Evidence for nitric oxide‐mediated sympathetic forearm vasodiolatation in humans.

Dietz, Niki M.; Engelke, K. A.; Samuel, Terri T.; Fix, R T; Joyner, Michael J.

doi:10.1113/jphysiol.1997.sp021879

Cited by 54 publications

(61 citation statements)

References 29 publications

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“…Finally, after a 15-minute rest period, a 5-minute period of intra-arterial infusion of phentolamine associated with L-NMMA (Clinalfa, 4 mg/min) was conducted. 12,13 Then, new baseline FBF, arterial pressure, heart rate, and MSNA were recorded for 3 minutes, followed by a 3-minute period of hypoxia with phentolamine and L-NMMA infusion. Saline and drugs were infused continuously at rate of 0.5 mL/min.…”

Section: Protocolmentioning

confidence: 99%

“…The ␣-adrenergic blockade phentolamine (Regitine, Ciba Pharmaceutical, Summit, NJ) was formulated at a specific concentration using sterile normal saline and infused into the brachial artery at a dose of 100 m/min, as described previously. [11][12][13] The N G -monomethyl-L-arginine (L-NMMA; Clinalfa, Laufelfingen, Switzerland) was formulated at a specific concentration using sterile normal saline and infused into the brachial artery at a dose of 4 mg/min, as described previously. 14,15 The vitamin C was infused into the brachial artery at a dose of 25 mg/min, a dose that has been shown previously to improve endothelial dysfunction in HF.…”

Section: Drug Preparation and Infusionsmentioning

confidence: 99%

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Mechanisms of Blunted Muscle Vasodilation During Peripheral Chemoreceptor Stimulation in Heart Failure Patients

et al. 2012

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Abstract-We described recently that systemic hypoxia provokes vasoconstriction in heart failure (HF) patients. We hypothesized that either the exaggerated muscle sympathetic nerve activity and/or endothelial dysfunction mediate the blunted vasodilatation during hypoxia in HF patients. Twenty-seven HF patients and 23 age-matched controls were studied. Muscle sympathetic nerve activity was assessed by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. Peripheral chemoreflex control was evaluated through the inhaling of a hypoxic gas mixture (10% O 2 and 90% N 2 ). Basal muscle sympathetic nerve activity was greater and basal FBF was lower in HF patients versus controls. During hypoxia, muscle sympathetic nerve activity responses were greater in HF patients, and forearm vasodilatation in HF was blunted versus controls. Phentolamine increased FBF responses in both groups, but the increase was lower in HF patients. Phentolamine and N G -monomethyl-L-arginine infusion did not change FBF responses in HF but markedly blunted the vasodilatation in controls. FBF responses to hypoxia in the presence of vitamin C were unchanged and remained lower in HF patients versus controls. In conclusion, muscle vasoconstriction in response to hypoxia in HF patients is attributed to exaggerated reflex sympathetic nerve activation and blunted endothelial function (NO activity). We were unable to identify a role for oxidative stress in these studies. (Hypertension. 2012;60:669-676.) • Online Data Supplement Key Words: heart failure � chemoreceptors � vasodilation � sympathetic nervous system � endothelium R esting sympathetic nerve activity is increased in patients with chronic systolic heart failure (HF), and patients with the greatest sympathetic activation have the highest mortality.1,2 Many potential mechanisms underlying the sympathetic excitation in HF have been proposed, including blunted baroreceptor control of central sympathetic outflow.3,4 Augmented peripheral chemoreceptor sensitivity in HF has also been described, which may also underlie the augmented central sympathetic outflow. 5,6 In healthy humans, hypoxia leads to increased blood flow directed to skeletal muscle, and this vasodilatation is mediated by NO release. 7 In a recent study, we reported that, paradoxically, the peripheral chemoreceptor stimulation resulted in skeletal muscle vasoconstriction in HF patients. 6 This unexpected vascular response led us to hypothesize that either the exaggerated sympathetic outflow attributable to chemoreceptor stimulation or the blunted endothelially mediated vasodilatation results in this muscle vasoconstriction during hypoxia in HF patients. In the present study, we describe muscle blood flow responses during peripheral chemoreceptor stimulation with local blockade of postsynaptic ␣-adrenergic receptors and in association with blockade of endothelial NO production in patients with severe HF and in healthy controls. In addition, we describe the effects of vitamin C, an antioxidant, alone, and an ant...

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Section: Protocolmentioning

confidence: 99%

Section: Drug Preparation and Infusionsmentioning

confidence: 99%

Mechanisms of Blunted Muscle Vasodilation During Peripheral Chemoreceptor Stimulation in Heart Failure Patients

et al. 2012

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“…[20][21][22] In addition, NO is involved in regulation of blood flow in organs after exercise and these actions may confound detection of NO effects in the eye during whole body exercise. [23][24][25][26][27] Therefore, NO may play an important role in the mechanism of blood flow changes in ocular and other tissues after exercise. It might be concluded that plasma NO changes explain the changes in ocular blood flow after dynamic exercise from the present experiments.…”

