Abstract:The roles of cyclooxygenase (COX) and prostaglandins (PGs) in the regulation of vasoreactivity of rat gingival arterioles in vivo were evaluated by using 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 PGI 2 ) or PGE 2 onto the gingiva significantly dilated the arterioles dose-dependently. The AALocal gingival blood flow plays a crucial role in maintaining dental health care in physiological conditions [1][2][3]. For evaluating local blood flow in the gingival tissues in vivo, laser-doppler and ultrasonic flowmetry have been used on animals and humans [4][5][6][7], but they are both disadvantageous for evaluating continuous changes in the diameter of gingival microvessels in vivo. On the other hand, an intravital microscope system enables us to continuously measure changes in the diameter of resistant microvessels, including small arteries and arterioles in vivo.PGs are produced via the arachidonic acid-COX pathway. COX is a limiting enzyme in this cascade and has been classified into two isoforms, COX-1 (constitutive type) and COX-2 (inducible type) [8][9][10][11]. 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. [The Japanese Journal of Physiology 55: [293][294][295][296][297][298][299][300][301][302] 2005]