© 1995 American Heart Association, Inc.
Articles |
Estrogen Relaxes Coronary Arteries by Opening BKCa Channels Through a cGMP-Dependent Mechanism
From the Department of Physiology & Biophysics, Wright State University School of Medicine, Dayton, Ohio.
Correspondence to Richard E. White, PhD, Department of Physiology and Biophysics, Room 158 Biological Science Bldg, Wright State University School of Medicine, Dayton, OH 45435. E-mail rwhite@sirius.bio.wright.edu
Abstract Women rarely suffer cardiovascular
dysfunction before menopause, but by the age of 65 a woman becomes as
vulnerable to cardiovascular mortality as a man. It has
been proposed that estrogens protect against
cardiovascular disease; however, the
physiological basis of estrogen protection is
unknown. In the present study the mechanism of estrogen-induced
relaxation of coronary arteries was investigated at the tissue,
cellular, and molecular levels. Tissue studies demonstrated that
17ß-estradiol relaxes porcine coronary arteries by an
endothelium-independent mechanism involving
K+ efflux, and subsequent studies employing the
patch-clamp technique confirmed that estrogen stimulates
K+ channel gating in coronary smooth muscle.
Perforated-patch recordings from metabolically
intact coronary myocytes revealed that 17ß-estradiol more
than doubles steady state outward currents in these cells at positive
voltages. Studies of on-cell patches demonstrated a potent
stimulatory effect of 17ß-estradiol on the gating of the
large-conductance, Ca2+- and
voltage-activated K+ (BKCa)
channels, while 17
-estradiol had no effect. Furthermore,
blocking BKCa channels in intact arteries inhibited
estrogen-induced relaxation. The effect of 17ß-estradiol on
BKCa channels was blocked by inhibiting cGMP-dependent
protein kinase (PKG) activity and was mimicked by exogenous cGMP or by
stimulating PKG activity. Therefore, we propose that
17ß-estradiol relaxes coronary arteries by opening
BKCa channels via cGMP-dependent
phosphorylation. This novel mechanism could account for
the hypotensive effect of estrogens and help explain, at least in part,
why postmenopausal estrogen therapy lowers the risk of
cardiovascular disease.
Key Words: estradiol • coronary artery • BKCa channel • cGMP • Ca2+-activated K+ channel
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M. Nara, P. D. K. Dhulipala, Y.-X. Wang, and M. I. Kotlikoff Reconstitution of beta -Adrenergic Modulation of Large Conductance, Calcium-activated Potassium (Maxi-K) Channels in Xenopus Oocytes. IDENTIFICATION OF THE cAMP-DEPENDENT PROTEIN KINASE PHOSPHORYLATION SITE J. Biol. Chem., June 12, 1998; 273(24): 14920 - 14924. [Abstract] [Full Text] [PDF]
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 D. O. Ruehlmann, J. R. Steinert, M. A. Valverde, R. Jacob, and G. E. Mann Environmental estrogenic pollutants induce acute vascular relaxation by inhibiting L-type Ca2+ channels in smooth muscle cells FASEB J, May 1, 1998; 12(7): 613 - 619. [Abstract] [Full Text]
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N. J. Alkayed, I. Harukuni, A. S. Kimes, E. D. London, R. J. Traystman, P. D. Hurn, and P. A. Grady Gender-Linked Brain Injury in Experimental Stroke • Editorial Comment Stroke, January 1, 1998; 29(1): 159 - 166. [Abstract] [Full Text] [PDF]
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D. F. Skafar, R. Xu, J. Morales, J. Ram, and J. R. Sowers Female Sex Hormones and Cardiovascular Disease in Women J. Clin. Endocrinol. Metab., December 1, 1997; 82(12): 3913 - 3918. [Abstract] [Full Text] [PDF]
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 D. B. Dixon and D. R. Copenhagen Metabotropic Glutamate Receptor-Mediated Suppression of an Inward Rectifier Current Is Linked via a cGMP Cascade. J. Neurosci., December 1, 1997; 17(23): 8945 - 8954. [Abstract] [Full Text] [PDF]
