Enhanced Nitric Oxide-Mediated Vascular Relaxation in Radial Artery Compared With Internal Mammary Artery or Saphenous Vein

Shapira, Oz M.; Xu, Aiming; Aldea, Gabriel S.; Vita, Joseph A.; Shemin, Richard J.; Keaney, John F.

doi:10.1161/01.cir.100.suppl_2.ii-322

Cited by 65 publications

(60 citation statements)

References 26 publications

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“…27 Furthermore, in a previous in vitro study, endotheliumdependent dilation was intact in segments of radial artery (which is adjacent to the brachial artery) obtained from patients with advanced coronary artery disease. 28 The present study may help clarify these apparent discrepancies because our data suggest that the observed reductions in hyperemiainduced FMD% in individuals with various CRFs are attributable largely to a reduction in the stimulus for dilation during hyperemia rather than impairment in local endothelial function in the brachial artery.…”

Section: Mitchell Et Al Shear Stress and Endothelial Functionmentioning

confidence: 68%

Local Shear Stress and Brachial Artery Flow-Mediated Dilation

et al. 2004

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Abstract-Endothelium-dependent flow-mediated dilation is a homeostatic response to short-term increases in local shear stress. Flow-mediated dilation of the brachial artery in response to postischemic reactive hyperemia is impaired in patients with cardiovascular disease risk factors and may reflect local endothelial dysfunction in the brachial artery. However, previous studies have largely neglected the effect of risk factors on evoked shear stress, which is the stimulus for dilation. We evaluated brachial artery percent dilation and evoked diastolic shear stress during reactive hyperemia using high-resolution ultrasound and Doppler in 2045 participants (1107 women, mean age 61 years) in the Framingham Offspring Study. In age-and sex-adjusted models, baseline and hyperemic shear stress were related to brachial artery percent dilation. In stepwise multivariable analyses examining clinical correlates of percent dilation (without shear stress in the model), age, sex, mean arterial pressure, pulse pressure, heart rate, body mass index, lipid medication use, and hormone replacement therapy were related to percent dilation (R 2 ϭ0.189; PϽ0.001). When hyperemic shear stress was incorporated, the overall R 2 improved (R 2 ϭ0.335; PϽ0.001), but relationships between risk factors and percent dilation were attenuated (age and mean arterial pressure) or no longer significant (all others). In contrast, risk factors were related to baseline and hyperemic shear stress in multivariable analyses. Evoked hyperemic shear stress is a major correlate of brachial artery flow-mediated dilation. The associations between many risk factors and brachial artery flow-mediated dilation may be attributable to reduced stimulus for dilation rather than impaired local conduit artery response during hyperemia. Key Words: endothelium Ⅲ microcirculation Ⅲ risk factors L ocal shear stress (SS) has important short-and long-term effects on the vascular endothelium that are relevant to atherogenesis. 1,2 Under normal conditions, the vascular endothelium responds to short-term increases in flow by releasing NO and other endothelium-dependent relaxing factors that dilate the artery and reduce SS toward normal. 3 Flow-mediated dilation (FMD) is impaired in atherosclerotic coronary arteries, 4 although the response is maintained in patients with hypercholesterolemia and angiographically normal arteries. 5 FMD has been studied noninvasively in the brachial artery by using reactive hyperemia after a short period of forearm ischemia as the flow stimulus and evaluating percentage increase in brachial artery diameter (FMD%). 6 Brachial artery FMD% is impaired in patients with cardiovascular disease risk factors (CRFs) or coronary atherosclerosis. 7 Reactive hyperemia largely reflects dilation of resistance vessels by ischemia-induced production of vasodilators including NO. 8 Although not widely appreciated, some studies have demonstrated a reduction in reactive hyperemia in patients with CRFs 9,10 or coronary artery disease. 7 Because reactive hyperemia is th...

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Section: Mitchell Et Al Shear Stress and Endothelial Functionmentioning

confidence: 68%

Local Shear Stress and Brachial Artery Flow-Mediated Dilation

et al. 2004

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“…5,6 Endothelial function is a predictor of coronary events in patients with coronary artery disease 7,8 and is associated with short-term coronary graft performance. 2 Greater endothelium-dependent relaxation occurs in vitro in precontracted IMA compared with SV after harvesting for coronary artery bypass surgery, 9,10 and although exposure of vein grafts to arterial pressure might be expected to result in further dysfunction of the endothelium, 11,12 heterogeneity in endothelium-dependent relaxation response, not related to duration of arterialization but to localized areas of intimal hyperplasia, has been reported. 13 Previous studies have shown preserved IMA graft vascular reactivity in vivo a number of years after surgery 14,15 ; however, at present there are few data describing the vascular function of the RA as an in vivo coronary conduit over the longer term.…”

