British Journal of Anaesthesia, Vol 81, Issue 6 925-931, Copyright © 1998 by The Board of Management and Trustees of the British Journal of Anaesthesia
C. F. Hung, C. H. Tsai and M. J. Su
We have examined the effects of morphine, a mu-opioid receptor agonist, on
various membrane ionic currents in rat ventricular and human atrial
myocytes, using patch-clamp techniques in the whole-cell configuration.
Morphine produced a concentration-dependent reduction in peak transient
sodium current. When the sodium current (INa) was evoked at 5-s intervals
the estimated IC50 for morphine was approximately 30 microgramsmol litre-1.
Morphine 10 microgramsmol litre-1 inhibited INa with a 5-mV shift in the
potential-dependent inactivation curve to negative potentials and retarded
the INa recovery rate from the inactivated state. Use- dependent INa block
was not observed when INa was elicited at frequencies varying from 0.2 to
20 Hz. Morphine did not significantly affect the inward calcium current
(ICa), transient outward current (Ito) or the inwardly rectifying potassium
current (IK1) at a concentration of 30 microgramsmol litre-1. The
inhibitory effect of morphine on INa could not be prevented or reversed by
treatment with the opioid antagonist naloxone. Therefore, we suggest that
morphine can directly inhibit the Na+ inward current and bind to
inactivated Na+ channels.
LABORATORY INVESTIGATIONS
Opioid receptor independent effects of morphine on membrane currents in single cardiac myocytes
Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan; Department of Surgery, College of Medicine, National Taiwan University, Taipei, Taiwan
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