63 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Marin-Grez ◽  
G. Schaechtelin ◽  
G. Bönner ◽  
G. Speck ◽  
D. Ganten ◽  
...  
Keyword(s):  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Rats ◽  
Control Value ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Experimental Renal Hypertension ◽  
Kallikrein Activity

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 ± 6 mmHg on day 8 after aortic ligature and 142 ± 6 mmHg on day 90; in controls pressures were 107 ± 3 and 110 ± 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6·5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animals 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

The Mechanism of Urinary Kallikrein Excretion in the Rat

1982 ◽  
Vol 63 (2) ◽  
pp. 217-218 ◽  
Author(s):  
A. Martínez Seeber ◽  
S. B. Vila ◽  
O. L. Catanzaro
Keyword(s):  
Wistar Rats ◽  
Filtration Rate ◽  
Glucose Solution ◽  
Urine Flow ◽  
Urinary Flow ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Male Wistar Rats

1. In male Wistar rats urinary kallikrein excretion was positively correlated with urinary flow and glomerular filtration rate (GFR). 2. Osmotic diuresis produced by a 30% (w/v) glucose solution increased urinary kallikrein, and a positive correlation between this variable and urine flow was observed. No correlation was observed with GFR. 3. The mechanism of urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

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

Gender Differences in Urinary Kallikrein Excretion in Man: Variation Throughout the Menstrual Cycle

1994 ◽  
Vol 86 (2) ◽  
pp. 227-231 ◽  
Author(s):  
J. D. M. Albano ◽  
S. K. Campbell ◽  
A. Farrer ◽  
J. G. B. Millar
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Physiological Role ◽  
Follicular Phase ◽  
Urinary Kallikrein ◽  
Plasma Aldosterone Concentration ◽  
Urinary Kallikrein Excretion ◽  
Post Menopausal ◽  
Cyclic Changes ◽  
Male Subjects

1. Urinary kallikrein excretion was measured in healthy male subjects and in healthy pre- and post-menopausal females. 2. Urinary kallikrein excretion was shown to be constant throughout a 24 h period. Individual male subjects showed little fluctuation in urinary kallikrein excretion; within-subject variance accounted for 1.65% of the total. 3. Female subjects with ovulatory menstrual periods excreted significantly more kallikrein than post-menopausal females and males. 4. Pre-menopausal females showed a much greater within-subject variation in urinary kallikrein excretion and this could be related to the stage of the menstrual cycle, with significantly greater urinary kallikrein excretion in the luteal phase than in the follicular phase. 5. Plasma renin activity and plasma aldosterone concentration also showed a menstrual variation, with concentrations in the luteal phase being significantly higher than those in the follicular phase. 6. The rise in urinary kallikrein excretion in the luteal phase could be abolished by oral administration of the aldosterone antagonist spironolactone. 7. Urinary kallikrein excretion in post-menopausal females was similar to the range found in males, and showed no cyclic changes over a 4 week period. 8. Gender and menstrual status should be taken into account in studies of the physiological role of tissue kallikreins.

Effects of Frusemide on the Renal Kallikrein–Kinin System of the Rat

1982 ◽  
Vol 63 (5) ◽  
pp. 447-453 ◽  
Author(s):  
G. Bönner ◽  
D. Beck ◽  
M. Deeg ◽  
M. Marin-Grez ◽  
F. Gross
Keyword(s):  
Renal Cortex ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Biphasic Response ◽  
Kinin System ◽  
Forced Diuresis ◽  
Renal Kallikrein ◽  
Male Wistar Rats ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

1. In male Wistar rats, three doses of frusemide (0·5, 5·0 and 50·0 mg/kg) were injected subcutaneously. A dose-related increase in urine flow and natriuresis occurred, whereas there was a biphasic response in kallikrein excretion with an initial, dose-related transient increase and a secondary reduction. When the urine losses were replaced by the infusion of 0·9% NaCl solution, the biphasic response of urinary kallikrein excretion was maintained. 2. In all experiments, urinary excretion of kallikrein correlated with the excretion of potassium. Frusemide enhanced the excretion of kinins, which correlated with the urine volume and the natriuresis, but not with kallikrein excretion. 3. In contrast to the initially increased excretion of kallikrein, kallikrein activity in the renal cortex remained unchanged or was even reduced. Kininogen content of the perfused tissue of the renal cortex did not vary throughout the experiment, but decreased markedly in the non-perfused tissue of the cortex 30 min after the injection of frusemide. 4. It is concluded that forced diuresis induced by frusemide causes a ‘wash out’ of renal kallikrein in urine, probably not indicating the true changes in the activity of the renal kallikrein-kinin system within the kidney. Kinin excretion in urine was not correlated with kallikrein excretion but with changes in diuresis. Thus it might be suggested that the renal kallikrein-kinin system could be involved by kinins in the regulation of renal water and sodium excretion as well as of renal plasma flow.

Effect of pH and amiloride on the intrarenal formation of kinins

1983 ◽  
Vol 245 (2) ◽  
pp. F198-F203
Author(s):  
A. G. Scicli ◽  
M. A. Diaz ◽  
O. A. Carretero
Keyword(s):  
Urinary Kallikrein ◽  
Urinary Ph ◽  
Kinin System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Lower Urinary

Changes in urinary kallikrein excretion are assumed to reflect changes in intrarenal formation of kinins. Yet factors that alter the enzymatic activity of renal kallikrein and kininases may alter the concentration of kinins in the nephron independent of amount of kallikrein excreted. In anesthetized rats, we measured excretion of urinary kallikrein (kininogenase activity) and kinin excretion during altered urinary pH and after amiloride, which reportedly inhibits urinary kallikrein. In rats fed a low sodium diet, urine was acidified by intravenous 0.28 M sodium sulfate. This decreased urinary pH from 6.1 +/- 0.09 to 5.3 +/- 0.17 and urinary kinin excretion from 28.0 +/- 9.0 to 10.5 +/- 5.0 pg/min. Urinary kallikrein excretion doubled from 43.0 +/- 5.0 to 82.5 +/- 13.5 ng/min. The optimum pH of kallikrein is congruent to 8.5, so the decreased excretion of urinary kinins is probably secondary to decreased kininogenase activity at lower urinary pH. Amiloride decreased urinary kinins from 35.5 +/- 7.3 to 18.2 +/- 2.5 pg/min and kallikrein from 18.7 +/- 4.9 to 9.3 +/- 1.8 ng/min, while urinary pH increased from 6.7 +/- 0.07 to 7.3 +/- 0.07. The depressed excretion of kallikrein and kinins with amiloride may not have been due to inhibition of kallikrein, since amiloride (1 mM) did not inhibit the kininogenase activity of rat urinary kallikrein (congruent to 1.2 nM) on dog or rat kininogen in vitro. We conclude that changes in urinary kallikrein may not reflect changes in intrarenal formation of kinins. These data also indicate that kallikrein excretion increases and kinin formation decreases when urine is acidified in the distal nephron and that there may be a link between the kallikrein-kinin system and the renal mechanisms affected by amiloride.

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