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

1981 ◽  
Vol 98 (1) ◽  
pp. 36-42 ◽  
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.

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

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.

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 renal kallikrein-kinin system

1980 ◽  
Vol 238 (4) ◽  
pp. F247-F255 ◽  
Author(s):  
O. A. Carretero ◽  
A. G. Scicli
Keyword(s):  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

scholarly journals ALDOSTERONE--A POTENT STIMULATOR OF THE RENAL KALLIKREIN-KININ SYSTEM DURING FETAL LIFE

1984 ◽  
Vol 18 ◽  
pp. 368A-368A
Author(s):  
Jean E Robillard ◽  
Kenneth T Nakamura ◽  
Oliva McWeeny ◽  
Sindy Wear ◽  
William Lawton
Keyword(s):  
Fetal Life ◽  
Kinin System ◽  
Potent Stimulator ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

The Renal Kallikrein-Kinin System in Renoparenchymal Hypertension

1989 ◽  
pp. 127-132 ◽  
Author(s):  
Toshiaki Ando ◽  
Kazuaki Shimamoto ◽  
Nobuyuki Ura ◽  
Toyoharu Yokoyama ◽  
Shuzaburo Fukuyama ◽  
...  
Keyword(s):  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

scholarly journals Bradykinin acutely inhibits activity of the epithelial Na+ channel in mammalian aldosterone-sensitive distal nephron

2011 ◽  
Vol 300 (5) ◽  
pp. F1105-F1115 ◽  
Author(s):  
Oleg Zaika ◽  
Mykola Mamenko ◽  
Roger G. O'Neil ◽  
Oleh Pochynyuk
Keyword(s):  
Critical Role ◽  
Na Channel ◽  
Open Probability ◽  
Kinin System ◽  
Renal Kallikrein ◽  
Subsequent Activation ◽  
Patch Clamp Electrophysiology ◽  
B2 Receptors ◽  
Renal Tubular ◽  
Kallikrein Kinin System

Activation of the renal kallikrein-kinin system results in natriuresis and diuresis, suggesting its possible role in renal tubular sodium transport regulation. Here, we used patch-clamp electrophysiology to directly assess the effects of bradykinin (BK) on the epithelial Na+ channel (ENaC) activity in freshly isolated split-opened murine aldosterone-sensitive distal nephrons (ASDNs). BK acutely inhibits ENaC activity by reducing channel open probability ( Po) in a dose-dependent and reversible manner. Inhibition of B2 receptors with icatibant (HOE-140) abolished BK actions on ENaC. In contrast, activation of B1 receptors with the selective agonist Lys-des-Arg9-BK failed to reproduce BK actions on ENaC. This is consistent with B2 receptors playing a critical role in mediating BK signaling to ENaC. BK has little effect on ENaC Po when Gq/11 was inhibited with Gp antagonist 2A. Moreover, inhibition of phospholipase C (PLC) with U73122, but not saturation of cellular cAMP levels with the membrane-permeable nonhydrolysable cAMP analog 8-cpt-cAMP, prevents BK actions on ENaC activity. This argues that BK stimulates B2 receptors with subsequent activation of Gq/11-PLC signaling cascade to acutely inhibit ENaC activity. Activation of BK signaling acutely depletes apical PI( 4 , 5 )P2 levels. However, inhibition of Ca2+ pump SERCA of the endoplasmic reticulum with thapsigargin does not prevent BK signaling to ENaC. Furthermore, caffeine, while producing a similar rise in [Ca2+]i as in response to BK stimulation, fails to recapitulate BK actions on ENaC. Therefore, we concluded that BK acutely inhibits ENaC Po in mammalian ASDN via stimulation of B2 receptors and following depletion of PI( 4 , 5 )P2, but not increases in [Ca2+]i.

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