Role of cyclooxygenase-1 and -2 in the generation of vasoactive prostanoids
Description
CYCLOOXYGENASE (COX) is the rate-limiting step in the formation of prostanoids from their essential fatty acid precursor arachidonic acid. Three COX isoforms have been described. COX-1 is constitutively expressed and involved in physiological processes, whereas COX-2 is an inducible enzyme upregulated by inflammatory cytokines (Akarasereenant et al., 1995; Masferrer et al., 1990; Bauer et al., 1994; Feng et al., 1993; Hela and Neilson 1992; Johnson et al., 1995; Kennedy et al., 1993; O'neil and Ford-Hutchinson 1993; Smith et al., 1998 and COX-3 is the splice variant of COX-1 (Chandrasekharan et al., 2002). Studies (Ermert et al., 1998; Asano et al., 1996; Camitta et al., 2001; Catella-Lawson et al., 1999; Harris et al., 2001; Vane et al.,) in the literature have shown that both COX-1 and -2 isoforms are expressed constituitively in many organs, including the lung, kidney, and heart. Because most previous studies (Bivalacqua et al., 1999; Champion et al., 1998; Chapnick et al., 1997; Feigen et al., 1978; Kadowitz 1975; Silldorf et al., 2002; Wood et al., 1994) were carried out using nonselective COX inhibitors, there is a possibility that prostanoids are formed by the COX-1 and -2 isoforms under physiological conditions and not only COX-1. Therefore the purpose of the present work was undertaken to investigate the role of COX-1 and -2 in the generation of vasoactive prostanoids in pulmonary and systemic arterial beds of the rat and the mouse