ArticleVascular medicine (London, England)2015
Contribution of endothelium-derived hyperpolarizing factor to exercise-induced vasodilation in health and hypercholesterolemia.
Article in Vascular medicine (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00166166 (Physiology and Pathologic Role of Endothelium-Derived Hyperpolarizing Factor in Humans), which is not on this map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Physiology and Pathologic Role of Endothelium-Derived Hyperpolarizing Factor in Humans
Who cites it
12 citing papers in PubMed.
- Nitric Oxide Contributes to Vasomotor Tone in Hypertensive African Americans Treated With Nebivolol and Metoprolol.Journal of clinical hypertension (Greenwich, Conn.) · 2016Trial
- Inhibition of superoxide and iNOS augment cutaneous nitric oxide-dependent vasodilation in non-Hispanic black young adults.Physiological reports · 2024Article
- Predictive biomarkers for the early detection and management of heart failure.Heart failure reviews · 2024Review
- Review
- Differential impact of severe familial hypercholesterolemia on regional skeletal muscle and organ blood flows during exercise: Effects of PDE5 inhibition.Microcirculation (New York, N.Y. : 1994) · 2019Article
- Peripheral Microvascular Function Reflects Coronary Vascular Function.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Rethinking Endothelial Dysfunction as a Crucial Target in Fighting Heart Failure.Mayo Clinic proceedings. Innovations, quality & outcomes · 2019Review
- Increased Vascular Permeability in the Bone Marrow Microenvironment Contributes to Disease Progression and Drug Response in Acute Myeloid Leukemia.Cancer cell · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Hypertensive response to exercise: mechanisms and clinical implication.Clinical hypertension · 2016Review
- Exaggerated Exercise Blood Pressure Response and Future Cardiovascular Disease.Journal of clinical hypertension (Greenwich, Conn.) · 2015Article
- Racial differences in arterial stiffness and microcirculatory function between Black and White Americans.Journal of the American Heart Association · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The role of endothelium-derived hyperpolarizing factor (EDHF) in either the healthy circulation or in those with hypercholesterolemia is unknown. In healthy and hypercholesterolemic subjects, we measured forearm blood flow (FBF) using strain-gauge plethysmography at rest, during graded handgrip exercise, and after sodium nitroprusside infusion. Measurements were repeated after l-NMMA, tetraethylammonium (TEA), and combined infusions. At rest, l-NMMA infusion reduced FBF in healthy but not hypercholesterolemic subjects. At peak exercise, vasodilation was lower in hypercholesterolemic compared to healthy subjects (274% vs 438% increase in FBF, p=0.017). TEA infusion reduced exercise-induced vasodilation in both healthy and hypercholesterolemic subjects (27%, p<0.0001 and -20%, p<0.0001, respectively). The addition of l-NMMA to TEA further reduced FBF in healthy (-14%, p=0.012) but not in hypercholesterolemic subjects, indicating a reduced nitric oxide and greater EDHF-mediated contribution to exercise-induced vasodilation in hypercholesterolemia. In conclusion, exercise-induced vasodilation is impaired and predominantly mediated by EDHF in hypercholesterolemic subjects. CLINICAL TRIAL REGISTRATION IDENTIFIER NCT00166166:
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