scholarly journals Renal artery stenosis with normal angiotensin II values. Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery.

Hypertension ◽  
1981 ◽  
Vol 3 (1) ◽  
pp. 53-58 ◽  
Author(s):  
A B Atkinson ◽  
J J Brown ◽  
D L Davies ◽  
B Leckie ◽  
A F Lever ◽  
...  
1979 ◽  
Vol 57 (s5) ◽  
pp. 139s-143s ◽  
Author(s):  
A. B. Atkinson ◽  
J. J. Brown ◽  
R. Fraser ◽  
B. Leckie ◽  
A. F. Lever ◽  
...  

1. The converting-enzyme inhibitor captopril has been given in doses up to 450 mg daily to hypertensive patients with renal artery stenosis and to patients resistant to other therapy. 2. Captopril alone was effective in controlling hypertension in renal artery stenosis, irrespective of whether pretreatment plasma angiotensin II was raised or normal, except in one man with overall renal impairment. 3. In one woman with the hyponatraemic hypertensive syndrome secondary to renal artery thrombosis, captopril restored depleted exchangeable sodium and potassium to normal. In the other cases of renal artery stenosis with normal renal function, exchangeable sodium and total body potassium were not significantly altered, and there were no marked changes in plasma sodium and potassium. 4. The combination of captopril with a diuretic controlled blood pressure long-term in every case of previously resistant hypertension. 5. Within 2 h, captopril induced highly significant falls in arterial pressure, in plasma angiotensin II and aldosterone, with converse increases in plasma active and total renin and blood angiotensin I. 6. The initial fall in plasma angiotensin II was closely related to the concomitant fall in diastolic pressure. 7. The pattern of change in circulating renin, angiotensins I and II and aldosterone was maintained during long-term therapy, whether or not a diuretic was added. There was no tendency for plasma angiotensin II to increase despite sustained elevation of active renin and angiotensin I.


Hypertension ◽  
1993 ◽  
Vol 21 (2) ◽  
pp. 173-184 ◽  
Author(s):  
P J Admiraal ◽  
A H Danser ◽  
M S Jong ◽  
H Pieterman ◽  
F H Derkx ◽  
...  

1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  

1987 ◽  
Vol 65 (8) ◽  
pp. 1559-1565 ◽  
Author(s):  
W. P. Anderson ◽  
R. L. Woods ◽  
K. M. Denton ◽  
D. Alcorn

In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. Angiotensin II also maintains GFR in less severe stenosis, which does not cause hypertension. This homeostatic action of angiotensin II to maintain GFR has minimal effects on blood flow. In renal-wrap hypertension, plasma renin levels are elevated for longer than after renal artery stenosis, but in other respects this initial phase of the hypertension is similar to that after renal artery stenosis. GFR is reduced, the rate of development of hypertension is accelerated by angiotensin II, and angiotensin II maintains the glomerular filtration fraction. Renal resistance is markedly increased owing to both compression of the kidney by the hypertrophying renal capsule and to angiotensin II. Thus angiotensin II apparently plays a primarily homeostatic role in renovascular hypertension to maintain glomerular ultrafiltration. It is suggested that the angiotensin II may be formed intrarenally and may act on sites other than resistance blood vessels.


1984 ◽  
Vol 2 (6) ◽  
pp. 605-614 ◽  
Author(s):  
David J. Webb ◽  
Alison M.M. Cumming ◽  
Frederick C. Adams ◽  
G Peter Hodsman ◽  
Brenda J. Leckie ◽  
...  

1988 ◽  
Vol 255 (2) ◽  
pp. H272-H279
Author(s):  
D. E. Dostal ◽  
J. A. Johnson ◽  
P. B. Langevin ◽  
N. Abas

Vascular rings from normal rabbit renal arteries, when bathed in processed plasma from 3-day renal artery stenosis (RAS) rabbits, had greater contractile responses to norepinephrine than did matched rings bathed in processed plasma from sham-operated rabbits. This vascular hyperresponsiveness of the rings produced by 3-day RAS plasma was abolished by the angiotensin II (ANG II) antagonist [Sar1, Ile8] ANG II but not by [Sar1, Ala8] ANG II at a dose that completely blocked the contractile responses of the rings to ANG II. The addition of [Sar1, Ala8]-ANG II to rings bathed in normal rabbit plasma did not alter the contractile responses to norepinephrine, indicating a lack of agonistic action by this ANG II analogue. These studies demonstrated that the ANG II receptors involved in the hormonally mediated vascular hyperresponsiveness in 3-day RAS rabbits are contained in the tissues that comprise these renal arterial rings.


Sign in / Sign up

Export Citation Format

Share Document