Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients

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


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

1978 ◽  
Vol 55 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Lechi ◽  
G. Covi ◽  
C. Lechi ◽  
A. Corgnati ◽  
E. Arosio ◽  
...  

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroups: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients β-adrenoreceptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.


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.


Diabetes ◽  
1974 ◽  
Vol 23 (10) ◽  
pp. 835-840 ◽  
Author(s):  
A. R. Christlieb ◽  
C. Munichoodappa ◽  
J. T. Braaten

1979 ◽  
Vol 56 (3) ◽  
pp. 255-259 ◽  
Author(s):  
A. C. Burden ◽  
H. Thurston

1. The plasma renin activity (PRA) was measured in 76 diabetic patients who were attending an outpatients clinic. Of these patients 16 had untreated hypertension and 28 had diabetic complications, which ranged from microaneurysms to renal failure and blindness. 2. Compared with age- and sex-matched normotensive control subjects, both normotensive and hypertensive diabetic patients had significantly higher PRA (P < 0·001). 3. Hypertensive diabetic patients also showed a higher PRA than matched hypertensive control subjects (P < 0·005). There were no significant differences between diabetic patients with hypertension or complications compared with those without these features. 4. Although this elevation of PRA could be due to a change in another component of the renin—angiotensin system, hypersecretion of renin is the most likely explanation.


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.


Sign in / Sign up

Export Citation Format

Share Document