Relaxations to SIN-1, Nitric Oxide, and Sodium Nitroprusside in Canine Arteries and Veins

1989 ◽  
Vol 14 ◽  
pp. S67-71 ◽  
Author(s):  
Virginia M. Miller ◽  
Paul M. Vanhoutte
2001 ◽  
Vol 280 (4) ◽  
pp. R959-R967 ◽  
Author(s):  
Peter S. Andrew ◽  
Yiming Deng ◽  
Richard Sultanian ◽  
Susan Kaufman

We hypothesized that nitric oxide (NO) contributes to intrasplenic fluid extravasation by inducing greater relaxation in splenic resistance arteries than veins such that intrasplenic microvascular pressure (PC) rises. Fluid efflux was estimated by measuring the difference between splenic blood inflow and outflow. Intrasplenic infusion of the NO donor S-nitroso- N-acetylpenicillamine (SNAP) (0.3 μg · 10 μl−1 · min−1) caused a significant increase in intrasplenic fluid efflux (baseline: 0.8 ± 0.4 ml/min, n = 10 vs. peak rise during SNAP infusion: 1.3 ± 0.4 ml/min, n = 10; P < 0.05). Intrasplenic PC was measured in the isolated, blood-perfused rat spleen. Intrasplenic infusion of SNAP (0.1 μg · 10 μl−1 · min−1) caused a significant increase in PC (saline: 10.9 ± 0.2 mmHg, n = 3 vs. SNAP: 12.2 ± 0.2 mmHg, n = 3; P < 0.05). Vasoreactivity of preconstricted splenic resistance vessels to sodium nitroprusside (SNP) (1 × 10−12-1 × 10−4 M) and SNAP (1 × 10−10-3 × 10−4 M) was investigated with the use of a wire myograph system. Significantly greater relaxation of arterioles than of venules occurred with both SNP (%maximal vasorelaxation: artery 96 ± 2.3, n = 9 vs. vein 26 ± 1.9, n = 10) and SNAP (%maximal vasorelaxation: artery 50 ± 3.5, n = 11 vs. vein 32 ± 1.7, n = 8). These results are consistent with our proposal that differential vasoreactivity of splenic resistance arteries and veins to NO elevates intrasplenic PC and increases fluid extravasation into the systemic lymphatic system.


1994 ◽  
Vol 77 (1) ◽  
pp. 51-57 ◽  
Author(s):  
C. M. Roos ◽  
G. F. Rich ◽  
D. R. Uncles ◽  
M. O. Daugherty ◽  
D. U. Frank

We localized the sites of vasodilation of inhaled nitric oxide (NO), a selective pulmonary vasodilator, and sodium nitroprusside (SNP) in isolated rat lungs. The sites were determined by analyzing the arterial, venous, and double-occlusion data with a two-resistor (small arteries and veins) three-capacitor (large arteries, large veins, and capillaries) model of the pulmonary vascular bed. Inhaled NO (170 and 670 ppm) and SNP (22.5 and 45.0 micrograms) decreased the small-artery resistance by 7.4 +/- 1.6, 17.2 +/- 2.2, 14.2 +/- 2.8, and 21.4 +/- 3.4% and the small-vein resistance by 13.5 +/- 3.2, 20.3 +/- 3.4 (SNP of 22.5 micrograms not significant), and 9.3 +/- 3.3%, respectively, in blood-perfused lungs (n = 12). Similar results were observed in Krebs-perfused lungs (n = 12). Capillary compliance was unaffected by inhaled NO and SNP. SNP increased the large-artery capacitance by 40.0 +/- 8.6 and 69.3 +/- 9.7%, whereas inhaled NO had no effect. SNP increased the large-vein capacitance by 31.0 +/- 8.7 and 48.0 +/- 10.7%, whereas inhaled NO had no effect in blood-perfused lungs. However, in Krebs-perfused lungs inhaled NO and SNP (45.0 micrograms only) increased the large-vein capacitance by 43.3 +/- 11.9, 41.4 +/- 14.2, and 44.2 +/- 11.0%. In conclusion, in blood-perfused isolated rat lungs inhaled NO and SNP dilate small-resistance arteries and veins, whereas SNP but not inhaled NO dilates larger capacitance arteries and veins. Furthermore, blood appears to prevent the downstream vasodilation by inhaled NO on larger capacitance pulmonary veins.


2011 ◽  
Vol 37 (1) ◽  
pp. 55-59
Author(s):  
Qing QUAN ◽  
Yong TAO ◽  
Xiao-rong ZHANG ◽  
Gui-dong YAO ◽  
Jin-ju WANG

Circulation ◽  
1997 ◽  
Vol 95 (9) ◽  
pp. 2303-2311 ◽  
Author(s):  
Nobuhiko Ito ◽  
Josef Bartunek ◽  
Kenneth W. Spitzer ◽  
Beverly H. Lorell

2009 ◽  
Vol 6 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Yang Li ◽  
Wang Xian-zhong ◽  
Yang Meng-bo ◽  
Zhang Jia-hua

AbstractTo illustrate the effect of nitric oxide (NO) on the microtubules of Sertoli cells (SC), SCs of piglets were treated with sodium nitroprusside (SNP). Changes in cell viability, anti-oxidant activity, enzyme activity and p38 mutagen-activated protein kinase (p38MAPK) activation were detected. The results were as follows. A low concentration of NO can keep SC microtubule and cell viability normal, and a high concentration of NO could increase p38MAPK activation, decrease anti-oxidant activity and transferrin secretion, and destroy the structure and distribution of the microtubules. The results suggest that SNP treatment results in an increase in NO in SCs and decreased cell anti-oxidant activity. The high concentration of NO destroys cell microtubules by activating p38MAPK.


2015 ◽  
Vol 33 (5) ◽  
pp. 1428-1440 ◽  
Author(s):  
Xiufang Ou ◽  
Tingting Zhuang ◽  
Wenchao Yin ◽  
Yiling Miao ◽  
Bo Wang ◽  
...  

Nitric Oxide ◽  
2009 ◽  
Vol 21 (2) ◽  
pp. 126-131 ◽  
Author(s):  
Darren C. Henstridge ◽  
Brian G. Drew ◽  
Melissa F. Formosa ◽  
Alaina K. Natoli ◽  
David Cameron-Smith ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document