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KMID : 0364019910240030229
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Korean Journal of Thoracic and Cardiovascular Surgery
1991 Volume.24 No. 3 p.229 ~ p.244
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Acting Mechanisms of Extracellular Ca^(2+) and Ca^(2+) -antagonists on Endothelium- Drived Relaxing Factor in Rabbit Aorta
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Abstract
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A bioassay technique and organ bath study were performed to analyze the effects of ext-rppf racellular Ca 21 and Ca2+antagonists on endothelium-derived relaxing factor(s) (EDRF) released from the endothelial cells of rabbit aorta. Transverse strips with intact endothelium or damaged endothelium were used for the mechanical contraction experiment using organ bath. Long segment includi ij, thoracic and abdominal aorta with endothelium (EDRF donor aorta) was perfused with Tyrode solution which was aerated with 95% 025% CO2 mixed gas and kept at 3510. The perfusate was bioassayed with a transverse strip of thoracic aorta with damaged endothelium. The test strip was contracted with nor-epinephrine and acetylcholine was used to stimulate the release of EDRF from endothelial cells.
The results obtained were as follows :
1) The endothelium-dependent relaxation(EDR) induced by acetylcholine was biphasic an initial rapid relaxation followed by a slow relaxation.
2) EDR induced by acetylcholine was reduced gradually with the decrease in the concentration of extracellular Ca2+. The effect of extracellular Ca2+ on EDR was more prominent in the late slow relaxation phase.
3) EDR to acetylcholine was not altered by acute exposure to organic Ca 21 antagonists. Pretreatment with verapamil to the EDRF donor aortic segment did not alter the mag-:sset nitude of EDR.
4) Among the inorganic Ca2+antagonists Mn2+ and Cd2+ did not inhibit EDR, whereas Coe+ and Lai+ inhibited EDR.
5) The inhibitory response of Coe+ to EDR developed when infused directly on the test strip. That of Lai+, however, was evoked when added to solution perfusing the donor aortic segment.
The above results suggest that Ca2+-antagonists do not affect EDR and the inhibitory effect of Coe+ results from influencing the action of EDRF on vascular smooth muscle, whereas that of Lai+ results from its action on the release of EDRI from endothelial cells.
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