Calcium-Induced Vasodilation Due to Increase in Nitric Oxide Formation in the Vascular Bed of Rabbit Ear Preparation.
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Participation of calcium-induced vasodilation (due to an increase in synthesized nitric oxide (NO)content in endothelial cells)in the arterio-venous circulation, including the vascular bed was investigated by the vessel perfusion method in the isolated rabbit ear preparation. The perfusion medium used was a tris-buffered solution. When CaCl<SUB>2</SUB> (6.25, 12.5 and 25 mg)was injected in the perfused vessel of the rabbit ear preparation, dose-dependent vasocontraction was observed when vascular tone was kept at a normal level. However, CaCl<SUB>2</SUB> dose-dependently induced vasodilation of the vessel when it was continuously contracted by norepinephrine (1.2 × 10<SUP>-7</SUP> M). This calcium-induced vasodilation was inhibited in the presence of <I>N</I><SUP>G</SUP>-nitro-L-arginine (5 × 10<SUP>-5</SUP>M), a selective inhibitor of NO synthesis, and methylene blue, a guanylate cyclase inhibitor, although it was rarely affected by indomethacin (10<SUP>-5</SUP> M), a cyclooxygenase inhibitor. Calcium-induced vasodilation was also obtained in the in situ circulation containing vascular bed, and this suggests that the vasodilation was due to a Ca<SUP>2+</SUP>-induced increase in the synthesis of NO derived from endothelial cells.
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