In vivo effects of angiotensin-ii receptor blockade and converting
enzyme inhibition on canine aortic viscoelasticity.
Barra, Juan Gabriel, Jaime Levenson, Ricardo Luis Armentano, Edmundo
Ignacio Cabrera Fischer, Ricardo Horacio Pichel, Alain Simon.
Basic Sciences Research Institute, The Ren[acute]e Favaloro
University Foundation, Sol's 453, 1078, Buenos Aires, ARGENTINA, and
Centre de M[acute]edicine Pr[acute]eventive Cardiovasculaire,
H[circumflex]opital Broussais, INSERM (CRI), 96 rue Didot, 75674
CEDEX 14 Paris, FRANCE
APStracts 3:0390H, 1996.
The influence of the renin-angiotensin system (RAS) on the aortic wall
mechanical properties under angiotensin-I converting enzyme
inhibition (enalaprilat, 0.3 mg/Kg iv), or angiotensin-II receptor
(AT1) blockade (E-3174, 1 mg/Kg iv) was examined in 8 normotensive
and 8 renovascular hypertensive conscious dogs. Aortic diameter (D,
sonomicrometry)-pressure (P, microtransducer) hysteresis loops during
steady-state and during rapid distal aortic occlusion allowed (after
hysteresis elimination) calculation of the aortic wall viscosity
index, the purely elastic P-D relationship, and derivation into
compliance-pressure curves. At the early stage of renovascular
hypertension when activation of RAS is more pronounced aortic wall
stiffness and wall viscosity were increased as compared with
normotensive states. Blood pressure remained unchanged in
normotensive animals and was reduced during hypertension after
antihypertensive treatments. In hypertensive animals, enalaprilat and
E-3174 decreased viscosity index and shifted the compliance-pressure
curve upward with respect to pre-treatment conditions. In
normotensive dogs, whereas E-3174 did not change the compliance
-pressure curve and viscosity index, enalaprilat increased compliance
and reduced viscosity index. We concluded that in normotensive dogs
converting enzyme inhibition modifies arterial visco-elastic
parameters by angiotensin-independent mechanism which contribute to
the modulation of the buffering function of large arteries.
Received 3 October 1995; accepted in final form 21 August 1996.
APS Manuscript Number H932-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996