AJP - Heart and Circulatory Physiology, Vol 271, Issue 6 2238-H2245, Copyright © 1996 by American Physiological Society
Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ
M. Szentivanyi Jr, G. L. Nadasy, L. Dezsi, G. Mozes, T. Tulassay and E. Monos
Clinical Research Department-Second Institute of Physiology, Semmelweis University of Medicine, Budapest, Hungary.
The vascular effects of somatostatin (ST) and its mechanism of action are
not well understood. In the present study, we investigated the direct
effects of ST on the vascular tone of rat saphenous artery and vein using
videomicroangiometry in situ. ST was administered either in superfusion or
in infusion. We found opposite effects in arteries and veins: ST
(10(-12)-10(-7) M) dilated the artery (outer diameter increased from 533
+/- 28 to 600 +/- 29 microns, administered in superfusion) and contracted
the vein (from 709 +/- 26 to 640 +/- 26 microns and from 775 +/- 30 to 708
+/- 60 microns in superfusion and infusion, respectively). These effects of
ST were completely abolished after deendothelization (air bolus maintained
for 6 min in vessel lumen) and after local infusion of NG-nitro-L-arginine
(L-NNA; 10(-4) M), a nitric oxide (NO) synthesis inhibitor. An NO-dependent
basal vasodilator tone in the rat saphenous vein responsible for 10.9 +/-
0.3% of the total vessel diameter was found. After ST administration the
venous diameter reduction was similar to that measured after
deendothelization or L-NNA. We conclude that ST in situ induces NO release
from endothelial cells of rat saphenous artery causing vasodilation,
whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone
of the saphenous vein inducing vasoconstriction.
