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• W2018743108 abstract "Cardiac hypertrophy occurs in as many as 47% of normotensive individuals who chronically use cocaine. We investigated the effects of cocaine, in concentrations commonly found in chronic cocaine users, on calcium/calmodulin kinase (CaMK), and whether cocaine can activate CaMK, increase cardiac myocyte protein expression, and cause cardiac hypertrophy in this manner. In series I to III, 0 (control) or cocaine in concentrations of 10−8 to 10−5 mol/L was added to cultured adult rat cardiac ventricular myocytes to determine by Western blots and by 32P incorporation the optimal treatment time and the optimal dose for CaMK activation. In series I, cocaine, 10−6 mol/L, increased myocyte CaMKII translocation from myocyte soluble to particulate fractions by ≥73 ± 9% (P < 0.01) in comparison with controls but did not cause the translocation of CaMKI or CaMKIV. In series II and III, cocaine treatment of myocytes for 15 minutes increased maximal CaMKII activity by 86.5 ± 13.3% (P < 0.001) and a cocaine dose of 5×10−6 mol/L increased CaMKII activity by 169.5 ± 18.1% (P < 0.001). In series IV we measured by silver staining β-myosin heavy chain protein (β-MHC) expression in myocytes before and after cocaine and also CaMK inhibition with KN-62 (1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine). In these experiments, cocaine, 5×10−6 mol/L, increased myocyte protein concentration by 29.2 ± 2.8%, and β-MHC by 93.2 ± 8.8% (P < 0.001). In series V and VI, cocaine effects on calcium currents (ICa) and intracellular Ca2+ ([Ca2+]i) were determined before and after CaMK inhibition with KN-62 in rat myocytes. Cocaine, 10−6 mol/L, enhanced ICa peak amplitude in a voltage-dependent manner (by 173.9 ± 14.9% at −20 mV and by 38.4 ± 6.9% at 0 mV P < 0.01). Cocaine, 10−6 to 10−5 mol/L, in series VI promoted Ca2+ transients from myocyte sarcoplasmic reticulum and increased [Ca2+]i to 607 ± 141 × 10−9 mol/L (P < 0.05). KN-62 decreased cocaine-induced myocyte protein expression by 76.6%, and β-MHC by 66.2% (P < 0.01) and significantly decreased cocaine-induced Ca2+ transients and [Ca2+]i. We conclude that CaMKII activation is an important mechanism whereby cocaine can cause myocyte hypertrophy." @default.
• W2018743108 created "2016-06-24" @default.
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• W2018743108 date "2006-07-01" @default.
• W2018743108 modified "2023-10-10" @default.
• W2018743108 title "Cocaine Activates Calcium/Calmodulin Kinase II and Causes Cardiomyocyte Hypertrophy" @default.
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• W2018743108 doi "https://doi.org/10.1097/01.fjc.0000211796.45281.46" @default.
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