Hypertension, Vol 5, 453-459, Copyright © 1983 by American Heart Association
JA Johnson, KD Kurz, S Siripaisarnpipat, DG Koivunen, DW Zeigler, T Sakamaki and CG Payne
Prehypertensive rabbits with renal artery stenosis of 3 days' duration
(one-kidney, one clip) are known to have increased pressor responses to
norepinephrine and vasopressin; this pressor hyperresponsiveness is
restored to normal by the angiotensin II (AII) antagonist, [ Sar1, Ile8 ]
AII, even though plasma renin activity (PRA) and plasma AII concentrations
are not elevated. In the present study, the cross- circulation of blood
between conscious one-kidney, 3-day renal artery stenosis rabbits and
conscious normal rabbits resulted in the transfer of pressor
hyperresponsiveness to the normal rabbits, although both groups of rabbits
had normal values for PRA. A similar cross- circulation of blood between
one-kidney rabbits without renal artery stenosis and normal rabbits did not
alter the pressor responsiveness of the normal rabbits to norepinephrine.
It was concluded that a circulating humoral factor is involved in mediating
pressor hyperresponsiveness in 3-day renal artery stenosis rabbits. To
evaluate the interrelationship between AII and the hormonal
hyperresponsiveness factor, an additional experiment was performed in which
blood was cross- circulated between one-kidney, 3-day renal artery stenosis
rabbits and normal rabbits, with the normal rabbits receiving [ Sar1, Ile8
] AII immediately following cross-circulation. Administration of this AII
antagonist to the normal rabbits prevented them from showing pressor
hyperresponsiveness following the cross-circulation of blood. It is
concluded that in this prehypertensive renal artery stenosis model the
humoral hyperresponsiveness factor exerts its effect through AII
mechanisms, rather than AII acting to increase the release or secretion of
the hyperresponsiveness factor.
ARTICLES
Humoral factor in pressor hyperresponsiveness in renal prehypertensive rabbits
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