期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 284, 期 5, 页码 H1577-H1584出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00665.2002
关键词
hemorheology; hemodynamics; regulation; cGMP
资金
- FIC NIH HHS [1R03 TW 01295] Funding Source: Medline
- NHLBI NIH HHS [HL 15722, HL 48484] Funding Source: Medline
In addition to its known action on vascular smooth muscle, nitric oxide ( NO) has been suggested to have cardiovascular effects via regulation of red blood cell (RBC) deformability. The present study was designed to further explore this possibility. Human RBCs in autologous plasma were incubated for 1 h with NO synthase ( NOS) inhibitors [N-omega-nitro-L-arginine methyl ester (L-NAME) and S-methylisothiourea], NO donors [ sodium nitroprusside ( SNP) and diethylenetriamine ( DETA)NONOate], an NO precursor (L-arginine), soluble guanylate cyclase inhibitors (1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one and methylene blue), and a potassium channel blocker [ triethylammonium ( TEA)]. After incubation, RBC deformability at various shear stresses was determined by ektacytometry. Both NOS inhibitors significantly reduced RBC deformability above a threshold concentration, whereas the NO donors increased deformability at optimal concentrations. NO donors, as well as the NO precursor L-arginine and the potassium blocker TEA, were able to reverse the effects of NOS inhibitors. Guanylate cyclase inhibition reduced RBC deformation, with both SNP and DETA-NONOate able to reverse this effect. These results thus indicate the importance of NO as a determinant of RBC mechanical behavior and suggest its regulatory role for normal RBC deformability.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据