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 G. M.C. Rosano, A. M. Caixeta, S. Chierchia, S. Arie, M. Lopez-Hidalgo, W. I. Pereira, F. Leonardo, C. M. Webb, F. Pileggi, and P. Collins Short-term Anti-Ischemic Effect of 17ß-Estradiol in Postmenopausal Women With Coronary Artery Disease Circulation, November 4, 1997; 96(9): 2837 - 2841. [Abstract] [Full Text]
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K. A. Roberts, M. M. Woo, and J. C. Rutledge Nitric Oxide Mediates LDL Uptake in the Artery Wall in Response to High Concentrations of 17ß-Estradiol Arterioscler Thromb Vasc Biol, October 1, 1997; 17(10): 2123 - 2131. [Abstract] [Full Text]
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R.-S. Zhang, P. H. Guth, O. U. Scremin, R. Singh, S. Pervin, and G. Chaudhuri Regulation of endometrial blood flow in ovariectomized rats: assessment of the role of nitric oxide Am J Physiol Heart Circ Physiol, October 1, 1997; 273(4): H2009 - H2017. [Abstract] [Full Text] [PDF]
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K. Node, M. Kitakaze, H. Kosaka, T. Minamino, H. Funaya, and M. Hori Amelioration of Ischemia- and Reperfusion-Induced Myocardial Injury by 17ß-Estradiol : Role of Nitric Oxide and Calcium-Activated Potassium Channels Circulation, September 16, 1997; 96(6): 1953 - 1963. [Abstract] [Full Text]
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E. Gilad, H. Matzkin, and N. Zisapel Interplay between Sex Steroids and Melatonin in Regulation of Human Benign Prostate Epithelial Cell Growth J. Clin. Endocrinol. Metab., August 1, 1997; 82(8): 2535 - 2541. [Abstract] [Full Text] [PDF]
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K. D. Dunlap, M. L. McAnelly, and H. H. Zakon Estrogen Modifies an Electrocommunication Signal by Altering the Electrocyte Sodium Current in an Electric Fish, Sternopygus J. Neurosci., April 15, 1997; 17(8): 2869 - 2875. [Abstract] [Full Text] [PDF]
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N. Bowling, W. E. Bloomquist, M. L. Cohen, H. U. Bryant, H. W. Cole, D. E. Magee, E. R. Rowley, and C. J. Vlahos Effects of Prolonged Ethinyl Estradiol Treatment on Calcium Channel Binding and In Vivo Calcium-Mediated Hemodynamic Responses in Ovariectomized Rats J. Pharmacol. Exp. Ther., April 1, 1997; 281(1): 218 - 225. [Abstract] [Full Text]
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G. C. Wellman, A. D. Bonev, M. T. Nelson, and J. E. Brayden Gender Differences in Coronary Artery Diameter Involve Estrogen, Nitric Oxide, and Ca2+-Dependent K+ Channels Circ. Res., November 1, 1996; 79(5): 1024 - 1030. [Abstract] [Full Text]
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K. J. Scheidegger, B. Cenni, D. Picard, and P. Delafontaine Estradiol Decreases IGF-1 and IGF-1 Receptor Expression in Rat Aortic Smooth Muscle Cells. MECHANISMS FOR ITS ATHEROPROTECTIVE EFFECTS J. Biol. Chem., December 1, 2000; 275(49): 38921 - 38928. [Abstract] [Full Text] [PDF]
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M. Di Fulvio, T. M. Lincoln, P. K. Lauf, and N. C. Adragna Protein Kinase G Regulates Potassium Chloride Cotransporter-3 Expression in Primary Cultures of Rat Vascular Smooth Muscle Cells J. Biol. Chem., June 8, 2001; 276(24): 21046 - 21052. [Abstract] [Full Text] [PDF]
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 M. Jankowski, G. Rachelska, W. Donghao, S. M. McCann, and J. Gutkowska Estrogen receptors activate atrial natriuretic peptide in the rat heart PNAS, September 25, 2001; 98(20): 11765 - 11770. [Abstract] [Full Text] [PDF]
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C. Dimitropoulou, G. Han, A. W. Miller, M. Molero, L. C. Fuchs, R. E. White, and G. O. Carrier Potassium (BKCa) currents are reduced in microvascular smooth muscle cells from insulin-resistant rats Am J Physiol Heart Circ Physiol, March 1, 2002; 282(3): H908 - H917. [Abstract] [Full Text] [PDF]
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