IN-VIVO ANGIOTENSIN-II RECEPTOR BLOCKADE AND CONVERTING-ENZYME INHIBITION ON CANINE AORTIC VISCOELASTICITY

The influence of the renin-angiotensin system (RAS) on the aortic wall mechanical properties under angiotensin I converting enzyme inhibitio n (enalaprilat, 0.3 mg/kg iv) or angiotensin II receptor (AT(1)) block ade (E-3174, 1 mg/kg iv) was examined in eight normotensive and eight renovascular hypertensive conscious dogs. Aortic diameter (D; sonomicr ometry)-pressure (P; microtransducer) hysteresis loops during steady s tate and during rapid distal aortic occlusion allowed (after hysteresi s elimination) calculation of the aortic wall viscosity index, the pur ely elastic P-D relationship, and derivation into compliance-pressure curves. At the early stage of renovascular hypertension when activatio n of RAS is more pronounced, aortic wall stiffness and wall viscosity were increased as compared with normotensive states. Blood pressure re mained unchanged in normotensive animals and was reduced during hypert ension after antihypertensive treatments. In hypertensive animals, ena laprilat and E-3174 decreased viscosity index and shifted the complian ce-pressure curve upward with respect to pretreatment conditions. In n ormotensive dogs, whereas E-3174 did not change the compliance-pressur e curve and viscosity index, enalaprilat increased compliance and redu ced viscosity index. We concluded that in normotensive dogs converting enzyme inhibition modifies arterial viscoelastic parameters by angiot ensin-independent mechanisms that contribute to the modulation of the buffering function of large arteries.