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Updated: May 11, 2026

Isolation and Cannulation of Cerebral Parenchymal Arterioles
Published on: May 23, 2016
Sarpogrelate dilates cerebral arteries in the absence of exogenous serotonin
Maiko Kawamura1, Masanori Ishiguro, Takashi Nagamine
1Department of Neurosurgery, School of Medicine, Sapporo Medical University, Sapporo, Japan.
Abstract:
Vasoconstriction of arteries induced by serotonin (5-hydroxytryptamine: 5-HT) is mediated by 5-HT2A and 5-HT1B receptors localized on smooth muscle. The present study investigated the impact of sarpogrelate, a 5-HT2A receptor antagonist, on cerebral artery diameter in the presence and absence of exogenous 5-HT. Diameter measurements were obtained in vitro from rabbit cerebral arteries pressurized to 60 mmHg. In the absence of 5-HT, arteries exhibiting pressure-induced myogenic tone dilated to sarpogrelate in a concentration-dependent manner (half maximal inhibitory concentration [IC50] ≈ 2.3 μM). In a separate experimental series, exogenous application of 5-HT (0.01 μM) caused further constriction of myogenically active arteries, decreasing cerebral artery diameter by an additional 25%. In the presence of 5-HT, sarpogrelate caused concentration-dependent vasodilation (IC50 ≈ 2.3 μM) that was similar to that observed in the absence of exogenous 5-HT. Dilation induced by sarpogrelate was not affected by physical removal of the endothelium or inhibition of nitric oxide synthase with Nω-nitro L-arginine. The highest concentration of sarpogrelate (100 μM) induced near maximal dilation, comparable to dilation induced by the L-type voltage-dependent calcium channel antagonist diltiazem. These findings suggest that in rabbit cerebral arteries, sarpogrelate has direct vasodilator effects on vascular smooth muscle.
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