scholarly journals Effect of Increased Nitric Oxide Bioavailability on Endothelial Function and Pulse Wave Velocity

2018 ◽  
Vol 50 (5S) ◽  
pp. 592-593
Author(s):  
Evan J. Bockover ◽  
Sierra Crowe ◽  
Brycen J. Ratcliffe ◽  
Caleb D. Harrison ◽  
Alberto Friedmann ◽  
...  
2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Juan Torrado ◽  
Yanina Zócalo ◽  
Ignacio Farro ◽  
Federico Farro ◽  
Claudio Sosa ◽  
...  

Introduction.Flow-mediated dilation (FMD), low flow-mediated constriction (L-FMC), and reactive hyperemia-related changes in carotid-to-radial pulse wave velocity (ΔPWVcr%) could offer complementary information about both “recruitability” and “resting” endothelial function (EF). Carotid-to-femoral pulse wave velocity (PWVcf) and pulse wave analysis-derived parameters (i.e., AIx@75) are the gold standard methods for noninvasive evaluation of aortic stiffness and central hemodynamics. If healthy pregnancy is associated with both changes in resting and recruitable EF, as well as in several arterial parameters, it remains unknown and/or controversial.Objectives.To simultaneously and noninvasively assess in healthy pregnant (HP) and nonpregnant (NP) women central parameters in conjunction with “basal and recruitable” EF, employing new complementary approaches.Methods.HP (n=11, 34.2 ± 3.3 weeks of gestation) and age- and cardiovascular risk factors-matched NP (n=22) were included. Aortic blood pressure (BP), AIx@75, PWVcf, common carotid stiffness, and intima-media thickness, as well as FMD, L-FMC, and ΔPWVcr %, were measured.Results.Aortic BP, stiffness, and AIx@75 were reduced in HP. ΔPWVcr% and FMD were enhanced in HP in comparison to NP. No differences were found in L-FMC between groups.Conclusion.HP is associated with reduced aortic stiffness, central BP, wave reflections, and enhanced recruitable, but not resting, EF.


Hypertension ◽  
2003 ◽  
Vol 42 (5) ◽  
pp. 915-918 ◽  
Author(s):  
Andrew D. Stewart ◽  
Sandrine C. Millasseau ◽  
Mark T. Kearney ◽  
James M. Ritter ◽  
Philip J. Chowienczyk

2018 ◽  
Vol 69 (9) ◽  
pp. 2351-2356 ◽  
Author(s):  
Angela Cozma ◽  
Adela Sitar Taut ◽  
Olga Orasan ◽  
Lucia Maria Procopciuc ◽  
Anca Daniela Farcas ◽  
...  

Metabolic syndrome (MS) is a clustering entity characterized by obesity, hypertension, hyperglycemia, dyslipidemia, and insulin resistance. Atherosclerotic lesions may be a complication of MS, arising from endothelial dysfunction and induced by decreased nitric oxide (NO) production. NO is synthesized by nitric oxide synthase (eNOS), encoded by the NOS3 gene, and displays anti-inflammatory, vasodilatory, and antiproliferative effects.We aimed to investigate the relationship between the G894T polymorphism of the eNOS gene and metabolic syndrome (including its components) and the association of this polymorphism with arterial function, assessed by determining pulse wave velocity and the augmentation index.The study included 100 consecutive patients, 55% with metabolic syndrome (based on IDF criteria -study group), 45% without MS (control group). Arterial stiffness was measured using TensioMedTMArteriograph. The presence of the homozygous (TT) or heterozygous (GT) state was associated, compared to subjects without the mutation (GG), with an increased prevalence of arterial hypertension, diabetes mellitus, with an increase of abdominal circumference, an increase of triglycerides, without significantly influencing the level of HDL. No significant differences were found between patients with G894T polymorphism compared to those without the mutation regarding the arterial stiffness. The eNOS gene polymorphism: 894G]T was significantly associated with the presence of MS; the polymorphism in homozygous and heterozygous state was associated with an increased risk of metabolic syndrome. G894T polymorphism did not significantly influence the values of the studied arterial parameters (pulse wave velocity, aortic and brachial augmentation index).


2005 ◽  
Vol 27 (3) ◽  
pp. 302-309 ◽  
Author(s):  
Katerina K. Naka ◽  
Ann C. Tweddel ◽  
Sagar N. Doshi ◽  
Jonathan Goodfellow ◽  
Andrew H. Henderson

2016 ◽  
Vol 101 (3) ◽  
pp. 1198-1206 ◽  
Author(s):  
Linda A. Jahn ◽  
Lee Hartline ◽  
Nagashree Rao ◽  
Brent Logan ◽  
Justin J. Kim ◽  
...  

Abstract Context: Insulin reportedly impairs endothelial function in conduit arteries but improves it in resistance and microvascular arterioles in healthy humans. No studies have assessed endothelial function at three arterial levels in healthy or metabolic syndrome (METSYN) subjects. Objective: The objective of the study was to compare endothelial responsiveness of conduit arteries, resistance, and microvascular arterioles to insulin in healthy and METSYN subjects. Design: We assessed conduit, resistance, and microvascular arterial function in the postabsorptive and postprandial states and during euglycemic hyperinsulinemia (insulin clamp). Setting: The study was conducted at a clinical research unit. Participants: Age-matched healthy and METSYN subjects participated in the study. Interventions: We used brachial flow-mediated dilation, forearm postischemic flow velocity, and contrast-enhanced ultrasound to assess the conduit artery, resistance arteriole, and microvascular arteriolar endothelial function, respectively. We also assessed the conduit artery stiffness (pulse wave velocity and augmentation index) and measured the plasma concentrations of 92 cardiovascular disease biomarkers at baseline and after the clamp. Results: Postabsorptive and postprandial endothelial function was similar in controls and METSYN in all tested vessels. METSYN subjects were metabolically insulin resistant (P < .005). In controls, but not METSYN subjects, during euglycemic hyperinsulinemia, endothelial function improved at each level of arterial vasculature (P < .05 or less for each). Conduit vessel stiffness (pulse wave velocity) was increased in the METSYN group. Twelve of 92 biomarkers differed at baseline (P < .001) and remained different at the end of the insulin clamp. Conclusions: We conclude that insulin enhances arterial endothelial function in health but not in METSYN, and this vascular insulin resistance may underlie its increased cardiovascular disease risk.


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