Exercise-induced vasodilation in forearm circulation of normal subjects and patients with congestive heart failure: Role of endothelium-derived nitric oxide

Katz, Stuart D.; Krum, Henry; Khan, Tehreen; Knecht, Mathius

doi:10.1016/0735-1097(96)00204-5

Cited by 124 publications

(82 citation statements)

References 34 publications

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“…22 An impairment in NO-dependent vascular function is a common finding in many cardiovascular diseases, including hypertension and heart failure. 11,32 The present findings corroborate the view that ET A receptor blockade is a useful tool in preventing the endogenous ET-dependent component of systemic and renal vasoconstriction secondary to NO deficiency.…”

Section: Montanari Et Al Effects Of L-name and Bq-123 In Human Kidneysupporting

confidence: 79%

Endothelin-A Blockade Attenuates Systemic and Renal Hemodynamic Effects of L-NAME in Humans

Montanari

Carra

et al. 2000

Hypertension

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Abstract-Eight Na-repleted volunteers underwent 3 separate 90-minute infusions of either N G -nitro-L-arginine methyl ester (L-NAME) 3.0 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 or endothelin-A receptor (ET-A) blocker BQ-123 (BQ) 0.125 nmol ⅐ kg Ϫ1 ⅐ min Ϫ1or both. Mean arterial pressure (MAP), glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistances (RVR), and sodium excretion rate (UNaV) were measured at baseline (b) and from 0 to 45 minutes (period 1) and 45 to 90 minutes (period 2) of infusion. BQ alone had no effect. GFR declined by 4.9% (PϽ0.001 versus b) in period 1, to 9.9% (PϽ0.001) in period 2 with L-NAME, and by 3.3% (PϽ0.01) to 6.6% (PϽ0.001) with L-NAME plus BQ (PϭNS between L-NAME and L-NAME plus BQ). UNaV fell equally with L-NAME or L-NAME plus BQ. MAP rose significantly in period 2 with L-NAME (6.9%; PϽ0.001) but not with coinfused BQ (2.1%; PϭNA versus b, Pϭ0.005 versus L-NAME alone). RBF declined by 12.2% (PϽ0.001) to 18.3% (PϽ0.001) with L-NAME and by 4.6% (PϽ0.005) to 8.2% (PϽ0.001) with L-NAME plus BQ. These changes were smaller with L-NAME plus BQ (PϽ0.05 in period 1 and PϽ0.02 in period 2). Blunted changes were also seen for RVR (PϽ0.005 in period 1 and PϽ0.001 in period 2 between L-NAME alone and L-NAME plus BQ). These findings show that systemic and renal vasoconstriction due to L-NAME are attenuated by BQ, which suggests that an interaction between endogenous nitric oxide production and ET-A activity participates in the maintenance of baseline systemic and renal vascular tone in humans.

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Section: Montanari Et Al Effects Of L-name and Bq-123 In Human Kidneysupporting

confidence: 79%

Endothelin-A Blockade Attenuates Systemic and Renal Hemodynamic Effects of L-NAME in Humans

Montanari

Carra

et al. 2000

Hypertension

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“…6,7,20,21,23 Katz et al observed that nitric oxide synthase inhibition reduced exercise-induced blood flow in normal subjects, but not in patients with heart failure, suggesting that nitric oxide-mediated vasodilation during exercise is impaired in individuals with heart failure. 23 In addition, Hirai et al have reported that inhibition of nitric oxide synthase resulted in reduced blood flow to exercising skeletal muscle in rats. 24 In a small human study, Gilligan et al observed that inhibition of nitric oxide synthase resulted in decreased forearm blood flow during hand-grip exercise.…”

Section: Discussionmentioning

confidence: 99%

Peripheral vascular endothelial function correlates with exercise capacity in women

et al. 2005

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SummaryBackground: Vascular endothelial function has been observed to correlate with exercise capacity in predominantly male populations. Gender-based differences exist in the clinical course of coronary artery disease, and previous studies indicate that estrogen may influence endothelial function. These observations raise the possibility that the relationship between endothelial function and exercise capacity in women may differ from that in men.Hypothesis: This study aimed to determine whether peripheral vascular endothelial function correlates with exercise capacity in women.Methods: Women who were referred for clinically indicated exercise testing with technetium-99 myocardial perfusion imaging were consecutively recruited. To ensure a population free of exercise limitation due to ischemic heart disease, women without myocardial perfusion defects were included for analysis in this study (n = 105). Endothelial function was assessed by brachial artery ultrasound flow-mediated vasodilation (FMD). Exercise capacity was defined as the duration of exercise on a symptom-limited Bruce protocol.Results: Mean FMD was 11.8 ± 0.6%, and median FMD was 12%. Subjects with an FMD less than the median of 12%

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“…NOS inhibition significantly reduced the forearm vasodilatation response to handgrip exercise in normal individuals, but did not change the response in patients with CHF suggesting that flow-induced NO-mediated vasodilatation during exercise is blunted in these patients [53]. In most CHF patients endothelial-mediated flow-dependent vasodilatation may be reduced as a consequence of physical deconditioning and the mechanistic evidence may be unmasked by studying the effects of exercise training on the endothelial function and exercise performance.…”

Section: The Endotheliummentioning

confidence: 98%

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

Piepoli

Guazzi

Boriani

et al. 2010

European Journal of Cardiovascular Prevention & Rehabilitat

112

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Muscular fatigue and dyspnoea on exertion are among the most common symptoms in chronic heart failure; however their origin is still poorly understood. Several studies have shown that cardiac dysfunction alone cannot fully explain their origin, but the contribution of the multiorgan failure present in this syndrome must be highlighted. In this study, divided in two parts (see part II: pp. 643-648), we aimed to summarize the existing evidence and the most controversial aspects of the complex interplay of different factors involved in symptom generation. In this first part of the review, six key factors are revised: the heart, the lung, the skeletal muscle, the hormonal changes, the O 2 delivery to the periphery, the endothelium. In the second part, the role of the excitatory reflexes and the cardiac cachexia will be presented, and finally, the potential therapeutic implications are discussed. We believe that a better knowledge of the pathophysiology of this syndrome may contribute to the management of the patients and to the improvement in their stress tolerance and quality of life.

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Exercise-induced vasodilation in forearm circulation of normal subjects and patients with congestive heart failure: Role of endothelium-derived nitric oxide

Cited by 124 publications

References 34 publications

Endothelin-A Blockade Attenuates Systemic and Renal Hemodynamic Effects of L-NAME in Humans

Endothelin-A Blockade Attenuates Systemic and Renal Hemodynamic Effects of L-NAME in Humans

Peripheral vascular endothelial function correlates with exercise capacity in women

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

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