Vasorelaxant effects of Ca(2+)-ATPase inhibitors were examined in the isolated adult and neonatal guinea pig thoracic aorta focusing on the functional alterations of endothelial cells with development. Cyclopiazonic acid produced an endothelium-dependent vascular relaxation in the adult aorta preconstricted with norepinephrine, whereas no relaxant response was obtained by the compound in the neonatal preparation. Endothelium-dependent vascular relaxation was also produced by another Ca(2+)-ATPase inhibitor, thapsigargin, in the adult aorta, but not in neonatal ones. The endothelium-dependent vascular relaxations produced by both Ca(2+)-ATPase inhibitors were suppressed either by NG-nitro-L-arginine or by methylene blue, suggesting that nitric oxide (NO) mediated the endothelium-dependent vascular relaxations. The present results suggest the possibility that mechanisms underlying the synthesis and/or release of NO change with development in the guinea pig aortic endothelial cells.
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