Possible interactions between neurotensin and prostaglandins in the isolated rat portal vein

Neurotensin (NT) was found to elicit a dose-dependent contractile effect in the isolated rat portal vein. This effect was not inhibited by phentolamine, atropine, methysergide, a mixture of diphenhydramine and cimetidine, or by Leu⁸]-angiotensin II, but it was markedly reduced or abolished by various antiinflammatory drugs such as indomethacin, acetylsalicylic acid, mefenamic acid, hydrocortisone and by mepacrine, an inhibitor of phospholipase A₂. The concentrations of antiinflammatory drugs used to inhibit NT, also antagonized the venoconstrictor effects of bradykinin and angiotensin, but did not affect the responses of the vein to noradrenaline. D-Trp¹¹]-NT, a previously described NT antagonist, was found to inhibit selectively and dose-dependently the stimulant effect of NT in the portal vein. The results suggest the existence of specific receptors for NT in the isolated rat portal vein. The response of this tissue to NT, and possibly to other peptides, appears to be dependent upon the presence of a functional PG biosynthetic pathway.