作者: Y. Yuan , H. J. Granger , D. C. Zawieja , D. V. DeFily , W. M. Chilian
DOI: 10.1152/AJPHEART.1993.264.5.H1734
关键词:
摘要: In this study, we hypothesized that histaminergic increases in venular permeability result from a cascade triggered by activation of phospholipase C (PLC), inducing the synthesis nitric oxide (NO) and activating guanylate cyclase. The apparent coefficient to albumin (Pa) was measured isolated porcine coronary venules subjected constant flow hydrostatic oncotic pressures. Histamine (2.5, 5, 10 microM) transiently progressively increased Pa. PLC inhibitor 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate (NCDC; 100 decreased baseline abolished effect histamine. NO synthase NG-monomethyl-L-arginine (L-NMMA; cyclase 6-anilinoquinoline-5,8-quinone (LY 83583; also blocked histamine-induced hyperpermeability. L-Arginine (3 mM) reversed inhibition L-NMMA. NG-monomethyl-D-arginine did not influence Furthermore, sodium nitroprusside (10 augmented Pa two- threefold; presence LY 83583 but altered NCDC. results suggest histamine direct action on endothelial cells through PLC-NO synthase-guanylate cyclase-signaling cascade.