Nitric oxide release from human corpus cavernosum induced by a purified scorpion toxin

Urology ◽  
2004 ◽  
Vol 63 (1) ◽  
pp. 184-189 ◽  
Author(s):  
Cleber E. Teixeira ◽  
Juliano F. de Oliveira ◽  
Juliana S. Baracat ◽  
Fernanda B.M. Priviero ◽  
Cristina E. Okuyama ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Corpus Cavernosum ◽  
Scorpion Toxin ◽  
Nitric Oxide Release

Comparative Relaxing Effects of Sildenafil, Vardenafil, and Tadalafil in Human Corpus Cavernosum: Contribution of Endogenous Nitric Oxide Release

Urology ◽  
2009 ◽  
Vol 74 (1) ◽  
pp. 216-221 ◽  
Author(s):  
Haroldo A. Toque ◽  
Fernanda B.M. Priviero ◽  
Cleber E. Teixeira ◽  
Mário A. Claudino ◽  
Juliana S. Baracat ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Corpus Cavernosum ◽  
Nitric Oxide Release ◽  
Endogenous Nitric Oxide

Estradiol-stimulated nitric oxide release in nervous tissue, vasculature, and gonads of the giant cockroachBlaberus craniifer

2004 ◽  
Vol 55 (1-4) ◽  
pp. 143-148 ◽  
Author(s):  
F. E. Nieto-Fernandez ◽  
F. Ianuzzi ◽  
Adriana Ruiz ◽  
Lilian Nodimele
Keyword(s):  
Nitric Oxide ◽  
Nervous Tissue ◽  
Nitric Oxide Release

Controlled Nitric Oxide Release Using Poly(lactic-co-glycolic acid) Nanoparticles for Anti-Inflammatory Effects

2020 ◽  
Vol 21 (12) ◽  
pp. 4972-4979
Author(s):  
Yoogyeong Oh ◽  
Hyejoong Jeong ◽  
Sungmin Lim ◽  
Jinkee Hong
Keyword(s):  
Nitric Oxide ◽  
Glycolic Acid ◽  
Nitric Oxide Release ◽  
Anti Inflammatory

Nitric oxide release in rat skeletal muscle capillary

1996 ◽  
Vol 270 (5) ◽  
pp. H1696-H1703 ◽  
Author(s):  
D. Mitchell ◽  
K. Tyml
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Leukocyte Adhesion ◽  
Microvascular Blood Flow ◽  
Capillary Length ◽  
Nitric Oxide Release ◽  
Longus Muscle ◽  
Potent Vasodilator ◽  
Capillary Bed ◽  
Synthase Inhibitor

Nitric oxide (NO) has been shown to be a potent vasodilator released from endothelial cells (EC) in large blood vessels, but NO release has not been examined in the capillary bed. Because the capillary bed represents the largest source of EC, it may be the largest source of vascular NO. In the present study, we used intravital microscopy to examine the effect of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on the microvasculature of the rat extensor digitorum longus muscle. L-NAME (30 mM) applied locally to a capillary (300 micron(s) from the feeding arteriole) reduced red blood cell (RBC) velocity [VRBC; control VRBC = 238 +/- 58 (SE) micron/s; delta VRBC = -76 +/- 8%] and RBC flux (4.4 +/- 0.7 to 2.8 +/- 0.7 RBC/s) significantly in the capillary, but did not change feeding arteriole diameter (Dcon = 6.3 +/- 0.7 micron, delta D = 5 +/- 7%) or draining venule diameter (Dcon = 10.1 +/- 0.6 micron, delta D = 4 +/- 2%). Because of the VRBC change, the flux reduction was equivalent to an increased local hemoconcentration from 1.8 to 5 RBCs per 100 micron capillary length. L-NAME also caused an increase in the number of adhering leukocytes in the venule from 0.29 to 1.43 cells/100 micron. L-NAME (30 mM) applied either to arterioles or to venules did not change capillary VRBC. Bradykinin (BK) locally applied to the capillary caused significant increases in VRBC (delta VRBC = 111 +/- 23%) and in arteriolar diameter (delta D = 40 +/- 5%). This BK response was blocked by capillary pretreatment with 30 mM L-NAME (delta VRBC = -4 +/- 27%; delta D = 5 +/- 9% after BK). We concluded that NO may be released from capillary EC both basally and in response to the vasodilator BK. We hypothesize that 1) low basal levels of NO affect capillary blood flow by modulating local hemoconcentration and leukocyte adhesion, and 2) higher levels of NO (stimulated by BK) may cause a remote vasodilation to increase microvascular blood flow.

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