scholarly journals Role of nitric oxide in the regulation of digital pulse volume amplitude in humans

2006 ◽  
Vol 101 (2) ◽  
pp. 545-548 ◽  
Author(s):  
Anju Nohria ◽  
Marie Gerhard-Herman ◽  
Mark A. Creager ◽  
Shauna Hurley ◽  
Debi Mitra ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Healthy Subjects ◽  
Reactive Hyperemia ◽  
Nitric Oxide Synthesis ◽  
Pulse Volume ◽  
Digital Pulse ◽  
Peripheral Arterial ◽  
Nitric Oxide Bioavailability

Measurement of the increase in digital pulse volume amplitude (PVA) during reactive hyperemia relative to baseline (PVA-RH) is being applied widely as a convenient test of nitric oxide bioavailability. However, evidence linking digital PVA-RH to nitric oxide is currently lacking. Accordingly, we investigated whether nitric oxide is responsible for the increase in digital PVA. During reactive hyperemia, we used a peripheral arterial tonometer to record digital PVA at baseline and during reactive hyperemia. The role of nitric oxide in these responses was investigated in 19 healthy subjects by inhibiting nitric oxide synthesis with NG-nitro-l-arginine methyl ester (l-NAME). Ten subjects underwent the identical protocol with saline and five with phenylephrine, a nonspecific vasoconstrictor, instead of l-NAME. The change in digital PVA after drug administration was compared between the three groups. Relative to the response with saline (−5 ± 2%), baseline PVA was unchanged by l-NAME infusion (−10 ± 2%), but it decreased significantly with phenylephrine (−50 ± 12%; P = 0.003). PVA-RH increased slightly with saline infusion (9 ± 4%). In comparison, PVA-RH was significantly blunted by l-NAME administration (−46 ± 21%; P = 0.002) and was relatively unchanged by phenylephrine (20 ± 9%). The present study establishes a central role for nitric oxide in the augmentation of PVA during reactive hyperemia. The measurement of digital PVA-RH may indeed provide a simple means of assessing endothelial function in humans.

Abstract P37: Evidence of Impaired Vascular Reactivity Following Dust Exposure in Participants in the World Trade Center Medical Monitoring and Treatment Program

2011 ◽  
Vol 4 (suppl_2) ◽  
Author(s):  
Simonette T Sawit ◽  
Mary Ann McLaughlin ◽  
Ana Garcia Alvarez ◽  
Dewan Kazi Fahima ◽  
Cynara Maceda ◽  
...  
Keyword(s):  
Treatment Program ◽  
Vascular Reactivity ◽  
Reactive Hyperemia ◽  
Medical Monitoring ◽  
Volume Changes ◽  
Peripheral Arterial Tonometry ◽  
Pulse Volume ◽  
Arterial Tonometry ◽  
Digital Pulse ◽  
Peripheral Arterial

INTRODUCTION: Exposure to particulate matter (PM) has been investigated as an additional risk factor for cardiovascular disease (CVD). It is likely that different mechanisms, including vascular dysfunction, are responsible for acute and chronic toxic effects. In participants of the Law Enforcement Cardiovascular Screening Program (LECS), a subset of the WTC Medical Monitoring and Treatment Program, we look to characterize the relationship between PM exposure and vascular reactivity (surrogate for endothelial function), as measured by peripheral arterial tonometry (PAT). METHODS: PAT, a system comprised of a finger probe to assess digital volume changes accompanying pulse waves, was used. Digital pulse volume changes during reactive hyperemia was assessed in 60 patients with either high (n=33) or low (n=27) PM exposure. PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pulse volume during reactive hyperemia divided by that at baseline. All data were prospectively obtained. We define highest inhaled PM exposure as occurring on 9/11/2001, and lower inhaled PM exposure as occurring on or after 9/13/2001. A PAT index of 1.67 or less was considered to represent abnormal vascular reactivity. RESULTS: Mean age was 49 years (range 45-53), 83% were male. There were no significant differences in baseline characteristics, including CVD risk factors. Median PAT was 1.87 (1.30-2.75) for subjects with lower exposure and 1.68 (1.15-3.22) for subjects with highest exposure to PM. Of subjects with highest exposure to PM, 68% (17/33) had a PAT index 1.67 or less, compared with 32% (8/27), of subjects with lower exposure (p value=0.17). The odds of having abnormal PAT index to normal PAT index was 2.1 times higher in subjects with highest exposure compared to those with lower exposure to PM (95%CI 0.7-6.2). CONCLUSION: We observe a trend correlating highest WTC inhaled PM exposure with abnormal vascular reactivity as measured by peripheral arterial tonometry index of 1.67 or less. The clinical impact of this finding, in this pilot study, requires further investigation.