Section: Discussionmentioning

confidence: 99%

Ocular blood flow changes after dynamic exercise in humans

Okuno

Sugiyama

Kohyama

et al. 2005

Eye

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Purpose To investigate control mechanisms for ocular blood flow changes after dynamic exercise using two different methods. Methods Changes over time in the tissue blood flow in the retina and choroid-retina of healthy volunteers were determined after dynamic exercise (Master's double two-step test), using scanning laser Doppler flowmetry (SLDF) and laser speckle flowgraphy (LSFG). Changes in intraocular pressure (IOP), blood pressure, plasma CO 2 gas concentration (pCO 2 ), and levels of nitric oxide (NO) metabolites were examined.Results Retinal blood flow measured by SLDF increased significantly only at 15 min after exercise. In contrast, normalized blur (NB) values in the choroid-retina, obtained by LSFG, increased significantly up to 60 min after exercise. Ocular perfusion pressure (OPP), calculated from IOP and blood pressure, increased significantly immediately and 15 min after exercise. The plasma NO metabolite levels increased significantly, although pCO 2 levels were unchanged. Conclusions Dynamic exercise changes OPP and produces increased tissue blood flow in the retina in the immediate postexercise period, while blood flow increases more persistently in the choroid-retina. Difference in control of blood flow in these two regions may be related to stronger autoregulatory mechanism of blood flow in the retina. Nitric oxide may play a role in the regulation of blood flow.

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“…The RMSSD and pNN50 were related to vagal activity. For the frequency domain method, the power spectrum was analyzed on three tracks, the components of the frequency band of from 0.04 to 0.15 Hz are considered low frequency, which reflect both sympathetic and parasympathetic modulation here (8). The components of between 0.15 and 0.40 Hz are considered high frequency (HF), and reflect the parasympathetic modulation (23).…”

Section: Spectral Analysis Of Heart Rate Variabilitymentioning

confidence: 99%

“…Acutely, the vasodilation during exercise depends upon the equilibrium between vasoconstrictor factors, mediated basically by ␣1-adrenergic and vasodilator forces, mediated by ␤2-adrenergic receptors (10, 36), and local nitric oxide (NO) release (8). The increase in vasodilation after exercise training is endothelium dependent (42) primarily by the shear stress stimulation (12) and by other mechanisms like enhanced acetylcholine (35) and circulating catecholamines (43).…”

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confidence: 99%

Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism

Lemos

Alves

Souza

et al. 2016

Physiological Genomics

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-Besides neuronal plasticity, the neurotrophin brain-derived neurotrophic factor (BDNF) is also important in vascular function. The BDNF has been associated with angiogenesis through its specific receptor tropomyosin-related kinase B (TrkB). Additionally, Val66Met polymorphism decreases activity-induced BDNF. Since BDNF and TrkB are expressed in vascular endothelial cells and aerobic exercise training can increase serum BDNF, this study aimed to test the hypotheses: 1) Serum BDNF levels modulate peripheral blood flow; 2) The Val66Met BDNF polymorphism impairs exercise training-induced vasodilation. We genotyped 304 healthy male volunteers (Val66Val, n ϭ 221; Val66Met, n ϭ 83) who underwent intense aerobic exercise training on a running track three times/wk for 4 mo. We evaluated pre-and post-exercise training serum BDNF and proBDNF concentration, heart rate (HR), mean blood pressure (MBP), forearm blood flow (FBF), and forearm vascular resistance (FVR). In the pre-exercise training, BDNF, proBDNF, BDNF/proBDNF ratio, FBF, and FVR were similar between genotypes. After exercise training, functional capacity (V O2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P ϭ 0.04) and BDNF/proBDNF ratio (interaction, P Ͻ 0.001). Interestingly, FBF (interaction, P ϭ 0.04) and the FVR (interaction, P ϭ 0.01) responses during handgrip exercise (HG) improved in Val66Val compared with Val66Met, even with similar responses of HR and MBP. There were association between BDNF/proBDNF ratio and FBF (r ϭ 0.64, P Ͻ 0.001) and FVR (r ϭ Ϫ0.58, P Ͻ 0.001) during HG exercise. These results show that peripheral vascular reactivity and serum BDNF responses to exercise training are impaired by the BDNF Val66Met polymorphism and such responsiveness is associated with serum BDNF concentrations in healthy subjects.BDNF Val66Met polymorphism; exercise training; vascular reactivity EXERCISE TRAINING HAS BEEN considered a key element in the improvement in brain-derived neurotrophic factor (BDNF) levels (39), which is the strongest factor linking exercise with cognitive benefits. However, the variability of individual responses may be linked to genetic differences.While BDNF promotes neuronal survival and enhanced synaptic plasticity by activating the tropomyosin kinase B (TrkB) receptor, the action of its precursor proBDNF results in apoptosis by interacting with the p75 neurotrophin receptor (p75NTR), and both are significantly involved in different physiological functions (15,53).Considering the fact that the BDNF gene and its TrkB receptor are expressed in several tissues, such as brain, heart, lungs, and endothelial cells (12, 28), besides neuronal plasticity, it is possible that the neurotrophin BDNF also is involved in the health of other tissues. Indeed, besides the hippocampus, the circulating BDNF is produced by a number of peripheral nonneuronal tissues, including vascular endothelial cells (28,53). Moreover, the neurotrophin BDNF has been associated with angiogenesis thro...

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Evidence for nitric oxide‐mediated sympathetic forearm vasodiolatation in humans.

Cited by 54 publications

References 29 publications

Mechanisms of Blunted Muscle Vasodilation During Peripheral Chemoreceptor Stimulation in Heart Failure Patients

Mechanisms of Blunted Muscle Vasodilation During Peripheral Chemoreceptor Stimulation in Heart Failure Patients

Ocular blood flow changes after dynamic exercise in humans

Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism

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