• T Saeki, M Nishimura, N Sato, T Fujinami, and Y Watanabe.
• Cardiovascular Institute, Fujita Health University School of Medicine, Aichi, Japan.
• J. Cardiovasc. Pharmacol. 1995 Jul 1;26(1):160-8.

AbstractTo investigate the presence of opioid receptors and their physiological role in cardiac pacemaker cells, we studied electrophysiological effects of fentanyl citrate, an activator of the mu-opioid receptors, on the spontaneous action potential (AP) and membrane currents, using small preparations (0.2 x 0.2 x 0.1 mm) of rabbit sinoatrial (SA) node (SAN). Fentanyl (0.1-3 microM) progressively decreased the AP amplitude (APA), maximal rate of depolarization (MRD), and spontaneous firing frequency (SFF) and prolonged the AP duration (APD) and diastolic interval in a concentration-dependent manner. At 1 microM, the spontaneous activity ceased in two of the eight preparations. These actions were blocked by a mu-opioid receptor antagonist, beta-funaltrexamine (beta-FNA), but were not modified by either kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI), or delta-opioid receptor antagonist ICI-174864. In voltage-clamp experiments using double microelectrode techniques, 1 microM fentanyl reduced the Ca2+ current (ICa) obtained on step depolarization from -40 to 0 mV by 19.9 +/- 9.3% (p < 0.05, n = 5), the fast and slow components of the delayed rectifying K+ current (IKfast, IKslow) tail obtained on repolarization from 10 to -60 mV by 54.7 +/- 4.7 and 41.4 +/- 2.4% (p < 0.05, n = 4), and the hyperpolarization-activated inward current at -90 mV by 12.6 +/- 0.5% (p < 0.05, n = 7), respectively. The gating kinetics of ICa and IKslow were not altered.(ABSTRACT TRUNCATED AT 250 WORDS)

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