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(Circulation. 2000;101:2277.)
© 2000 American Heart Association, Inc.

Clinical Investigation and Reports

Modulation of Sympathetic Coronary Vasoconstriction by Cardiac Renin-Angiotensin System in Human Coronary Heart Disease

Antonio Saino, MD; Guido Pomidossi, MD; Rodolfo Perondi, MD; Alberto Morganti, MD; Lucia Turolo, PhD; Giuseppe Mancia, MD

From Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Ospedale Maggiore IRCCS, Milan, Italy (A.S., G.P., R.P., A.M., L.T., G.M.); and Clinica Medica, Università di Milano-Bicocca, Ospedale San Gerardo, Monza, Milan (A.S., G.M.).

Correspondence to Prof Giuseppe Mancia, Clinica Medica, Ospedale San Gerardo, Via Donizetti 106, 20052 Monza, Milano, Italy.

Background—In humans, angiotensin II enhances the sympathetic coronary vasoconstriction elicited by the cold pressor test (CPT) and diving. Whether this enhancement depends on the circulating angiotensin II or on the locally produced angiotensin II is unknown, however.

Methods and Results—We addressed this issue in 14 patients with severe coronary artery disease by evaluating the effects of a 2-minute CPT (n=14) and a 30-second dive (n=8) on mean arterial pressure (MAP, arterial catheter), heart rate (ECG), coronary sinus blood flow (CBF, thermodilution technique), and coronary vascular resistance (MAP/CBF ratio). The 2 stimuli were applied at the end of left intracoronary infusion of either saline or benazeprilat diluted at the concentration of 25 µg/mL. The rate of benazeprilat infusion had been preliminarily demonstrated to reduce angiotensin II concentration in the coronary sinus without affecting its arterial concentration. The changes in MAP and heart rate induced by CPT and diving were superimposable during saline and benazeprilat infusions. The decrease in CBF induced by CPT and diving during saline infusion was changed into an increase during benazeprilat infusion with a significant attenuation of the coronary vasoconstrictor response.

Conclusions—In patients with coronary artery disease, an attenuation of sympathetic coronary vasoconstriction can be obtained by reducing cardiac angiotensin II formation without involving circulating angiotensin II. This suggests a role of the tissue renin-angiotensin system in modulating autonomic cardiac drive in humans.

Key Words: circulation • nervous system, sympathetic • renin • angiotensin • coronary disease

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