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AIM:To observe the role of calcium-sensing receptor (CaSR) in the regulation of pulmonary artery tension.METHODS:The intracellular calcium concentration ([Ca2+]i) was detected by laser-scanning confocal micros-copy, and the pulmonary artery tension was determined by the pulmonary arterial ring technique .RESULTS: Increased levels of [Ca2+]o or Gd3+(an agonist of CaSR) induced the increase in [Ca2+]i and pulmonary artery constriction in a concentration-dependent manner.Additionally, the effects of Ca2+and Gd3+were inhibited by U73122 and D609 (specific inhibitor of PLC), and 2-APB and heparin (specific antagonist of IP3 receptor).However, U73343 (U73122 inactive ana-logue) did not take effect.CONCLUSION: CaSR may be involved in the regulation of pulmonary artery tension by in-creasing [Ca2+]i through G-protein-PLC-IP3 pathway.
RESUMEN
Objective To investigate the effects of tissue inhibitor-3 of matrix metalloproteinases(TIMP-3)Gene-transfected vascular smooth muscle cells(VSMCs)transplantation on heart function after acute myocardial infarction(AMI)in rats and to explore the potential mechanisms.Methods Wistar rats were produced AMI models by ligating the descending left coronary artery.Rats were survived and divided into 3 groups randomly(n=18):0.5mlDMEM containing 1?106 TIMP-3 gene-transfected VSMCs(group A),1?106 VSMCs(group B)or 0.5 ml DMEM without cell(group C)were injected into the ischemic myocardium immediately.Ischemic myocardium samples were harvested at 3 day after operation.The heart function was observed through the tissue functional examination.The activity of TIMP-3 gene-transfected VSMCs were measured by immunohistochemical method.mRNA of TIMP-3 and matrix metalloproteinase 9(MMP-9)were determined by RT-PCR.Results VSMCs were cultivated and had a high purity(98%).TIMP-3 gene was transfected into VSMCs successfully.Three day after operation in group A the average percentage of LVIDd、LVIDs、EDV and ESV were significantly higher than group normal(P