Section: Editorial See P 857 Clinical Perspective On P 867mentioning

confidence: 99%

Vascular Reactivity and Flow Characteristics of Radial Artery and Long Saphenous Vein Coronary Bypass Grafts

et al. 2010

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Background-Radial artery (RA) aortocoronary bypass grafts anastomosed to a branch of the circumflex coronary artery have significantly better patency rates than saphenous vein (SV) grafts at 5 years, but the physiological characteristics and mechanisms involved are not clearly defined. We compared RA and SV graft vasomotor and flow responses to endothelium-dependent and -independent stimuli 5 years after surgery in a subgroup of patients enrolled in the Radial artery versus Saphenous Vein Patency (RSVP) trial. Methods and Results-Twenty-seven patients were included in the study (RA, nϭ15; SV, nϭ12). Graft blood flow was calculated from flow velocity, measured by intracoronary Doppler, and luminal diameter, measured by quantitative coronary angiography, before and after intragraft infusions of adenosine, acetylcholine, and isosorbide dinitrate. At rest, RA luminal diameters were significantly smaller than SV luminal diameters (Pϭ0.029), blood flow velocity was greater in RA than SV (Pϭ0.008), and volume blood flows were similar. RA but not SV dilated in response to adenosine and isosorbide dinitrate (all PϽ0.05, RA versus SV, percent change from baseline), and there were no significant differences in the diameter responses to acetylcholine. Volume blood flow responses to adenosine, acetylcholine, and isosorbide dinitrate were comparable. Conclusions-Five years after surgery, RA coronary bypass conduits grafted to a single coronary territory demonstrated preserved flow-mediated vasodilatation, whereas SV grafts did not. Our results may provide insight into the more favorable patency of RA grafts over SV grafts. Clinical Trial Registration-http://www.clinicaltrials.gov.

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“…Other studies suggest that the endothelial function of radial artery is similar to that of the IMA (25,26). However, other investigators have reported differences in endothelium-derived NO release and hyperpolarizing factor in the IMA and radial artery (27,28 This has led researchers to look for experimental models for functional experiments in an attempt to avoid the detrimental impact of these cardiovascular risk factors on vasoreactivity. Recently, we addressed the neurogenic contractions produced in porcine radial artery using a combined histological/functional approach (4).…”

Section: +mentioning

confidence: 99%

Modulation of Noradrenergic Neurotransmission in Isolated Rat Radial Artery

et al. 2009

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Abstract. The present study was designed to characterize the neurogenic contraction of rat radial artery. Electrical field stimulation (EFS) evoked frequency-dependent contraction that was abolished by tetrodotoxin (neuronal Na + channel blocker), guanethidine (sympathetic neuron blocker), or phentolamine (α-adrenoceptor blocker). The α 1 -adrenoceptor antagonist prazosin inhibited endothelium-independent contractions to EFS, noradrenaline (NA), and the α 1 -adrenoceptor agonist phenylephrine. Rauwolscine, an α 2 -adrenoceptor antagonist, augmented nerve-mediated contractions and reduced sensitivity to NA and the α 2 -adrenoceptor agonist BHT-920. The β-adrenoceptor antagonist propranolol diminished EFS-elicited contractions, while sensitivity to NA was enhanced by propranolol. Relaxations evoked by isoproterenol, a β-adrenoceptor agonist, were abolished by propranolol. N G -Nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, increased both nerve-mediated and NA-induced responses in endothelium-intact, but not in endothelium-denuded arteries. Moreover, endothelium-dependent responses to BHT-920 and isoproterenol were modified by L-NOARG. Tetraethylammonium (TEA) or 4-amynopyridine, the Ca 2+ -activated (K Ca ) or voltage-dependent K + (K V ) channel blockers, respectively, enhanced the neurogenic contractions observed. TEA but not 4-amynopyridine increased NA-induced contractions. The ATP-sensitive K + (K ATP )-channel blocker glibenclamide failed to modify adrenergic contractions. Blockade of capsaicin-sensitive primary afferents increased EFS-induced contractions. In conclusion, adrenergic contractions are predominantly mediated by muscular α 1 -adrenoceptors, while endothelial α 2 -and β-adrenoceptors play a minor role. Presynaptic α 2 -and β-adrenoceptors cannot be precluded. Noradrenergic neurotransmission in rat radial artery seems to be modulated by both stimulation of endothelial NO, K Ca , and K V channels and sensory C-fiber activation.

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Enhanced Nitric Oxide-Mediated Vascular Relaxation in Radial Artery Compared With Internal Mammary Artery or Saphenous Vein

Cited by 65 publications

References 26 publications

Local Shear Stress and Brachial Artery Flow-Mediated Dilation

Local Shear Stress and Brachial Artery Flow-Mediated Dilation

Vascular Reactivity and Flow Characteristics of Radial Artery and Long Saphenous Vein Coronary Bypass Grafts

Modulation of Noradrenergic Neurotransmission in Isolated Rat Radial Artery

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