Roles of adenosine and nitric oxide in skeletal muscle in acute and chronic hypoxia

Marshall, Janice M.

doi:10.1007/978-1-4757-3401-0_23

Cited by 22 publications

(17 citation statements)

References 21 publications

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“…Systemic hypoxia per se is known to induce acute vasodilation [9][10][11]. In addition, Thomson et al and Vedam et al have shown a significant reduction in augmentation index, used to assess arterial stiffness, in healthy men breathing hypoxic gas [12,13].…”

Section: Introductionmentioning

confidence: 99%

Vascular adaptations to hypobaric hypoxic training in postmenopausal women

et al. 2010

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The objective of this study was to examine the effects of exercise training in hypoxia on arterial stiffness and flow-mediated vasodilation (FMD) in postmenopausal women. Sixteen postmenopausal women (56±1 years) were assigned to a normoxic exercise group (Normoxic group, n=8) or a hypoxic exercise group (Hypoxic group, n=8). The Hypoxic group performed exercise under hypobaric hypoxic conditions corresponding to 2000 m above sea level, and was exposed to these conditions for 2 h per session. Aquatic exercise was performed at an intensity of around 50% peak oxygen uptake for 30min, 4days per week, for 8 weeks. Arterial stiffness was assessed by brachial-ankle pulse wave velocity (baPWV), and FMD was evaluated by peak diameter of the popliteal artery during reactive hyperemia. After the 8 weeks of training, the Normoxic group showed no significant changes. In contrast, baPWV (P < 0.05) was significantly reduced and peak diameter (P<0.05) and %FMD (P<0.01) were significantly increased in the Hypoxic group after training. These results suggest that exercise training under mild intermittent hypoxic conditions could more effectively reduce arterial stiffness in postmenopausal women, compared with exercise training performed at the same relative intensity under normoxic conditions. Our data also indicate that hypoxic exercise training may induce vascular functional adaptation, for example an increase in FMD response. These findings therefore could have important implications for the development of a new effective exercise prescription program.

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Section: Introductionmentioning

confidence: 99%

Vascular adaptations to hypobaric hypoxic training in postmenopausal women

et al. 2010

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“…86 Similarly, adenosine promotes vascular growth in vivo in several tissues, including skeletal muscle, myocardium and wound beds. 87,88 For example, Ziada et al showed that intravenous delivery of adenosine in rabbits resulted in approximately a 27% increase in capillary density in the myocardium and in approximately a 26% increase capillary-to-muscle fiber ratio in skeletal muscles. 89 The main pro-angiogenic effects of adenosine have so far been attributed to adenosine-induced secretion of pro-angiogenic growth factors, such as VEGF and bFGF in an A 2A receptor-mediated fashion.…”

Section: Lysophosphatidic Acidmentioning

confidence: 99%

Engineering vascularized tissues using natural and synthetic small molecules

2008

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Vascular growth and remodeling are complex processes that depend on the proper spatial and temporal regulation of many different signaling molecules to form functional vascular networks. The ability to understand and regulate these signals is an important clinical need with the potential to treat a wide variety of disease pathologies. Current approaches have focused largely on the delivery of proteins to promote neovascularization of ischemic tissues, most notably VEGF and FGF. Although great progress has been made in this area, results from clinical trials are disappointing and safer and more effective approaches are required. To this end, biological agents used for therapeutic neovascularization must be explored beyond the current well-investigated classes. This review focuses on potential pathways for novel drug discovery, utilizing small molecule approaches to induce and enhance neovascularization. Specifically, four classes of new and existing molecules are discussed, including transcriptional activators, receptor selective agonists and antagonists, natural product-derived small molecules, and novel synthetic small molecules.

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“…In acute systemic hypoxia such as one might expect in apnea, adenosine and NO dilate the arterioles and so help to maintain oxygen consumption in skeletal muscle. 38 Diet is also important to the development of fatigue 39,40 as well as to NO output in the nasal airway. 41 This effect is also seen in other tissues.…”

Section: The Respiratory Musclesmentioning

confidence: 99%

Nitric Oxide (NO) and Obstructive Sleep Apnea (OSA)

Haight

Djupesland

2003

Sleep Breath

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Nitric oxide (NO) and obstructive sleep apnea are inseparable. Obstructive sleep apnea could be described as the intermittent failure to transport the full complement of nasal NO to the lung with each breath. There NO matches perfusion to ventilation. NO is utilized by the efferent pathways that control the unequal, inspiratory battle between the pharyngeal dilators and the closing negative pressures induced by the thoracic musculature. Recurrent cortical arousals are a major short-term complication, and the return to sleep after each arousal uses NO. The long-term complications, namely hypertension, myocardial infarction, and stroke, might be due to the repeated temporary dearth of NO in the tissues, secondary to a lack of oxygen, one of NO's two essential substrates.

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Roles of adenosine and nitric oxide in skeletal muscle in acute and chronic hypoxia

Cited by 22 publications

References 21 publications

Vascular adaptations to hypobaric hypoxic training in postmenopausal women

Vascular adaptations to hypobaric hypoxic training in postmenopausal women

Engineering vascularized tissues using natural and synthetic small molecules

Nitric Oxide (NO) and Obstructive Sleep Apnea (OSA)

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