The effect of verapamil, nifedipine and diltiazem on formalin-induced pain response in mice
Subject Areas : Veterinary Clinical PathologyM.H Khayat Nouri 1 * , جواد Mahmody 2 , M.R Hoseinchi Ghareaghaji 3
1 - Department of Basic Sciences, Faculty of Veterinary Medicine, Islamic Azad University-Tabriz Branch, Tabriz, Iran
2 - Graduate of Veterinary Pharmacology, Faculty of Veterinary Medicine, Islamic Azad University-Science and Research Branch, Tehran, Iran
3 - Department of Basic Sciences, Faculty of Veterinary Medicine, Islamic Azad University-Urmia Branch, Urmia, Iran
Keywords: Mice, Verapamil, Nifedipine, Diltiazem, pain, Formalin,
Abstract :
Voltage-gated calcium channels play a major role in the control of cellular processes in cardiac, vascular and neuronal tissues. Verapamil, nifedipine and diltiazem are calcium channel blockers widely used in the treatment of cardiovascular ailments in humans. A number of studies have shown that calcium channel blockers have antinociception and antiinflammatory effects in a range of animal models (but not in all animal models). The aim of this study was to investigate the effect of verapamil, nifedipine and diltiazem on formalin-induced pain and inflammation in mice. In this experimental study, verapamil, nifedipine and diltiazem (10 mg/kg) were intraperitoneally injected 30 minutes before the injection of 20µl of 5% formalin solution into the paw region. The time of licking and biting of injected paw was measured as pain response at 5 minute intervals for 1 hour. The results showed that formalin induced a biphasic pain response (first phase: 0-5 and second phase: 20-45 minute after injection). Intraperitoneal injection of verapamil, nifedipine and diltiazem before formalin reduced the second phase (inflammatory pain) of pain response significantly (p<0.05) and only verapamil reduced the first phase (neurogenic pain) of pain response significantly (p<0.05). Based on the results of this study it can be concluded that verapamil, nifedipine and diltiazem possess antinociceptive and antiinflammatory activity probably via a decrease in calcium influx that in turn interferes with the release of neurotransmitters and other substances that promote nociception and inflammation.