Responses in muscle sympathetic activity to acute hypoxia in humans

Saito, Mitsuru; Mano, Tadaaki; Iwase, Satoshi; Koga, Kazushi; Abe, Hiroshi; Yamazaki, Yoji

doi:10.1152/jappl.1988.65.4.1548

Cited by 161 publications

(140 citation statements)

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“…We conclude that the greater blood flow during hypoxia in healthy humans compared with HF patients is attributable to endothelium-mediated vasodilatation, because L-NMMA infusion during hypoxia eliminated this augmented FBF in healthy humans. As reported previously, 9,[17][18][19] chemoreceptor stimulation by systemic hypoxia provokes increases in sympathetic nerve activity. Our study is consistent with these previous studies.…”

Section: Discussionsupporting

confidence: 75%

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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: Discussionsupporting

confidence: 75%

“…Vitamin C protects cellular damage by scavenging reactive oxygen species. 20 In addition, vitamin C recycles the endothelial NO synthase cofactor tetrahydrobiopterin, which increases endothelial NO synthase function 19 and, in consequence, NO bioavailability. Vitamin C has an important role in influencing vascular function.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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“…[13][14][15][16][17] In studies using direct microneurographic measurements of muscle sympathetic nerve activity (MSNA) in humans, brief and/or mild hypoxia caused little or no change in MSNA, whereas more sustained and severe hypoxia rather consistently stimulated sympathetic activity. 15,16,18,19 Part of the discrepancy between norepinephrine plasma concentration and MSNA findings in these human studies could be related to the stimulation of norepinephrine clearance by hypoxia. 20 Thus, although there is evidence that hypoxia stimulates postganglionic sympathetic nerve activity in humans, no data are available at high altitude and in HAPE-susceptible subjects.…”

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confidence: 77%

Augmented Sympathetic Activation During Short-Term Hypoxia and High-Altitude Exposure in Subjects Susceptible to High-Altitude Pulmonary Edema

et al. 1999

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Background-Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. Methods and Results-We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to high-altitude pulmonary edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a high-altitude laboratory (4559 m). We also measured systolic pulmonary artery pressure to examine the relationship between sympathetic activation and pulmonary vasoconstriction. In subjects prone to pulmonary edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2-to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to edema (PϽ0.001). At high altitude, in subjects prone to edema, the increase in the meanϮSE sympathetic firing rate was Ͼ2 times larger than in those resistant to edema (36Ϯ7 versus 15Ϯ4 bursts per minute, PϽ0.001) and preceded the development of lung edema. We observed a direct relationship between sympathetic nerve activity and pulmonary artery pressure measured at low and high altitude in the 2 groups (rϭ0.83, PϽ0.0001). Conclusions-With the use of direct measurements of postganglionic sympathetic nerve discharge, these data provide the first evidence for an exaggerated sympathetic activation in subjects prone to high-altitude pulmonary edema both during short-term hypoxic breathing at low altitude and during actual high-altitude exposure. Sympathetic overactivation may contribute to high-altitude pulmonary edema. (Circulation. 1999;99:1713-1718.)

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“…Moreover, greater elevations in MSNA than observed here might be anticipated. Compared to other physiological stimuli such as cold (Victor, Leimbach, Seals, Wallin & Mark, 1987; Seals, 1990), exercise (Mark, Victor, Nerhed & Wallin, 1985;Seals et al 1988), or hypoxia (Saito, Mano, Iwase, Koga, Abe & Yamazaki, 1988;Rowell, Johnson, Chase, Comess & Seals, 1989), which may stimulate MSNA more directly and with greater consistency among subjects, the level of MSNA excitation observed during mental stress is relatively weak.…”

Section: Discussionmentioning

confidence: 98%

Sympathetic activity is influenced by task difficulty and stress perception during mental challenge in humans.

Callister

Suwarno

Seals

1992

The Journal of Physiology

197

179

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SUMMARY1. Our aim was to determine the influence of the type of task, the absolute and relative difficulty of the task, and the perceived stress associated with performance of the task on sympathetic circulatory regulation during cognitive challenge in humans.2. Sympathetic nerve activity to skeletal muscle (MSNA) determined from peroneal microneurography, heart rate and arterial blood pressure were recorded continuously in twelve subjects during a modified Stroop colour word test (CWT) and mental arithmetic (MA), each performed over six levels of increasing absolute task difficulty. Performance (percentage correct) on each task was assessed and ratings of perceived stress obtained. Responses to CWT and MA were compared at similar levels of performance and perceived stress. 3. MSNA decreased at task onset, remained below baseline levels at low levels of difficulty which were not perceived as stressful, increased above baseline levels at higher levels of difficulty which were perceived as stressful, and increased further during recovery. Thus, the regulation of MSNA was stress dependent. At similar levels of stress perception there were no differences in MSNA between CWT and MA. Although performance declined as task difficulty increased, there was no particular 'threshold' level of performance associated with the stimulation of MSNA.4. Arterial pressure and heart rate were elevated above baseline levels throughout the mental tasks. Arterial pressure increased over the first 3-4 levels of each task and then plateaued whereas heart rate did not vary across increasing levels of task difficulty. Heart rate and arterial pressure responses to CWT were higher than those to MA.5. These data demonstrate that during cognitive challenge the stimulation of MSNA is governed primarily by perceived stress which is dependent, in part, on the absolute level of task difficulty. In contrast, neither performance nor the type of cognitive task appear to be important determinants of MSNA. Arterial pressure is influenced by the task and level of difficulty. Heart rate is independent of task difficulty but may be task dependent.

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Responses in muscle sympathetic activity to acute hypoxia in humans

Cited by 161 publications

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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

Augmented Sympathetic Activation During Short-Term Hypoxia and High-Altitude Exposure in Subjects Susceptible to High-Altitude Pulmonary Edema

Sympathetic activity is influenced by task difficulty and stress perception during mental challenge in humans.

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