Inhibition of Urinary Kallikrein Excretion by Semi-Purified Renin in the Rat

1979 ◽  
Vol 57 (s5) ◽  
pp. 243s-245s ◽  
Author(s):  
H. R. Croxatto ◽  
G. Silva ◽  
M. Boric

1. Rat kidney extracts obtained at successive stages of a purification procedure, which allows the separation of renin and kallikrein, were used in order to investigate their effect upon urinary excretion of kallikrein, sodium, potassium and water in hyperhydrated rats. 2. Only the purified fraction containing renin reduced kallikrein excretion. The decrease of kallikrein coincided with a considerable increase in sodium, potassium and water excretion. 3. The natriuretic effect of renin extract did not depend on the presence of kallikrein. The injection of a mixture of renin and kallikrein attenuated the effect of renin alone, indicating that both enzymes exert antagonistic actions on the excretion of electrolytes and water by the kidneys. 4. A purified fraction of kidney extract containing no kallikrein and only traces of renin activity, had a stimulatory effect on kallikrein, water and elctrolyte excretion.

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza

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.


1976 ◽  
Vol 51 (s3) ◽  
pp. 283s-286s
Author(s):  
C. I. Johnston ◽  
P. G. Matthews ◽  
E. Dax

1. Urinary kallikrein excretion was measured in rats by an enzyme kinetic method employing radioimmunoassay of generated bradykinin. 2. Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin. 3. Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin. 4. A close and significant direct relation between plasma renin activity and urinary kallikrein excretion was demonstrated. 5. The diuresis and natriuresis induced by frusemide in rats was associated with increased urinary kallikrein excretion and acute rises in plasma renin. 6. In chronic renal hypertensive rats urinary kallikrein excretion was increased only in the animals with two-kidney Goldblatt hypertension. This group was also the only group that demonstrated a significant rise in plasma renin activity.


1982 ◽  
Vol 63 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Marin-Grez ◽  
G. Schaechtelin ◽  
G. Bönner ◽  
G. Speck ◽  
D. Ganten ◽  
...  

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.


Life Sciences ◽  
1981 ◽  
Vol 28 (2) ◽  
pp. 175-184 ◽  
Author(s):  
P. Boscolo ◽  
G. Galli ◽  
A. Iannaccone ◽  
F. Martino ◽  
G. Porcelli ◽  
...  

1978 ◽  
Vol 55 (s4) ◽  
pp. 187s-189s
Author(s):  
H. R. Croxatto ◽  
R. Arriagada ◽  
M. Rojas ◽  
J. Roblero ◽  
R. Rosas

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.


1988 ◽  
Vol 11 (1-2) ◽  
pp. 50-59
Author(s):  
Gregory W. Stephens ◽  
Wilfred Lieberthal ◽  
Narendra B. Oza ◽  
Robert Valeri ◽  
Norman G. Levinsky

1983 ◽  
Vol 65 (5) ◽  
pp. 487-490 ◽  
Author(s):  
José M. López ◽  
Eugenio Arteaga ◽  
José A. Rodriguez ◽  
Héctor Croxatto

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.


1990 ◽  
Vol 27 (4) ◽  
pp. 337-342 ◽  
Author(s):  
Shyam Bala Lall ◽  
Shanti Kunchaparty ◽  
Hefazat Husain Siddiqui ◽  
Jasbir Singh Bajaj

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