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Komatsu, Sumio; Sawada, Shohei; Tamagaki, Toshiyuki; Tsuda, Yutaka; Kono, Yoshihito; Higaki, Tadashi; Imamura, Hitoshi; Tada, Yuusuke; Yamasaki, Seiki; Toratani, Akihisa; Sato, Toshiyuki; Akamatsu, Naoaki; Tsuji, Hajime; Nakagawa, Masao
Journal of pharmacological and toxicological methods, 02/1999, Letnik: 41, Številka: 1Journal Article
We investigated the effect of probucol on the intracellular pH (pHi) and proliferation of human umbilical vein endothelial cells (HUVEC), as well as their production of prostacyclin (PGI 2). The addition of probucol produced a biphasic shift in pHi, with a brief initial acidification followed by a rapid alkaline shift. After pretreatment with EGTA, the initial decrease in pHi was abolished, and the subsequent increase was inhibited. After pretreatment with amiloride, only the increase of pHi was abolished. These results suggest that the probucol-induced increase of pHi was mainly dependent on Na +/H + exchange and partly on extracellular Ca 2+. In contrast, the addition of LDL produced a decrease of pHi. Under Ca 2+-free condition, pHi was further decreased by LDL. In cells pretreated with amiloride, however, pHi was not further decreased by LDL. It was found that probucol promoted cell proliferation, and LDL inhibited cell proliferation. Addition of probucol also enhanced prostacyclin generation by HUVEC. This enhancement of PGI 2 generation resulted from increased release of Ca 2+ from the storage sites, due not only to increased production of inositol 1,4,5-triphosphate (IP 3) but also to the increase of pHi. These findings may help to explain the antiatherosclerotic action of probucol.
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