Vascular Hyporesponsiveness in Aortic Rings from Cirrhotic Rats: Role of Nitric Oxide and Endothelium

1996 ◽  
Vol 91 (6) ◽  
pp. 733-738 ◽  
Author(s):  
M. Clara Oriíz ◽  
Lourdes A. Fortepiani ◽  
Concha Martínez ◽  
Noemí M. Atucha ◽  
Joaquín García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Bile Duct ◽  
Methyl Ester ◽  
Nitric Oxide Synthesis ◽  
Experimental Conditions ◽  
Nitric Oxide Release ◽  
Oxide Synthase ◽  
And Control ◽  
Inducible Nitric Oxide

1. The role of nitric oxide as mediator of the vascular alterations present in different models of experimental liver cirrhosis is controversial. In the present study, we evaluated the role of nitric oxide and that of the endothelium in the response to phenylephrine and acetylcholine of isolated aortic rings from chronic bile duct-ligated (29 days) rats and their corresponding controls. Experiments were performed in rings with or without endothelium, in rings pretreated with N-ω-nitro-l-arginine methyl ester (10−4 mol/l) to inhibit nitric oxide synthesis and in rings pretreated with aminoguanidine (10−4 mol/l) to inhibit inducible nitric oxide synthesis. 2. Under basal conditions, the maximum absolute tension developed in response to cumulative addition of phenylephrine was significantly decreased in rings from bile duct-ligated animals (1.62 ± 0.06 g) compared with the control rings (2.15 ± 0.099). This hyporesponsiveness to phenylephrine of rings from bile duct-ligated animals was corrected after treatment with N-ω-nitro-l-arginine methyl ester and reduced, but not completely eliminated, in rings without endothelium. In contrast, aminoguanidine did not modify the lower response to phenylephrine rings from bile duct-ligated animals. ED50 values were not different between groups under any experimental conditions. 3. The endothelium-dependent vasodilatation to acetylcholine in phenylephrine-constricted rings was similar in both groups of animals, control and bile duct ligated, under all experimental conditions. N-ω-nitro-l-arginine methyl ester pretreatment and removal of the endothelium completely abolished the response to acetylcholine in cirrhotic and control rings. 4. These results demonstrate that in aortic rings from cirrhotic, bile duct-ligated rats, increased production of nitric oxide, mainly of endothelial origin, is responsible for the lower contractile response to phenylephrine. Our data, however, do not support the involvement of the inducible nitric oxide synthase isoform in this alteration. In contrast, endothelial vasodilatory response to acetylcholine is not altered in this model of cirrhosis, which indicates that not all mechanisms of nitric oxide release are abnormal.

On the role of mechanosensitive mechanisms eliciting reactive hyperemia

2002 ◽  
Vol 283 (6) ◽  
pp. H2250-H2259 ◽  
Author(s):  
Akos Koller ◽  
Zsolt Bagi
Keyword(s):  
Nitric Oxide ◽  
Tyrosine Kinases ◽  
Reactive Hyperemia ◽  
Nitric Oxide Synthesis ◽  
Rat Skeletal Muscle ◽  
Flow Shear ◽  
Hemodynamic Forces ◽  
Flow Shear Stress ◽  
Isolated Rat

