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Structurally diverse groups of compounds are known to be effective as Calcium antagonists. The most potent class of antagonists comprises derivatives of 1, 4 Dihydropyridine of which the most widely known agent is Nifedipine. This class of compounds has been subject of many structure-activity relationship studies. In this research we evaluated the Calcium channel antagonists activity of various diester analogues of Nifedipine on rat ileal smooth muscle. In these analogues, the Orthophenyl group at position 4 is replaced by 1 Methyl-2-Meythlusulfonyl or Methylthio-5 Imidazolyl. Wistar rats (180-250 g) were killed by a blow to the head. The intestine was removed above the ileocecal junction and longitudinal smooth muscle segments of 2 cm length were maintained at 37°C in a 10 ml jacket organ bath containing oxygenated intestinal Krbps solution. The contraction were recorded with a forced displacement transducer connected to a physiograph. The contraction was elicited with 80 mmol kcl. Test compounds were cumulatively added to produce 50% relaxation of contracted ileal smooth muscle (IC50) that was determined from the concentration response trace recorded by physiograph. The comparison of activities of symmetrical esters indicates that increasing the length of methylen chain in C3 and C5 esters substituent decreased the activity and comparison of activities of a symmetrical ester, compound indicate when at C3 was a small substituent, increasing the length of methylen chain increase activity.

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Background and Objective: Brain ischemia is one of the most important factor of morbidity and mortality and leaving many people with mental and physical disabilities. Until now there are no appropriate medications to prevent and cure ischemic injury. This study was done to evaluate the protective effect of Adenosine A1 receptor and ascorbic acid on hippocampal neuronal density and memory disorder in ischemia reperfusion induced Rats. Materials and Methods: This experimental study was performed on the hippocampus pyramidal neurons on 56 male BALB/c mice. Animals randmly allocated into 8 groups (N=7) including: 1) intact, 2) ischemic control group, 3) ischemic, plus agonist and adenosine of A1 receptor, 4) ascorbic acid (100 mg/daily), 5) ischemic plus agonist adenosine receptor (1 mg/1 kg) one week after ischemia, 6) ischemia, ascorbic acid befor and after ischemia and A1 receptor (1 mg/1 kg) agonist after ischemia, 7) A1 receptor, antagonist (2.25 / 1 kg), one weed after ischemia, 8) Ascorbic acid (100 mg/1kg) before and after ischemia plus A1 receptor antagonist (2.25 / 1 kg) after ischemia. Ischemia induced by clamping of common carotid artery and the drugs was injected subsequently into peritoneum after reduction of inflammation of ischemic zone. The Y-maze memory test performed after completing the treatment period, afterward brains fixed and prepared for microscopic nissl staining method. The counting of pyramidal cells were performed at 53500 square micrometer of CA1. Data were analyzed using SPSS-15 and ANOVA test. Results: The Y-maze test showed extensive deficit in short-term memory in ischemic group (PA=200) but in treatment groups this deficit significantly reduced (PA=243, 248 and 265). The normal neuronal cell in ischemic group was significantly lowered (n=87) than treatment groups (n=111, 105 and 125) including ascorbic acid group (125), adenosine receptor agonist (105) and ascorbic acid plus agonist adenosine receptor (111). The number of normal neuronal cell in ischemic groups significantly is reduced compared to treatment group (P<0.05). Conclusion: This study showed that concurrent treatment of ascorbic acid and Adenosine A1 receptor agonist can significantly reduce the complications caused by brain ischemia in CA1 area of hippocampus.