Alterations in vascular reactivity in isolated vessel segments from dogs with naturally occurring heart failure

Abstract

To investigate if functional vascular reactivity is altered in heart failure, the reactivity of isolated canine saphenous vein (SV) and femoral artery (FA) rings, from control dogs and dogs with naturally occurring heart failure was examined. In both vessels, relaxation responses to the endothelium-dependent vasodilator, acetylcholine were unaffected by heart failure. In the FA, in heart failure, there was a significant reduction in the potency of the agonist noradrenaline (pEC506·05±0·07 (N = 8) and 5·54 ± 0·13 (N = 7) for control and heart failure respectively). There was no significant alteration in potency in the SV. In addition, in the FA the maximum responses to both noradrenaline (control 3·64 ± 0·31 KPa, (N = 8); failure 5·11 ± 0·35 KPa, (N = 7) P = 0·004) and potassium chloride (control 2·18 ± 0·26 KPa, (N = 8); failure 4·46 ± 0·25 KPa, (N = 7) P = 0·001) were significantly increased in heart failure. It is suggested that enhanced agonist induced responses, in the femoral artery, in dogs with heart failure, may limit blood flow to exercising skeletal muscle and subsequently reduce exercise tolerance.