AJP - Heart and Circulatory Physiology, Vol 243, Issue 6 869-H875, Copyright © 1982 by American Physiological Society
Renin-angiotensin and development of collateral circulation after renal ischemia
L. A. Fernandez, V. J. Caride, J. Twickler and R. E. Galardy
Aortic ligation between the origins of the renal arteries in the rat
produces a left renal ischemia, renin-dependent hypertension, and a
transitory hindlimb paralysis of less than 2 h. Removal of the left
ischemic kidney at the time of aortic ligation curtails the rise of blood
pressure, plasma renin activity is normal, and paralysis is still present
24 h after surgery. Administration of an angiotensin-converting enzyme
inhibitor or saralasin also prevents recuperation from paralysis after
aortic ligation. Independent manipulation of the mean arterial pressure or
plasma renin activity by pretreatment with reserpine or deoxycorticosterone
before surgery shows that the presence or absence of paralysis is dependent
on the plasma renin activity and not on the high blood pressure. Blood flow
measurements show that paralysis is due to a persistent impairment of blood
supply to the hindlimb muscle and not to ischemia of the spinal cord.
Infusion of angiotensin II to aortic-ligated, left-renoprival animals tends
to restore blood flow to muscle. It is concluded that after renal ischemia
the renin-angiotensin system, independent of its hypertensive effect,
restores blood flow by stimulating the development of collateral
circulation.
