Nitric Oxide-Induced Intracellular Ca2+ Modulation in Macrovascular Endothelial Cells.
10.4070/kcj.2004.34.6.600
- Author:
Seong Hee JEON
1
;
Geun Hee SEOL
;
Suk Hyo SUH
;
Seong Hoon PARK
Author Information
1. Department of Internal Medicine, Bupyung Serim Hospital, Inchon, Korea.
- Publication Type:Original Article
- Keywords:
Endothelium;
Intracellular calcium;
Cyclic GMP;
Nitric oxide
- MeSH:
Animals;
Cyclic GMP;
Endothelial Cells*;
Endothelium;
Guanylate Cyclase;
Human Umbilical Vein Endothelial Cells;
Humans;
Mice;
Myocytes, Smooth Muscle;
Nitric Oxide;
Nitroprusside;
Protein Kinases;
Tissue Donors
- From:Korean Circulation Journal
2004;34(6):600-609
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Nitric 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: In primary cultured MAEC and HUVEC, cells were loaded with fura 2-AM and [Ca2+]i and measured using a microfluorometer. RESULTS: The 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: These results suggest that NO inhibits the [Ca2+]i through a cGMP-dependent mechanism and increases the [Ca2+]i through a cGMP-independent mechanism.
