Author + information
- Received September 26, 1994
- Revision received March 16, 1995
- Accepted April 26, 1995
- Published online September 1, 1995.
- Krishnankutty Sudhir, MD, PhD, FRACPa,*,
- Tony M. Chou, MDa,
- William L. Mullen, MDa,
- Dirk Hausmann, MDa,
- Peter Collins, MD, FRCP†,
- Paul G. Yock, MD, FACCa and
- Kanu Chatterjee, MB, FRCP, FACCa,2
- ↵*Present address and address for correspondence:Dr. Krishnankutty Sudhir, Alfred and Baker Medical Unit, Baker Medical Research Institute, Commercial Road, Prahran, Victoria 3181, Australia.
- ↵1Address for reprints:Dr. Kanu Chatterjee, Box 0124, Moffit Hospital 1186M, University of California, San Francisco, California 94143.
Objectives We sought to examine the immediate vasodilator effect of intracoronary estrogen on epicardial and resistance coronary arteries in 19 dogs.
Background Although estrogen reportedly dilates coronary arteries in vitro, the site and mechanisms of its action have not been fully defined in vivo.
Methods Epicardial coronary artery dimensions and coronary flow velocity were assessed using simultaneous intracoronary two-dimensional and Doppler ultrasound.
Results Estrogen (0.1 and 1 μmol/liter) induced a significant increase in coronary cross-sectional area, flow velocity and volumetric blood flow. Estrogen-induced vasodilation was not influenced either by pretreatment with Nω-nitro-l-arginine methyl ester (l-NAME) (100 μmol/liter intracoronary), indomethacin (5 mg/kg body weight intravenously), propranolol (0.75 mg/kg intravenously) or the classic estrogen receptor antagonist ICI 182,780 (10 μmol/liter). Balloon denudation of the endothelium did not attenuate estrogen-induced epicardial vasodilation. Pretreatment with glibenclamide (10 μmol/liter) attenuated estrogeninduced vasodilation only in epicardial arteries, as did verapamil (0.1 μmol/liter). Estrogen had no effect on a phenylephrine dose-response curve in either epicardial coronary arteries or the microcirculation.
Conclusions Acute estrogen-induced dilation in canine coronary arteries is endothelium independent and is not mediated by the classic intracellular estrogen receptor but through nongenomic mechanisms, presumably at the membrane level, which in epicardial arteries may include effects on adenosine triphosphate-sensitive potassium or calcium channels, or both.
This study was funded in part by the Cardiac Research Foundation, University of California at San Francisco, San Francisco, California. Dr. Sudhir was supported as a C.J. Martin fellow of the National Health and Medical Research Council of Australia, Canberra, Australia and as a postdoctoral fellow of the American Heart Association, California affiliate. Dr. Chou was supported in part by an educational grant from Devices for Vascular Intervention, Redwood, California and by Grant F32 HL090969-01 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Dr. Hausmann was supported by the German Research Society (Deutsche Forchungsgemeinschaft), Bonn, Germany. Dr. Yock is a consultant to Cardiovascular Imaging Systems, Sunnyvale, California.
- Received September 26, 1994.
- Revision received March 16, 1995.
- Accepted April 26, 1995.
- American College of Cardiology