Abstract:
:The purpose of this study was to elucidate the mechanism by which bradykinin (BK) enhances prostacyclin (PGI(2)) production in human umbilical vein endothelial cells (HUVEC). BK-induced enhancement of PGI(2) synthesis was observed in a dose- and time-dependent manner, and it also increased [Ca(2+)](i) followed by enhancement of cytosolic phospholipase A(2) (cPLA(2)) activity. The PKC inhibitors GF109203X and H7 attenuated the BK-induced increase in [Ca(2+)](i) and inhibited the BK-induced PGI(2) synthesis. Phorbol 12-myristate 13-acetate increased cPLA(2) activity and PGI(2) synthesis but failed to alter [Ca(2+)](i). BK increased cPLA(2) mRNA eightfold by 15 min, and this increase was inhibited by pretreatment with the PKC inhibitors. In response to cycloheximide pretreatment, cPLA(2) mRNA was superinduced. These results suggest that BK stimulates PGI(2) synthesis in HUVEC by activation of cPLA(2) by dual mechanisms: an elevation of [Ca(2+)](i) and a PKC-dependent pathway. Moreover, changes in calcium kinetics and expression of cPLA(2) mRNA may underlie the BK-induced PGI(2) enhancement in these cells.
journal_name
Microvasc Resjournal_title
Microvascular researchauthors
Higaki T,Sawada S,Kono Y,Imamura H,Tada Y,Yamasaki S,Toratani A,Sato T,Komatsu S,Akamatsu N,Tamagaki T,Tsuda Y,Tsuji H,Nakagawa Mdoi
10.1006/mvre.1999.2163keywords:
subject
Has Abstractpub_date
1999-09-01 00:00:00pages
144-55issue
2eissn
0026-2862issn
1095-9319pii
S0026-2862(99)92163-5journal_volume
58pub_type
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