There is strong evidence demonstrating that nifedipine dissolved in ethanol selectively ‎inhibits only L-TYPE Ca^2+ current. In addition, acute ethanol exposure reduces ‎voltage-dependent CALCIUM currents. In the present study, we investigated the ‎antagonistic effect of fixed concentration of nifedipine dissolved in different ‎concentration of ethanol on L-TYPE Ca^2+ current. In a Na^+-K^+ free solution, ‎nifedipine dissolved in 60 and 120 mM ethanol decreased resting membrane potential ‎of Ca^2+ spikes and caused a significant reduction in amplitude, duration and an ‎increase in threshold of Ca^2+ spikes. Furthermore, Ca^2+ current was inhibited by ‎ethanol in a concentration-dependent manner, so that the reduction of L-TYPE Ca^2+ ‎current by nifedipine/60 and 120 mM ethanol was statistically significant. Meanwhile; ‎ethanol concentration-dependent response of Ca2+ currents was observed at its late ‎component in more positive potentials. These results may be consistent with ethanol-‎dependent inhibition of L-TYPE Ca^2+ currents and ethanol-dependent enhancement of ‎a Ca^2+-activated potassium current‏.‏

Wound healing is a natural response to restore the injured tissue to normal. Wound healing is also complicated process involving different cellular, molecular and biochemical mechanisms and various types of cytokines and growth factors. CALCIUM CHANNEL blockers belong to cardiovascular medicine and administrated to treatment of hypertension, angina and cardiac arrhythmia because of vasodilatory effect. CALCIUM CHANNEL blockers is divided to dihydropyridine and non-dihydropyrine. The potential of both dihydropyridine and non-dihydropyrine CALCIUM CHANNEL blockers in wound healing have been reported in different animal models and in vitro previously. Amlodipine, verapamil, diltiazem, nifedipine, and azelnidipine are CALCIUM CHANNEL blockers that indicated wound healing property. The various mechanisms that involve in wound healing effect of CALCIUM CHANNEL blockers are discussed in this article.

Introduction: Alzheimer’ s disease (AD) is the mos t common type of dementia in the elderly. Memory impairment usually occurs gradually and progressively. AD has not only been associated with decreased cerebral acetylcholine concentration, oxidative s tress, and beta-amyloid protein deposition, but more recent s tudies have shown that neurodegeneration induced by dis turbance of the intracellular CALCIUM homeos tasis is also involved in the pathophysiology of the disease. It has been reported that CALCIUM CHANNEL blockers (CCBs) have beneficial effects in different models of memory impairment. Here, we review and discuss the effects of CCBs, especially N-types, as novel agents that have effects on memory deficits in animal models of AD. on contrary to the L-TYPE CALCIUM CHANNELs, which are presented in the other organs in addition to nerve cells, N-type CALCIUM CHANNELs are commonly located on the neurons. The main advantage of N-type CCBs is their lower side effects than other CCBs. Conclusion: Targeting the N-type CCBs may contribute to the new s trategies for the treatment of AD.