We hypothesized that changes in hemodynamic forces such as pressure (P) and flow (F) contribute importantly to the development of reactive hyperemia. To exclude the effects of vivo factors, isolated rat skeletal muscle arterioles (∼130 μm) were utilized. We found that changes in P or P + F following occlusions elicited reactive dilations (RD). The peak of RD (up to ∼45 μm), but not the duration of RD, increased to changes in P (80 to 10, then back to 80 mmHg) as a function of the length of occlusions (30, 60, and 120 s). However, changes in P + F (80–10 -80 mmHg + 25–0-25 μl/min) increased both the peak and duration of RD (from ∼25 to 90 s) with longer occlusions. When only P changed, inhibition of nitric oxide synthesis or endothelium removal (E−) reduced only the peak of RD, whereas when P + F were changed, both the peak and duration of RD became reduced. Inhibition of stretch-activated cation channels by gadolinium reduced the peak but enhanced the duration of RD (both to P or P + F) that was unaffected by N G-nitro-l-arginine methyl ester (l-NAME) or by E−. When only P changed, inhibition of tyrosine kinases by genistein reduced peak RD but did not affect the RD duration. However, when P + F changed, genistein reduced both the peak and the duration of RD, additional l-NAME reduced the peak RD, but did not affect the duration of RD. Thus in isolated arterioles an RD resembling the characteristics of reactive hyperemia can be generated that is elicited by deformation, stretch, pressure, and flow/shear stress-sensitive mechanisms and is, in part, mediated by nitric oxide.

Role of NO in goat basal cerebral circulation and after vasodilatation to hypercapnia or brief ischemias

1993 ◽  
Vol 265 (6) ◽  
pp. R1410-R1415 ◽  
Author(s):  
G. Dieguez ◽  
J. L. Garcia ◽  
N. Fernandez ◽  
A. L. Garcia-Villalon ◽  
L. Monge ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
Systemic Arterial Pressure ◽  
Nitric Oxide Production ◽  
Hemodynamic Effects ◽  
Arterial Pco2 ◽  
Different Levels

The role of nitric oxide (NO) in the cerebral circulation under basal conditions and after vasodilatation to hypercapnia or reactive hyperemias was studied in 17 anesthetized goats. The intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME, 3-4 or 8-10 mg/kg), an inhibitor of nitric oxide production, reduced middle cerebral artery (MCA) flow (electromagnetically measured) by 19 and 30% and increased systemic arterial pressure by 21 and 26%, respectively, whereas heart rate did not significantly change; MCA resistance increased by 48 and 86%, respectively. These hemodynamic effects were reversed by L-arginine (200-300 mg/kg iv; 5 goats). Different levels of hypercapnia (PCO2 of 30-35, 40-45, and 55-65 mmHg) (12 goats) produced arterial PCO2-dependent increases in MCA flow that were similar under control and L-NAME treatment. Graded cerebral hyperemia occurred after 5, 10, and 20 s of MCA occlusion in 5 goats, but its magnitude was decreased during L-NAME treatment. It suggests that, in the cerebral circulation, nitric oxide 1) produces a basal vasodilator tone and 2) is probably not involved in the vasodilatation to hypercapnia but may mediate hyperemic responses after short brain ischemias.

scholarly journals A mathematical model for the role of N 2 O 3 in enhancing nitric oxide bioavailability following nitrite infusion

Nitric Oxide ◽  
2016 ◽  
Vol 60 ◽  
pp. 1-9 ◽  
Author(s):  
Yien Liu ◽  
Donald G. Buerk ◽  
Kenneth A. Barbee ◽  
Dov Jaron
Keyword(s):  
Nitric Oxide ◽  
Mathematical Model ◽  
Nitric Oxide Bioavailability

scholarly journals a possible role of endogenous inhibitors for nitric oxide synthesis in the lower urinary tracts

2000 ◽  
Vol 82 ◽  
pp. 57
Author(s):  
Hitoshi Masuda ◽  
Toshihiko Tsujii ◽  
Hiroyuki Oshima ◽  
Moritaka Goto ◽  
Hiroshi Azuma
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthesis ◽  
Endogenous Inhibitors ◽  
Lower Urinary

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

1996 ◽  
Vol 271 (1) ◽  
pp. G27-G35
Author(s):  
J. G. Wood ◽  
Q. Zhang ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Question Mark ◽  
Endothelin 1 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

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