Renin—angiotensin and Kallikrein—kinin Systems in Sodium Homeostasis and Hypertension in Rats

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 ◽  
...  

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

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.


1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.


1982 ◽  
Vol 63 (2) ◽  
pp. 121-125 ◽  
Author(s):  
S. Swart ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal response had normal responses after chronic diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular ‘low renin hypertension’ may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.


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.


Sign in / Sign up

Export Citation Format

Share Document