(Circulation. 1997;96:148-153.)
© 1997 American Heart Association, Inc.
Articles |
Intracoronary Angiotensin II Potentiates Coronary Sympathetic Vasoconstriction in Humans
From the Centro di Fisiologia Clinica e Ipertensione, Università
di Milano, Ospedale Maggiore, (A.S., G.P., R.P., A.R., G.M.); Cattedra di
Medicina Interna, Università di Milano, Ospedale San Gerardo, Monza
(G.M.); Ospedale di Vimercate, (R.V.); and Centro Cuore Columbus
(L.D.F.),
1 Milan, Italy.
Correspondence to Prof Giuseppe Mancia, Cattedra di Medicina Interna, Ospedale S. Gerardo, via Donizetti 106, Monza, Milano, Italy.
Background In humans with coronary artery disease, ACE inhibition attenuates coronary sympathetic vasoconstriction. Whether this is due to removal of angiotensin (Ang) II production or to a reduced bradykinin breakdown, however, is unknown.
Methods and Results In eight normotensive patients with
angiographic evidence of mild left coronary artery lesions
(
50%), mean arterial pressure (MAP,
intra-arterial catheter), heart rate (HR, ECG lead),
coronary sinus blood flow (CBF, thermodilution method), and
coronary vascular resistance (CVR, ratio between MAP and CBF)
were measured before and during a 15-minute left intracoronary
infusion of Ang II at a dose that had no direct coronary or
systemic vasomotor effects. The same measurements were made before and
during a 15-minute infusion of saline. A 2-minute cold pressor test
(CPT) and a 45-second diving were performed at the end of either
infusion period. These maneuvers were used because their
coronary vasomotor effects are abolished by
phentolamine and thus depend on sympathetic activation. During
saline infusion, both CPT and diving caused a marked increase in MAP.
HR increased with CPT and fell with diving. CBF increased in parallel
to the MAP increase, with little change 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 additional patients,
the diameter of the stenotic vessels remained unchanged during
the CPT performed under saline and Ang II infusion.
Conclusions Ang II markedly enhances sympathetic influences on coronary circulation in humans, presumably by acting at the arteriolar level. This may explain the blunting effect of ACE inhibition on sympathetic coronary vasoconstriction in patients with coronary artery disease.
Key Words: angiotensin • nervous system, autonomic • reflex • coronary disease
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