Depolarizing cardiac arrest and endothelium-derived hyperpolarizing factor–mediated hyperpolarization and relaxation in coronary arteries: The effect.

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Presentation transcript:

Depolarizing cardiac arrest and endothelium-derived hyperpolarizing factor–mediated hyperpolarization and relaxation in coronary arteries: The effect and mechanism Guo-Wei He, MD, PhD, Cheng-Qin Yang, MD, Jian-An Yang, MD The Journal of Thoracic and Cardiovascular Surgery Volume 113, Issue 5, Pages 932-941 (May 1997) DOI: 10.1016/S0022-5223(97)70267-8 Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 1 Schematic diagram describing the possible pathway by which hyperkalemia may affect the interaction between endothelium and smooth muscle. In response to the increase of the intracellular (cytosolic free) calcium level, endothelial cells derive three major EDRFs (prostaglandin I2, EDNO, and EDHF). These EDRFs decrease the intracellular calcium concentration in the smooth muscle cell through different mechanisms and ultimately relax the smooth muscle cell. The mechanism of EDHF to relax vessels is to open K channels and hyperpolarize the membrane. Subsequently, the voltage-operated Ca2+ channels (VOC) are inhibited and therefore the Ca2+ influx is reduced and this causes relaxation. The present study suggests that exposure to hyperkalemia reduces the EDHF-mediated relaxation through affecting KCa channels (and to a lesser extent Katp channels) and prolonged depolarization. When EDHF-mediated relaxation is reduced, the coronary artery may have a tendency to contract and the coronary vascular tone increases. cGMP, Cyclic guanosine monophosphate; cAMP, cyclic adenosine monophosphate; PGI 2 , Prostaglandin I2. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 2 Mean concentration-relaxation curves for substance P (concentration: −log M; relaxation: percent of contraction by U46619, 30 nmol/L). Symbols represent data averaged from a group of rings. Vertical bars are 1 standard error of the mean of the response at each concentration. Indo + GBM, response in presence of indomethacin (7 μmol/L) and glibenclamide (3 μmol/L) (n = 5); Indo + LNNA, response in presence of indomethacin (7 μmol/L) and L-NNA (300 μmol/L) (n = 6); Indo + LNNA + GBM, response in presence of indomethacin (7 μmol/L), L-NNA (300 μmol/L), and glibenclamide (3 μmol/L) (n = 6); Indo + LNNA + TEA, response in presence of indomethacin (7 μmol/L), L-NNA (300 μmol/L), and tetraethylammonium (1 mmol/L) (n = 8); E−, endothelium denuded (n = 4). Significance p < 0.0001 among the groups (analysis of variance). **p < 0.01; ***p < 0.0001 compared with indomethacin + L-NNA and indomethacin + glibenclamide (Scheffe's F test). The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 3 Mean concentration-relaxation curves (concentration: −log M; relaxation: percent of contraction by U46619 30 nmol/L) for substance P in the coronary arteries exposed to hyperkalemia (K 20 mmol/L) for 1 hour. See Fig. 2 for the meaning of the symbols. Indo + GBM, response in presence of indomethacin (7 μmol/L) and glibenclamide (3 μmol/L) (n = 6); Indo + LNNA, response in presence of indomethacin (7 μmol/L) and L-NNA (300 μmol/L) (n = 6); Indo + LNNA + TEA, response in presence of indomethacin (7 μmol/L), L-NNA (300 μmol/L), and tetraethylammonium (1 mmol/L) (n = 8); E−, endothelium denuded (n = 4). **p < 0.01 (Scheffe's F test) compared with the arteries treated with the same inhibitors but not exposed to K (see Fig. 2). The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 4 Mean concentration-relaxation curves (concentration: −log M; relaxation: percent of contraction by U46619 30 nmol/L) for substance P in the coronary arteries exposed to hyperkalemia (K 50 mmol/L) for 1 hour. See Fig. 2 for the meaning of the symbols. Indo + GBM, response in presence of indomethacin (7 μmol/L) and glibenclamide (3 μmol/L) (n = 6); Indo + LNNA, response in presence of indomethacin (7 μmol/L) and L-NNA (300 μmol/L) (n = 6); E−, endothelium denuded (n = 4). ***p < 0.0001 (Scheffe's F test) compared with the arteries treated with the same inhibitors but not exposed to K (see Fig. 2). The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 5 An actual tracing of the membrane potential measurement in a single smooth muscle cell of the porcine coronary artery. Concentration-response (membrane potential) curves were established for substance P in the presence of indomethacin (7 μmol/L) and L-NNA (300 μmol/L) in the endothelium-intact artery before (a) and after (b) the exposure to K (20 mmol/L). This hyperpolarization is abolished in the endothelium-denuded preparation (c). The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 6 Membrane potential measurement of the porcine coronary artery. Concentration-response (membrane potential) curves were established for substance P in the presence of indomethacin (7 μmol/L) and L-NNA (300 μmol/L). Symbols represent data averaged from six preparations in each group of coronary arteries. Vertical bars are 1 standard error of the mean of the response at each concentration. Control, without exposure to hyperkalemia; K20, the arteries were exposed to hyperkalemia (K 20 mmol/L replacing Na+) for 1 hour before the concentration-response curves were established; TEA, in the presence of tetraethylammonium (1 mmol/L) in addition to indomethacin and L-NNA. *p < 0.05 compared with the control. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 932-941DOI: (10.1016/S0022-5223(97)70267-8) Copyright © 1997 Mosby, Inc. Terms and Conditions