NITRIC OXIDE-DEPENDENT OPPOSITE EFFECTS OF SOMATOSTATIN ON ARTERIAL AND VENOUS CALIBER IN-SITU

The vascular effects of somatostatin (ST) and its mechanism of action are not well understood. In the present study, we investigated the dir ect effects of ST on the vascular tons of rat saphenous artery and vei n using videomicroangiometry in situ. ST was administered. either in s uperfusion or in infusion. We found opposite effects in arteries and v eins: ST (10(-12)-10(-7) M) dilated the artery (outer diameter increas ed from 533 +/- 28 to 600 +/- 29 mu m, administered in superfusion) an d contracted the vein (from 709 +/- 26 to 640 +/- 26 mu m and from 775 +/- 30 to 708 +/- 60 um in superfusion anti infusion, respectively). These effects of ST st ere completely abolished after deendothelizatio n lair bolus maintained for 6 min in vessel lumen and after local infu sion of N-G-nitro-L-arginine (L-NNA; 10(-4) M), a nitric oxide (NO) sy nthesis inhibitor. An NO-dependent basal vasodilator tone in the rat s aphenous vein responsible for 10.9 +/- 0.3% of the total vessel diamet er was found. After ST administration the venous diameter reduction wa s similar to that measured after deendothelization or L-NNA. We conclu de that ST in situ induces NO release from endothelial cells of rat sa phenous artery causing vasodilation, whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone uf the saphenous vein inducin g vasoconstriction.