Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0368120040340060600
Korean Circulation Journal
2004 Volume.34 No. 6 p.600 ~ p.609
Nitric Oxide-Induced Intracellular Ca2+ Modulation in Macrovascular Endothelial Cells
Áø¼ºÈñ/Jeon SH
¼³±ÙÈñ/¼­¼®È¿/¹Ú¼ºÈÆ/Seol GH/Suh SH/Park SH
Abstract
Background and Objectives£ºNitric oxide (NO) reduces the intracellular Ca2+ concentration ([Ca2+]i) in smooth muscle cells, whereas the effect of NO on [Ca2+]i in endothelial cells is still controversial. Therefore, the effect of NO on the [Ca2+]i, and its mechanism in mouse aortic endothelial cells (MAEC) and human umbilical vein endothelial cells (HUVEC) were examined.

Materials and Methods£ºIn primary cultured MAEC and HUVEC, cells were loaded with fura 2-AM and [Ca2+]i and measured using a microfluorometer.

Results£ºThe NO donor, sodium nitroprusside (SNP), reduced the [Ca2+]i in 72% of the cells tested (n=100). In the remaining cells, the effect of SNP was biphasic, or the [Ca2+]i was increased. In addition, the membrane-permeable cGMP, 8-bromo cGMP, decreased the [Ca2+]i. The effects of SNP and 8-bromo cGMP were inhibited by the soluble guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazole[4,3-a]quinoxalin-1-one (ODQ), and the cGMP-dependent protein kinase inhibitor, KT5823, respectively. In contrast, in the presence of 8-bromo cGMP or ODQ, SNP increased the [Ca2+]i.

Conclusion£ºThese results suggest that NO inhibits the [Ca2+]i through a cGMP-dependent mechanism and increases the [Ca2+]i through a cGMP-independent mechanism.
KEYWORD
FullTexts / Linksout information
 
Listed journal information
SCI(E) ÇмúÁøÈïÀç´Ü(KCI) KoreaMed ´ëÇÑÀÇÇÐȸ ȸ¿ø