Authors
Kento Yoshioka, Minami Inagaki, Tam Minh Phi, Haruki Kimura, Keigo Osa, Keisuke Obara, Noritaka Nakamichi, Yoshio Tanaka
Published in
Biological & pharmaceutical bulletin. Volume 49. Issue 9. Pages 1416-1419.
Abstract
γ-Linolenic acid (GLA) is an n-6 polyunsaturated fatty acid (PUFA) with reported vasoprotective effects. GLA has been shown to inhibit contractions in pig coronary arteries via competitive antagonism at prostanoid TP receptors. α-Linolenic acid (ALA), an n-3 PUFA and a structural isomer of GLA, has been shown to inhibit contractions in pig basilar arteries (PBAs) via prostanoid TP receptor antagonism and activation of K+ channels. However, the actions of GLA in cerebral arteries remain unclear. In this study, we examined the effects of GLA on contractile responses in PBAs. GLA (10-5-10-4 M) concentration-dependently inhibited contractions induced by the TP receptor agonist U46619 (3 × 10-8 M) and prostaglandin F2α (PGF2α; 3 × 10-6 M). GLA (3 × 10-6-3 × 10-5 M) shifted the concentration-response curve for U46619 to the right. Schild analysis yielded a slope of 1.33 (95% confidence interval: 0.70-1.96), which was not significantly different from unity, but GLA also reduced the maximal response to U46619. The apparent pA2 value was 5.43. GLA (10-4 M) also inhibited PGF2α-induced contractions in the presence of the TP receptor antagonist SQ 29,548 (10-6 M); this inhibitory effect was attenuated by Ba2+ (10-3 M) but not by other tested K+ channel inhibitors. GLA also inhibited endothelin-1 (10-8-3 × 10-8 M)-induced contractions, and this effect was attenuated by Ba2+. These findings indicate that GLA, like ALA, suppresses contractile responses in PBAs through dual mechanisms involving TP receptor antagonism and activation of Ba2+-sensitive K+ channels.
PMID:
42702555
Bibliographic data and abstract were imported from PubMed on 07 Sep 2026.
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