Orai1 Contributes to Platelet-Activating Factor (PAF)-Induced Contraction in Association with Voltage-Dependent Ca²⁺ Channel-Mediated Mechanisms in Guinea Pig Urinary Bladder Smooth Muscle
Abstract
Platelet-activating factor (PAF) is known to induce smooth muscle contraction; however, its mechanisms in urinary bladder smooth muscle (UBSM) remain unclear. We investigated the involvement of Orai1 in PAF-induced contraction in guinea pig UBSM. PAF (10−6 M)-induced contraction was markedly inhibited by the Orai1 inhibitor Synta66 (10−5 M) and the L-type voltage-dependent Ca2+ channel (VDCC) inhibitor verapamil (10−5 M). Similarly, under Ca2+-free conditions with store depletion induced by cyclopiazonic acid (3 × 10−5 M), Ca2+-induced contraction was suppressed by Synta66 and verapamil. In contrast, Synta66 only partially inhibited contractions induced by acetylcholine (10−5 M) and α,β-methylene ATP (3 × 10−6 M), and it had no effect on high-potassium chloride (80 mM)-induced contraction. Inhibition of Na+/Ca2+ exchanger 1 (NCX1), transient receptor potential canonical (TRPC) 1/4/5 channels, or anoctamin 1 (ANO1) did not significantly affect PAF-induced contraction. These findings suggest that Orai1 contributes to PAF-induced contraction in association with VDCC-dependent mechanisms, whereas NCX1, TRPC1/4/5 channels, and ANO1 play limited roles under these conditions.
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BibTeX
@article{obara2026orai1,
title = {{Orai1 Contributes to Platelet-Activating Factor (PAF)-Induced Contraction in Association with Voltage-Dependent Ca²⁺ Channel-Mediated Mechanisms in Guinea Pig Urinary Bladder Smooth Muscle}},
author = {Keisuke Obara and Daiki Kato and Marina Yuguchi and Momoko Tanaka and Kento Yoshioka and Noritaka Nakamichi and Yoshio Tanaka},
journal = {Biological and Pharmaceutical Bulletin},
year = {2026},
month = aug,
doi = {10.1248/bpb.b26-00187},
url = {https://www.jstage.jst.go.jp/article/bpb/49/8/49_b26-00187/_article},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Orai1 Contributes to Platelet-Activating Factor (PAF)-Induced Contraction in Association with Voltage-Dependent Ca²⁺ Channel-Mediated Mechanisms in Guinea Pig Urinary Bladder Smooth Muscle
AU - Keisuke Obara
AU - Daiki Kato
AU - Marina Yuguchi
AU - Momoko Tanaka
AU - Kento Yoshioka
AU - Noritaka Nakamichi
AU - Yoshio Tanaka
PY - 2026
DA - 2026/08/25
JO - Biological and Pharmaceutical Bulletin
DO - 10.1248/bpb.b26-00187
UR - https://www.jstage.jst.go.jp/article/bpb/49/8/49_b26-00187/_article
AB - Platelet-activating factor (PAF) is known to induce smooth muscle contraction; however, its mechanisms in urinary bladder smooth muscle (UBSM) remain unclear. We investigated the involvement of Orai1 in PAF-induced contraction in guinea pig UBSM. PAF (10−6 M)-induced contraction was markedly inhibited by the Orai1 inhibitor Synta66 (10−5 M) and the L-type voltage-dependent Ca2+ channel (VDCC) inhibitor verapamil (10−5 M). Similarly, under Ca2+-free conditions with store depletion induced by cyclopiazonic acid (3 × 10−5 M), Ca2+-induced contraction was suppressed by Synta66 and verapamil. In contrast, Synta66 only partially inhibited contractions induced by acetylcholine (10−5 M) and α,β-methylene ATP (3 × 10−6 M), and it had no effect on high-potassium chloride (80 mM)-induced contraction. Inhibition of Na+/Ca2+ exchanger 1 (NCX1), transient receptor potential canonical (TRPC) 1/4/5 channels, or anoctamin 1 (ANO1) did not significantly affect PAF-induced contraction. These findings suggest that Orai1 contributes to PAF-induced contraction in association with VDCC-dependent mechanisms, whereas NCX1, TRPC1/4/5 channels, and ANO1 play limited roles under these conditions.
SN - 1347-5215
SN - 0918-6158
ER -