Physiological concentrations of estradiol attenuate endothelin 1-induced coronary vasoconstriction in vivo

• Published in: Circulation (New York, N.Y.) N.Y.), 1997-11, Vol.96 (10), p.3626-3632
• Main Authors: SUDHIR, K, KO, E, ZELLNER, C, WONG, H. E, HUTCHISON, S. J, CHOU, T. M, CHATTERJEE, K
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Flow Velocity - drug effects; Coronary Circulation - drug effects; Coronary Vessels - diagnostic imaging; Coronary Vessels - drug effects; Coronary Vessels - physiology; Endothelin-1 - antagonists & inhibitors; Endothelin-1 - pharmacology; Estradiol - pharmacology; Female; Hormones. Endocrine system; Medical sciences; Pharmaceutical Vehicles - pharmacology; Pharmacology. Drug treatments; Serotonin - pharmacology; Swine; Ultrasonography, Interventional; Vasoconstriction - drug effects; Vasoconstrictor Agents - pharmacology; Viper Venoms - pharmacology
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.96.10.3626

Estrogens are cardioprotective hormones and are reported to have antianginal properties. We examined the effect of physiological concentrations of 17beta-estradiol on coronary reactivity in anesthetized female farm pigs. Epicardial coronary cross-sectional area (CSA) was assessed by two-dimensional intravascular ultrasound, average coronary peak flow velocity (APV) by intravascular Doppler velocimetry, and coronary blood flow (CBF) was calculated. Dose-response curves to intracoronary endothelin-1 (ET-1, 1 pmol/L to 10 nmol/L), the selective ET(B) receptor agonist sarafotoxin (1 pmol/L to 10 nmol/L), and serotonin (0.1 nmol/L to 1 micromol/L) were assessed before and after a 10-minute infusion of intracoronary estradiol (1 nmol/L). Before estradiol administration, ET-1 induced significant dose-dependent decreases in CSA, APV, and CBF. Estradiol attenuated ET-1-induced epicardial vasoconstriction (P