Investigation of the role of prostaglandins in nitroglycerin-induced relaxation of isolated rabbit blood vessels

Abstract

The effect of inhibition of prostaglandin synthesis on nitroglycerin-induced relaxation was examined in isolated rabbit mesenteric and celiac arterial rings. An indomethacin dose of 5 μM was selected as adequate to inhibit prostaglandin synthesis as this dose prevented relaxation of the arterial rings by sodium arachidonate (3.3 μM) and by bradykinin, a peptide thought to induce vasodilation via stimulation of prostaglandin synthesis. Following 20 min pretreatment with indomethacin (5 μM), indomethacin solvent, or Krebs solution (control), the arterial rings were contracted submaximally with phenylephrine (0.5–10 μM). The degree of inhibition of phenylephrine-induced tone produced after cumulative additions of nitroglycerin (10−10 – 5 × 10−7 M) was assessed. In control celiac and mesenteric rings the responses to nitroglycerin were as follows: mean effective dose (ED50), 5.6 × 109 ± 4.5 × 10−9 M (SD) and 1.1 × 10−8 ± 5 × 10−9 M (SD), respectively; maximum relaxation, 97 ± 3% (SD) and 93 ± 7% (SD), respectively. Neither indomethacin nor indomethacin solvent affected the ED50 or maximum relaxation with nitroglycerin. We conclude that nitroglycerin-induced relaxation of rabbit celiac and mesenteric arteries appears to be mediated through a mechanism other than stimulation of prostaglandin synthesis.