Abstract
This study was designed to examine the effects of arachidonic acid (AA) on atrial myocytes from patients with coronary heart disease. The patch clamp technique was used to record sodium current in human atrial myocytes, before and after administration of intracellular AA. The suppression of sodium current induced by AA was voltage- and dose-dependent, with an IC50 of 10.3 microM. The activation curves of relative conductance in absence versus presence of AA, 10 microM, nearly overlapped. The 50% channel activation was at 40.8 +/- 2.7 mV in the control state versus 42.5 +/- 3.1 mV in presence of AA (n = 10, P > 0.05). AA at 10 microM shifted the steady-state inactivation relationship significantly, from 94.5 +/- 3.4 mV to 116.6 +/- 4.1 mV (n = 11, P < 0.01) at the 50% channel inactivation point. The 50% recovery time from the inactivation state was significantly longer in the presence of 10 microM AA (27.3 +/- 1.7 ms), than in the control state (5.9 +/- 0.4 ms n = 8, P < 0.01). In conclusion, AA suppressed the sodium current and prolonged the duration of recovery from inactivation in atrial myocytes from patients with coronary heart disease.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
