Direct measurement of nitric oxide release from vascular endothelial cells

1996 ◽  
Vol 81 (2) ◽  
pp. 774-779 ◽  
Author(s):  
J. P. Guo ◽  
T. Murohara ◽  
M. Buerke ◽  
R. Scalia ◽  
A. M. Lefer
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Methyl Ester ◽  
Vascular Endothelial Cells ◽  
Calmodulin Antagonist ◽  
Nitric Oxide Release ◽  
A 23187 ◽  
No Release ◽  
Basal Release ◽  
Isolated Rat

A nitric oxide (NO)-selective electrode was used to directly measure NO release from isolated rat aortic endothelium and cultured rat aortic endothelial cells (RAECs). Basal release of NO was significantly attenuated by a NO synthase inhibitor NG-nitro-L-arginine methyl ester (1 mM) to 42 +/- 14 pmol/1 x 10(5) cells (P < 0.01). The basal release of NO was also significantly inhibited by a calmodulin antagonist W-7 at 15 microM (P < 0.01). L-Arginine (1 mM), significantly stimulated NO release (P < 0.05 vs. control basal release). Stimulation of cultured RAECs with two endothelium-dependent vasodilators, acetylcholine (100 nM) and A-23187 (1 microM), significantly increased NO release [574 +/- 112 pmol/1 x 10(5) cells (n = 5) and 658 +/- 119 pmol/1 x 10(5) cells (n = 5) in acetylcholine- and A-23187-stimulated RAECs, respectively]. Basal release of NO was also detectable in isolated rat aortic rings with intact endothelium. NO release was significantly attenuated by NG-nitro-L-arginine methyl ester and augmented by human superoxide dismutase. These data indicate the physiological usefulness of the amperometric measurement of NO employing a NO-specific electrode in biological systems.

Reduced perivascular Po2 increases nitric oxide release from endothelial cells

2003 ◽  
Vol 285 (2) ◽  
pp. H507-H515 ◽  
Author(s):  
G. P. Nase ◽  
J. Tuttle ◽  
H. G. Bohlen
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Parenchymal Cell ◽  
Oxygen Availability ◽  
No Production ◽  
Main Site ◽  
Nitric Oxide Release ◽  
No Release ◽  
Parenchymal Cells

Many studies have suggested that endothelial cells can act as “oxygen sensors” to large reductions in oxygen availability by increasing nitric oxide (NO) production. This study determined whether small reductions in oxygen availability enhanced NO production from in vivo intestinal arterioles, venules, and parenchymal cells. In vivo measurements of perivascular NO concentration ([NO]) were made with NO-sensitive microelectrodes during normoxic and reduced oxygen availability. During normoxia, intestinal first-order arteriolar [NO] was 397 ± 26 nM ( n = 5), paired venular [NO] was 298 ± 34 nM ( n = 5), and parenchymal cell [NO] was 138 ± 36 nM ( n = 3). During reduced oxygen availability, arteriolar and venular [NO] significantly increased to 695 ± 79 nM ( n = 5) and 534 ± 66 nM ( n = 5), respectively, whereas parenchymal [NO] remained unchanged at 144 ± 34 nM ( n = 4). During reduced oxygenation, arteriolar and venular diameters increased by 15 ± 3% and 14 ± 5%, respectively: NG-nitro-l-arginine methyl ester strongly suppressed the dilation to lower periarteriolar Po2. Micropipette injection of a CO2 embolus into arterioles significantly attenuated arteriolar dilation and suppressed NO release in response to reduced oxygen availability. These results indicated that in rat intestine, reduced oxygen availability increased both arteriolar and venular NO and that the main site of NO release under these conditions was from endothelial cells.

