Effects of exercise‐training on hypoxia and angiotensin II‐induced pulmonary vasoconstrictions

Kashimura, Osamu; Sakai, Akio; Yanagidaira, Yasunori

doi:10.1111/j.1748-1716.1995.tb09976.x

Cited by 20 publications

(17 citation statements)

References 13 publications

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“…Alveolar hypoxia may potentially act by inducing increased in situ expression of vasoconstricting substances in the lung. In this connection, increased levels of catecholamines, vasopressin, angiotensin or ET-1 have been described during exercise [31][32][33]. However, their physiopathological significance in the exerciseinduced pulmonary haemodynamic and gas exchange abnormalities has not as yet been established.…”

Section: Discussionmentioning

confidence: 99%

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise

Yamakami

Taguchi²,

Gabazza³

et al. 1997

Eur Respir J

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Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise. T. Yamakami, O. Taguchi, E.C. Gabazza, M. Yoshida, T. Kobayashi, H. Kobayashi, H. Yasui, H. Ibata, Y Adachi. ERS Journals Ltd 1997. ABSTRACT: This study was undertaken to assess the arterial plasma levels of endothelin-1 (ET-1) and their relationship with pulmonary haemodynamic and gas exchange variables during exercise in patients with emphysema and interstitial lung disease (ILD).Incremental cycle ergometry was performed in all patients up to maximal capacity. At rest, arterial ET-1 levels were higher in emphysema (1.86±0.35 pg·mL -1 ; p<0.02) and ILD (1.75±0.25 pg·mL -1 ; p<0.03) patients than in controls (1.35±0.18 pg·mL -1 ). Emphysema (2.08±0.26 versus 1.70±0.40 pg·mL -1 ) and ILD (1.98±0.21 versus 1.67±0.02 pg·mL -1 ) patients with pulmonary hypertension (PH) presented significantly (p<0.05) higher arterial ET-1 levels than those without. At rest, arterial ET-1 levels were significantly correlated with mean pulmonary arterial pressure (Ppa) in both ILD (r=0.8, p=0.01) and emphysema (r=0.5, p=0.03) patients. During exercise, the arterial ET-1 levels were significantly correlated with arterial oxygen (Pa,O 2 ) (r=-0.6, p=0.04), alveolar-arterial oxygen difference (r=0.8, p=0.01), and Ppa (r=0.6, p=0.04) in ILD patients, but not in those with emphysema.In brief, the results of this study suggest that arterial endothelin-1 is markedly increased in interstitial lung disease and emphysema patients, and that, it is related to the exercise-induced exacerbation of pulmonary hypertension in patients with interstitial lung disease, but not in those with emphysema. Eur Respir J 1997; 10: 2055-2060. Pulmonary artery hypertension is the major cardiovascular complication of emphysema and advanced interstitial lung disease (ILD) [1]. Pulmonary hypertension (PH) is important, not only because it is associated with right ventricular hypertrophy (or cor pulmonale) but also because it adversely affects prognosis in these patients [2]. The mechanisms responsible for PH include thrombotic obstruction of pulmonary blood vessels, reduced distensibility of the pulmonary vascular bed, pulmonary vascular obstruction produced by medial hypertrophy or intimal proliferation, and pulmonary vasoconstriction elicited by acute or chronic alveolar hypoxia [3,4]. Of these, hypoxic vasoconstriction has been considered one of the major factors involved in the pathogenesis of sustained PH or in the development of acute exacerbation of PH in patients with emphysema or advanced ILD [5]. However, the precise mechanism by which hypoxia induces pulmonary vasoconstriction and the structural changes that ensue from chronic hypoxia have not been fully elucidated. Endothelin-1 (ET-1), a vasoconstricting peptide originally isolated from cultured human endothelial cells, may play a relevant role in the pathogenesis of PH during hypoxia [6][7][8]. This assumption is supported by previous findings that showed that the e...

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Section: Discussionmentioning

confidence: 99%

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise

Yamakami

Taguchi²,

Gabazza³

et al. 1997

Eur Respir J

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“…Rats were trained for 4 and 6 weeks under hypobaric hypoxia (equivalent to altitudes of 2500 and 5500 m). Kashimura et al 196 found that the increase in resting mean pulmonary arterial pressure with increasing equivalent altitude was lower in the 2 trained groups than in the control group and greater after 6 than after 4 weeks of exercise. 195 In a follow-up study, they showed that 6 weeks of training can attenuate the hypoxia-induced and angiotensin II-induced PH.…”

Section: Animal Experimentsmentioning

confidence: 99%

Cardiovascular Effects of Exercise Training

2010

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“…2000). Regarding the Ang II pathway, an exercise‐induced decrease in Ang II‐induced pulmonary vasoconstriction was present in rats that trained for 6 weeks (Kashimura et al . 1995).…”

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confidence: 99%

Physical (in)activity and endothelium‐derived constricting factors: overlooked adaptations

Thijssen¹,

Rongen

Smits

et al. 2008

The Journal of Physiology

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The inner surrounding of arterial vessels, the endothelium, is optimally located to detect changes in blood characteristics or blood flow that may result from changes in physical activity or from diseases. In response to physical stimuli, the endothelium varies its release of circulating vasoactive substances and serves as a source of local and systemic endothelium-derived dilator and vasoconstrictor factors. Endothelial dysfunction is one of the earliest markers of vascular abnormalities observed in cardiovascular disease and ageing. Exercise training is an efficient therapeutic strategy to improve endothelial function. Traditionally, studies on endothelial dysfunction and physical (in)activity-related effects on vascular adaptations are primarily focused on vasodilator substances (i.e. nitric oxide). One may suggest that augmentation of vasoconstrictor pathways (such as endothelin-1 and angiotensin II) contributes to the endothelial dysfunction observed after physical inactivity. Moreover, these pathways may also explain the exercise-induced beneficial cardiovascular adaptations. This review summarizes the current knowledge on the effects of physical (in)activity on several endothelium-derived vasoconstrictor substances.

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Effects of exercise‐training on hypoxia and angiotensin II‐induced pulmonary vasoconstrictions

Cited by 20 publications

References 13 publications

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise

Cardiovascular Effects of Exercise Training

Physical (in)activity and endothelium‐derived constricting factors: overlooked adaptations

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