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

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.

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Effect of vasopressin on renal kallikrein excretion

AJP Renal Physiology ◽

10.1152/ajprenal.1980.239.4.f388 ◽

1980 ◽

Vol 239 (4) ◽

pp. F388-F392 ◽

Cited By ~ 2

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

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Effect of pH and amiloride on the intrarenal formation of kinins

AJP Renal Physiology ◽

10.1152/ajprenal.1983.245.2.f198 ◽

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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The renal kallikrein-kinin system in Brattleboro rats with hereditary hypothalamic diabetes insipidus

Acta Endocrinologica ◽

10.1530/acta.0.0980036 ◽

1981 ◽

Vol 98 (1) ◽

pp. 36-42 ◽

Cited By ~ 5

Author(s):

G. Bonner ◽

W. Rascher ◽

G. Speck ◽

M. Marin-Grez ◽

F. Gross

Keyword(s):

Diabetes Insipidus ◽

Water Deprivation ◽

Brattleboro Rats ◽

Urinary Kallikrein ◽

Similar Reduction ◽

Kinin System ◽

Urinary Kallikrein Excretion ◽

Basic Activity ◽

Renal Kallikrein ◽

Kallikrein Kinin System

Abstract. The activity of the renal kallikrein-kinin system was investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI); LongEvans rats (LE) were taken as controls. In the rats with DI, urinary kallikrein excretion was lower (P < 0.05) than in the LE rats. However, when related to total renal mass or to body weight, there was no difference between the two strains. Kallikrein activity in the renal cortex was similar in the Brattleboro and the LE rats. Antidiuretic hormone (vasopressin tannate) in a dose of 100 mU given once daily for 3 days had no effect on urinary kallikrein excretion in either of the strains. Water deprivation for 24 h resulted, also in both strains, in a similar reduction in urinary kallikrein excretion. The renal kallikrein-kinin system of LE rats and that of DI rats does not principally differ in basic activity, nor in response to the administration of vasopressin, nor to water deprivation.

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The Renal Kallikrein-Kinin System: Its Role as a Safety Valve for Excess Sodium Intake, and Its Attenuation as a Possible Etiologic Factor in Salt-Sensitive Hypertension

Critical Reviews in Clinical Laboratory Sciences ◽

10.1080/713609329 ◽

2003 ◽

Vol 40 (1) ◽

pp. 43-115 ◽

Cited By ~ 38

Author(s):

Makoto Katori ◽

Masataka Majima

Keyword(s):

Safety Valve ◽

Sodium Intake ◽

Etiologic Factor ◽

Kinin System ◽

Renal Kallikrein ◽

Excess Sodium ◽

Kallikrein Kinin System ◽

Salt Sensitive Hypertension

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

Clinical Science ◽

10.1042/cs055187s ◽

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.

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