Arachidonic Acid-Induced COX-1 and COX-2-Mediated Vasodilation in Rat Gingival Arterioles In Vivo

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  • Nakatsuka Atsushi
    Department of Physiology, Shinshu University School of Medicine
  • Mizuno Risuke
    Department of Physiology, Shinshu University School of Medicine
  • Ono Nobuyuki
    Department of Electronics and Control Engineering, Nagano National College of Technology
  • Nakayama Jun
    Department of Pathology, Shinshu University School of Medicine
  • Ohhashi Toshio
    Department of Physiology, Shinshu University School of Medicine

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The roles of cyclooxygenase (COX) and prostaglandins (PGs) in the regulation of vasoreactivity of rat gingival arterioles in vivo were evaluated by sing an intravital microscope. The superfusion of indomethacin (a nonselective COX inhibitor) or SC-560 (a selective COX-1 inhibitor) onto the gingiva significantly constricted the arterioles, though NS-398 (a selective COX-2 inhibitor) did not affect the diameter of the arterioles. The SC-560–mediated constriction of the arterioles was completely reversed by an additional treatment with arachidonic acid (AA). The superfusion of AA, beraprost-Na (an analogue of PGI2) or PGE2 onto the gingival significantly dilated the arterioles dose-dependently. The AA-induced dilation of the arterioles was significantly reduced by the treatment with SC-560 or NS-398. The expression of COX-1 and COX-2 were positive in the endothelium, but not the smooth muscles, of the arterioles. The expression of PGE synthase (PGES) was found only in the smooth muscles, but not the endothelium, of the arterioles. Neither the endothelium nor the smooth muscles of the arterioles expressed PGI synthase (PGIS). These findings suggest that the COX-2–mediated PG cascade may collaborate with the COX-1 pathway in the regulation of arteriolar myogenic activity in rat gingiva in the case of the supply of a large amount of AA.<br>

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