Effects of cocaine on nitric oxide production in bovine coronary artery endothelial cells.

نویسندگان

  • Jiale He
  • Shumei Yang
  • Lubo Zhang
چکیده

Cocaine decreases coronary artery endothelial-dependent vasorelaxation. To explore the potential mechanisms, the present study examined the effect of cocaine on nitric oxide release in bovine coronary artery endothelial cells (BCAECs). In the absence of cocaine, basal nitric oxide release from BCAECs continued to accumulate in the medium over the period from 6 to 72 h. Cocaine significantly decreased nitric oxide release at each time point of the study. At 48-h treatment, cocaine (3-30 muM) produced a concentration-dependent decrease in nitric oxide release in BCAECs. In accordance with its inhibition of nitric oxide release, cocaine decreased endothelial nitric-oxide synthase (eNOS) protein levels in BCAECs in a concentration-dependent manner. In addition to the prolonged effect, cocaine pretreatment for 1 h significantly decreased basal and ATP-induced nitric oxide release in BCAECs. Whereas acute cocaine treatment did not affect basal levels of free intracellular calcium concentrations in BCAECs, it significantly decreased the ATP-induced elevation of intracellular calcium and increased its time lag to reach the peak. A quantitative approach by immunofluorescence microscopy revealed that cocaine significantly increased eNOS localized at the cell membrane in BCAECs. Collectively, the results suggest that cocaine inhibits nitric oxide release in BCAECs by decreasing intracellular calcium mobilization, increasing the inactive state of eNOS, and decreasing eNOS protein levels.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Association between T-786C polymorphism of endothelial nitric oxide synthase gene and level of the vessel dilation factor in patients with coronary artery disease

Various polymorphisms on endothelial nitric oxide synthase (eNOs) gene cause reduced production of NO, the endothelial relaxing factor, and may accelerate the process of atherosclerosis. The study designed to investigate the frequency of T-786C polymorphism of the eNOs gene in patients suffering from coronary artery disease (CAD) in north-west of Iran. One hundred twenty subjects including 60 p...

متن کامل

Cocaine-mediated apoptosis in bovine coronary artery endothelial cells: role of nitric oxide.

The present study examined the role of nitric oxide in cocaine-induced apoptosis in bovine coronary artery endothelial cells (BCAECs). Cocaine produced a time-dependent decrease in cell viability and an increase in apoptosis in BCAECs, which were blocked by the nitric oxide donors DETA-NONOate (DETA-NO) and S-nitroso-N-acetyl-penicillamine. In accordance, cocaine decreased nitric oxide producti...

متن کامل

Effect of the Sera of Patients with Multiple Sclerosis on Apoptosis and Nitric Oxide Production of Endothelial Cells

Background & Aims: Multiple sclerosis (MS) is one of the chronic autoimmune diseases of the central nervous system with unknown etiology. The present study aimed to investigate the apoptosis and nitric oxide (NO) production of endothelial cells treated with serum of patients with MS and response to interferon beta (IFN- ) therapy. Methods: Human umbilical vein endothelial cells were treated wit...

متن کامل

Xiu Q. Wang and Nosratola D. Vaziri Erythropoietin Depresses Nitric Oxide Synthase Expression by Human Endothelial Cells

We have recently shown that erythropoietin (EPO)-induced hypertension is unrelated to the rise in hematocrit and is marked by elevated cytosolic [Ca] and nitric oxide (NO) resistance. The present study was done to determine the effect of EPO on NO production and endothelial NO synthase (eNOS) expression by endothelial cells. Human coronary artery endothelial cells were cultured to subconfluence...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Journal of pharmacology and experimental therapeutics

دوره 314 3  شماره 

صفحات  -

تاریخ انتشار 2005