TY - JOUR
T1 - Regulation of K+ and Ca2+ channels in experimental cardiac failure
AU - Gopalakrishnan, M.
AU - Triggle, D. J.
AU - Rutledge, A.
AU - Kwon, Y. W.
AU - Bauer, J. A.
AU - Fung, H. L.
PY - 1991
Y1 - 1991
N2 - To examine the status of ATP-sensitive K+ (K+(ATP)) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+(DHP)) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (B(max)) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, B(max) values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, β-adrenoceptors and α1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol and [3H]prazosin showed reductions in left ventricular muscarinic and β-adrenoceptor densities but not in α1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.
AB - To examine the status of ATP-sensitive K+ (K+(ATP)) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+(DHP)) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (B(max)) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, B(max) values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, β-adrenoceptors and α1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol and [3H]prazosin showed reductions in left ventricular muscarinic and β-adrenoceptor densities but not in α1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.
KW - Adenosine triphosphate-sensitive potassium channels
KW - Ion channel regulation
KW - Muscarinic receptors
KW - Myocardial infarction
KW - Receptor regulation
KW - Voltage-gated calcium channels
KW - α-adrenoceptors
KW - β-adrenoceptors
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U2 - 10.1152/ajpheart.1991.261.6.h1979
DO - 10.1152/ajpheart.1991.261.6.h1979
M3 - Article
C2 - 1661095
AN - SCOPUS:0026309766
SN - 0002-9513
VL - 261
SP - H1979-H1987
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 6 30-6
ER -