scholarly journals Polycystin deficiency induces dopamine-reversible alterations in flow-mediated dilatation and vascular nitric oxide release in humans

2015 ◽  
Vol 87 (2) ◽  
pp. 465-472 ◽  
Author(s):  
Aurélien Lorthioir ◽  
Robinson Joannidès ◽  
Isabelle Rémy-Jouet ◽  
Caroline Fréguin-Bouilland ◽  
Michèle Iacob ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Release ◽  
Flow Mediated Dilatation

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.

Flow-mediated dilatation following wrist and upper arm occlusion in humans: the contribution of nitric oxide

2001 ◽  
Vol 101 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Sagar N. DOSHI ◽  
Katerina K. NAKA ◽  
Nicola PAYNE ◽  
Christopher J.H. JONES ◽  
Moira ASHTON ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Peak Flow ◽  
Ultrasound Probe ◽  
Upper Arm ◽  
Flow Mediated Dilatation ◽  
Synthase Inhibitor ◽  
Increased Blood Flow ◽  
Similar Peak

Flow-mediated dilatation (FMD) of the brachial artery assessed by high-resolution ultrasound is widely used to measure endothelial function. However, the technique is not standardized, with different groups using occlusion of either the wrist or the upper arm to induce increased blood flow. The validity of the test as a marker of endothelial function rests on the assumption that the dilatation observed is endothelium-dependent and mediated by nitric oxide (NO). We sought to compare the NO component of brachial artery dilatation observed following wrist or upper arm occlusion. Dilatation was assessed before and during intra-arterial infusion of the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA) following occlusion of (i) the wrist (distal to ultrasound probe) and (ii) the upper arm (proximal to ultrasound probe) for 5min in ten healthy males. Dilatation was significantly greater after upper arm occlusion (upper arm, 11.62±3.17%; wrist, 7.25±2.49%; P = 0.003). During l-NMMA infusion, dilatation after wrist occlusion was abolished (from 7.25±2.49% to 0.16±2.24%; P < 0.001), whereas dilatation after upper arm occlusion was only partially attenuated (from 11.62±3.17% to 7.51±2.34%; P = 0.006). The peak flow stimulus was similar after wrist and upper arm occlusion. We conclude that dilatation following upper arm occlusion is greater than that observed after wrist occlusion, despite a similar peak flow stimulus. l-NMMA infusion revealed that FMD following wrist occlusion is mediated exclusively by NO, while dilatation following upper arm occlusion comprises a substantial component not mediated by NO, most probably related to tissue ischaemia around the brachial artery. FMD following wrist occlusion may be a more valid marker of endothelial function than dilatation following upper arm occlusion.

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