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Abstract

Angiotensin II from the renin-angiotensin system is proposed to be pro-inflammatory induces reactive oxygen species, nuclear factor kappa B. It sensitizes pain receptors to mediators of pain (via PGE2). ACEI block these actions increase endogenous opioids by inhibiting enzyme enkephalinase. Voltage-gated calcium channels (VGCC) causing calcium influx are involved in exocytosis of synaptic vesicle (glutamate, substance-P) post membrane depolarization while pain processing. N and T types of VGCC are implicated in the central sensitization of pain stimuli. The current study aims at evaluating the analgesic properties of trandolapril and nimodipine in mice. This was an experimental study. Twenty-four swiss albino mice were randomly divided into four groups. Reaction time was assessed on Eddy's hot plate (±55°C) in trandolapril group (5mg/kg), Nimodipine group (2.5mg/kg) and compared with standard (tramadol 20mg/kg) and percentage change was evaluated at 30, 60, 90, 120 min. ANOVA did a statistical evaluation. A significant increase (p<0.05) in reaction time was seen in the trandolapril group at 60, 90,120 min whereas at 30, 60, 90,120 min in the tramadol group. No significant change occurred in the control and nimodipine groups. Trandolapril is therefore proposed to possess analgesic activity in mice. However, no effect was seen with nimodipine at this dose. INTRODUCTION:Pain is one of the most common symptoms in patients who visit a clinician. It is a distressing experience that is associated with actual or potential tissue damage involving sensory, emotional, cognitive, and social components, according to the QUICK RESPONSE CODE