Calcium-induced vasodilation due to increase in nitric oxide formation in the vascular bed of rabbit ear preparation.

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 CaCl2 (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, CaCl2 dose-dependently induced vasodilation of the vessel when it was continuously contracted by norepinephrine (1.2 x 10(-7) M). This calcium-induced vasodilation was inhibited in the presence of NG-nitro-L-arginine (5 x 10(-5) M), a selective inhibitor of NO synthesis, and methylene blue, a guanylate cyclase inhibitor, although it was rarely affected by indomethacin (10(-5) 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(2+)-induced increase in the synthesis of NO derived from endothelial cells.