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.

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.

On the interaction of calcium, sodium, and water transport in the diuresing kidney

1968 ◽  
Vol 46 (2) ◽  
pp. 275-280 ◽  
Author(s):  
O. Schück ◽  
J. H. Cort
Keyword(s):  
Renal Function ◽  
Linear Relation ◽  
Filtration Rate ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Osmotic Diuresis ◽  
Anesthetized Dogs ◽  
Permeability For Water ◽  
Solute Excretion ◽  
Tubular Permeability

Diuresis was induced in cats by infusion of 3% glucose in 10% ethanol. When urine flow had stabilized at high levels a solution of the Ca salt of ethylenediaminetetraacetate (Na2CaEDTA) was infused as a control for the effect of the EDTA molecule on renal function. The infusion was then changed over to the same molar rate of Na2EDTA, which resulted in a 30% decrease in serum Ca levels. Ca was then repleted rapidly as CaCl2 given intravenously, and the infusion was shifted back to Na2CaEDTA. The decrease in extracellular Ca concentration was associated with a significant antidiuresis. In further experiments on anesthetized dogs, osmotic diuresis was induced either by (a) infusion of hyperosmotic mannitol solutions, which were then shifted over to hypertonic NaCl, or (b) the same solutions in reverse order. Ca excretion correlated in linear fashion with Na excretion, but not with total solute excretion or with filtration rate. When Ca was added to the mannitol infusion, Na excretion increased in linear relation to Ca. It is suggested that Ca (a) decreases tubular permeability for water reabsorption and (b) decreases Na reabsorption, while Na (c) decreases Ca reabsorption. Mechanisms a and b would appear to involve membrane transport directly in the proximal tubule.

Effect of sodium lactate on urate clearance in the Dalmatian and in the mongrel

1964 ◽  
Vol 207 (1) ◽  
pp. 113-117 ◽  
Author(s):  
Gabrielle H. Reem ◽  
Parker Vanamee
Keyword(s):  
Filtration Rate ◽  
Inhibitory Effect ◽  
Sodium Lactate ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Osmotic Diuresis ◽  
Significant Drop ◽  
Urate Reabsorption

Sodium lactate was infused and urate clearance was measured under conditions of osmotic diuresis alone, as well as during simultaneous urate infusion. Urate clearance in the Dalmatian was not depressed by the administration of sodium lactate of 1.2–9.3 mEq/kg dl-sodium lactate, indicating that sodium lactate has no inhibitory effect on tubular secretion of urate. dl-Sodium lactate, 0.54–11.8 mEq/kg, was administered to four mongrel dogs in five experiments. In three experiments a significant drop of urate clearance in relation to filtration rate was observed. In two experiments in which urine flows exceeded 10 ml/min no significant decrease in urate clearance was recorded following dl-sodium lactate administration. The depression of urate clearance in the mongrel under conditions of moderate urine flow where reabsorption of solutes is more easily accomplished, and the absence of this effect in the Dalmatian as well as in the mongrel under conditions of vigorous diuresis where reabsorption of solutes is greatly diminished, lends support to the belief that sodium lactate depresses urate clearance by facilitating urate reabsorption in the mongrel.

Renal response to atrial peptides is reduced in experimental nephrosis

1987 ◽  
Vol 252 (4) ◽  
pp. F654-F660 ◽  
Author(s):  
N. Perico ◽  
F. Delaini ◽  
C. Lupini ◽  
G. Remuzzi
Keyword(s):  
Flow Rate ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Bolus Injection ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Constant Infusion ◽  
Urinary Flow ◽  
Single Intravenous Injection ◽  
Renal Response

The aim of this study was to evaluate the renal response to atrial extracts (AE) and synthetic atrial natriuretic factor (ANF) in control rats and in rats with experimental nephrotic syndrome (NS). NS was obtained by a single intravenous injection of adriamycin (7.5 mg/kg). Bolus injection of AE from normal or NS rats resulted in marked increase of diuresis and natriuresis in bioassay control rats (AE from normal rats, urine flow rate, 14.87 +/- 2.94 to 186.18 +/- 55.86 microliters/min; Na excretion, 0.68 +/- 0.26 to 21.80 +/- 5.45 mu eq/min; AE from NS, urine flow rate, 13.49 +/- 4.30 to 167.14 +/- 51.44 microliters/min; Na excretion, 0.98 +/- 0.57 to 20.71 +/- 9.76 mu eq/min). In contrast, blunted diuretic (from 11.26 +/- 3.05 to 65.20 +/- 27.30 microliters/min) and natriuretic (from 0.58 +/- 0.15 to 4.52 +/- 1.59 mu eq/min) effect was observed when AE were injected in rats with NS. Injection of the vehicle in which AE were dissolved or ventricular extracts did not increase urinary flow rate or Na excretion in both control and NS animals. Bolus injection of synthetic ANF (Arg-101-Tyr-126) induced marked diuretic and natriuretic response in control but not in NS rats. Similar results were obtained when AE were infused by constant infusion in control or in NS bioassay rats. AE given by constant infusion induced comparable increase in glomerular filtration rate (GFR) over basal values both in control and NS animals (controls, 39%; NS rats, 40%).(ABSTRACT TRUNCATED AT 250 WORDS)

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

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.

Inactive Urinary Kallikrein Excretion and Urine Flow Rate

1985 ◽  
Vol 69 (s12) ◽  
pp. 67P-67P ◽  
Author(s):  
D.G. Waller ◽  
S.K. Campbell ◽  
J.D.M Albano ◽  
J.G.B Millar
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urinary Kallikrein ◽  
Urinary Kallikrein Excretion

scholarly journals Effects of water deprivation on renal hydroelectrolytic excretion in chronically Trypanosoma cruzi-infected rats

1995 ◽  
Vol 28 (1) ◽  
pp. 7-11 ◽  
Author(s):  
T.T. Rosa ◽  
L.F. Junqueira Junior ◽  
F.J.C. Mangia ◽  
J.P.R. Veiga ◽  
F.V. Pádua
Keyword(s):  
Trypanosoma Cruzi ◽  
Wistar Rats ◽  
Water Deprivation ◽  
Renal Excretion ◽  
Fractional Excretion ◽  
The Other ◽  
Urinary Flow ◽  
Fractional Excretion Of Sodium ◽  
Male Wistar Rats ◽  
Age And Sex

The effect of an 8 hour-period of water deprivation on fluid and electrolyte renal excretion was investigated in male Wistar rats infected with the strain São Felipe (12SF) of Trypanosoma cruzi, in comparison with age and sex matched non-infected controls. The median percent reductions in the urinary flow (-40% v -63%) and excretion ofsodium (-57% v-79%) were smaller in chagasic than in control rats, respectively. So, chagasic rats excreted more than controls. On the other hand, the median percent decrement in the clearance of creatinine was higher in chagasic (-51%) than in controls (-39%). Thus, chagasic rats showed some disturbed renal hydroelectrolytic responses to water deprivation, expressed by smaller conservation, or higher excretion of water and sodium in association with smaller glomerularfiltration rate. This fact denoted an elevation in the fractional excretion of sodium and water.

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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