1-Adrenoceptor blockade mitigates excessive norepinephrine release into cardiac interstitium in mitral regurgitation in dog
نویسندگان
چکیده
Gerald H. Hankes, Jeffrey L. Ardell, José Tallaj, Chih-Chang Wei, Inmaculada Aban, Merrilee Holland, Patricia Rynders, Ray Dillon, Rene Cardinal, Donald B. Hoover, J. Andrew Armour, Ahsan Husain, and Louis J. Dell’Italia Auburn University of Veterinary Medicine, Auburn, Alabama; Department of Pharmacology, East Tennessee State University, Johnson City, Tennessee; Center for Heart Failure Research, Departments of Medicine and Physiology and Biophysics, Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama; and Department of Pharmacology, University of Montreal, Montreal, Quebec, Canada
منابع مشابه
Beta1-adrenoceptor blockade mitigates excessive norepinephrine release into cardiac interstitium in mitral regurgitation in dog.
Mitral regurgitation (MR) is associated with increased neuronal release of norepinephrine (NE) and epinephrine (EP) into myocardial interstitial fluid (ISF) that may be necessary in sustaining left ventricular (LV) function via activation of cardiomyocyte beta-adrenergic receptors (ARs). However, activation of neuronal beta-ARs on cardiac neurons may lead to further catecholamine release, with ...
متن کاملBeta1-adrenergic receptor blockade attenuates angiotensin II-mediated catecholamine release into the cardiac interstitium in mitral regurgitation.
BACKGROUND This study tested the hypothesis that beta1-adrenoreceptor blockade modulates the angiotensin II (Ang II)-evoked neural release of norepinephrine (NE) and epinephrine (Epi) into the cardiac interstitial fluid (ISF) space in experimentally induced mitral regurgitation (MR) in the dog. METHODS AND RESULTS Normal dogs (n=8) were compared with dogs with MR of 2 (n=8) and 4 (n=6) weeks'...
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