1-Adrenoceptor blockade mitigates excessive norepinephrine release into cardiac interstitium in mitral regurgitation in dog

نویسندگان

  • 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
  • Louis J. Dell’Italia
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

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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 ...

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Beta1-adrenergic receptor blockade attenuates angiotensin II-mediated catecholamine release into the cardiac interstitium in mitral regurgitation.

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Follow up the Treatment Process of Mitral Valve Diseases by Radiography and Echocardiography in Dogs

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تاریخ انتشار 2006