Background In humans with coronary artery disease, ACE inhibition atte
nuates coronary sympathetic vasoconstriction. Whether this is due to r
emoval of angiotensin !Ang) II production or to a reduced bradykinin b
reakdown, however, is unknown. Methods and Results In right normotensi
ve patients with angiographic evidence of mild left coronary artery le
sions (less than or equal to 50%), mean arterial pressure (MAP, intra-
arterial catheter), heart rate (HR, ECG lead), coronary sinus blood fl
ow (CBF, thermodilution method), and coronary vascular resistance (CVR
, ratio between MAP and CBF) were measured before and during a 15-minu
te left intracoronary infusion of Ang II at a dose that had no direct
coronary or systemic vasomotor effects. The same measurements were mad
e before and during a 15-minute infusion of saline. A 2-minute cold pr
esser test (CPT) and a 45-second diving were performed at the end of e
ither infusion period. These maneuvers were used because their coronar
y vasomotor effects are abolished by phentolamine and thus depend on s
ympathetic activation. During saline infusion. both CPT and diving cau
sed a marked increase in MAP. I-IR increased with CPT and fell with di
ving. CBF increased in parallel to the MAP increase, with little chang
e in CVR. The MAP and HR responses were similar during Ang II infusion
, which, however, caused either no change or a reduction in CBF with a
consequent marked increase in CVR with both CPT and diving. In four a
dditional patients. the diameter of the stenotic vessels remained unch
anged during the CPT performed under saline and Ang II infusion. Concl
usions Ang II markedly enhances sympathetic influences on coronary cir
culation in humans, presumably by acting at the arteriolar level. This
may explain the blunting effect of ACE inhibition on sympathetic coro
nary vasoconstriction in patients with coronary artery disease.