Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ

Mátyás Szentiványi, György L. Nádasy, László Dézsi, Géza Mózes, Tivadar Tulassay, Emil Monos

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Abstract

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 μm, administered in superfusion) and contracted the vein (from 709 ± 26 to 640 ± 26 μm and from 775 ± 30 to 708 ± 60 μm 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 N(G)-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.

Original languageEnglish
Pages (from-to)H2238-H2245
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume271
Issue number6 40-6
Publication statusPublished - Dec 1 1996

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Keywords

  • basal vasodilator tone
  • endothelium-dependent relaxation
  • saphenous artery
  • saphenous vein
  • vasoactive peptides

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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