Shear Stress Induces ATP-Independent Transient Nitric Oxide Release From Vascular Endothelial Cells, Measured Directly With a Porphyrinic Microsensor

1995 ◽  
Vol 77 (2) ◽  
pp. 284-293 ◽  
Author(s):  
Anthony J. Kanai ◽  
Harold C. Strauss ◽  
George A. Truskey ◽  
Anne L. Crews ◽  
Saul Grunfeld ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Nitric Oxide Release

Nitric oxide and vascular reactivity in developing zebrafish,Danio rerio

2000 ◽  
Vol 279 (6) ◽  
pp. R2200-R2207 ◽  
Author(s):  
Regina Fritsche ◽  
Thorsten Schwerte ◽  
Bernd Pelster
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Methyl Ester ◽  
Vascular Reactivity ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vessel Diameter ◽  
No Donor ◽  
Dorsal Vein ◽  
Vasoactive Substances

We used a newly developed digital motion analysis video technique to study the effects of nitric oxide (NO) and epinephrine on the early larval arterial and venous vasculature of zebrafish. Application of the NO donor sodium nitroprusside resulted in a significant increase in both the venous and arterial vessel diameters, whereas N G-nitro-l-arginine methyl ester caused a significant decrease in the same diameters. Thus our results show that both the venous and arterial vasculature of the 5- and 6-day-old zebrafish larvae are influenced by endogenously produced NO. By use of immunohistochemistry, NO synthase immunoreactivity was demonstrated in endothelial cells of the dorsal vein. Local application of epinephrine onto the dorsal artery had no effect on vessel diameter. However, if the embryos were preincubated with N ω-nitro-l-arginine methyl ester, addition of epinephrine resulted in a significant reduction in both arterial and venous vessel diameters. Thus this study provides increasing evidence that before a functional autonomic innervation of the peripheral vascular system, vascular tone in larval tissue is regulated by a complex interaction of vasoactive substances that are produced locally by vascular endothelial cells.

Difference in Endothelium-Derived Hyperpolarizing Factor–Mediated Hyperpolarization and Nitric Oxide Release Between Human Internal Mammary Artery and Saphenous Vein

Circulation ◽  
2000 ◽  
Vol 102 (suppl_3) ◽  
Author(s):  
Zhi-Gang Liu ◽  
Zhi-Dong Ge ◽  
Guo-Wei He
Keyword(s):  
Nitric Oxide ◽  
Saphenous Vein ◽  
Internal Mammary Artery ◽  
Resting Membrane Potential ◽  
Nitric Oxide Release ◽  
No Release ◽  
Basal Release ◽  
Internal Mammary ◽  
Sensitive Electrode

Background —The greater nitric oxide (NO) release that occurs in the internal mammary artery (IMA) when compared with the saphenous vein (SV) has been suggested by more endothelium-dependent relaxation in the IMA or measured by bioassay; however, no direct measurement of NO- or endothelium-derived hyperpolarizing factor (EDHF)–mediated hyperpolarization has been reported. The present study measured such hyperpolarization, as well as NO release, in these vessels. Methods and Results —IMA (n=46) and SV (n=61) segments taken from patients undergoing coronary surgery were studied in the organ chamber. Hyperpolarization (by intracellular glass microelectrode) and NO release (by NO-sensitive electrode) in response to acetylcholine and bradykinin, with and without incubation with N G -nitro- l -arginine, indomethacin, and oxyhemoglobin, were measured. The resting membrane potential of the smooth muscle cells from the IMA (58±0.8 mV; n=15) was higher than that in those from the SV (−62±0.9 mV; n=23; P =0.0001). The EDHF-mediated hyperpolarization induced by acetylcholine (10 −5 mol/L: −9.4±1.5 mV in IMA, n=10, versus −4.5±1.0 mV in SV, n=17; P <0.01) and bradykinin (10 −7 mol/L: −10.9±1.5 mV in IMA, n=8, versus −5.1±0.5 mV in SV, n=8; P <0.01) and the basal release of NO (16.8±1.6 nmol/L in IMA, n=13, versus 9.9±2.8 nmol/L in SV, n=13; P <0.001) were significantly greater in the IMA than in the SV. The duration of acetylcholine- and bradykinin-induced NO release was longer in the IMA than in the SV. Conclusions —The basal release of NO and EDHF-mediated hyperpolarization were significantly greater in the IMA than in the SV. In addition, the duration of the stimulated release of NO was longer in the IMA than in the SV. These differences may contribute to the superior long-term patency of IMA grafts.

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