Increased Intraluminal Pressure Changes Mechanism of Flow-Mediated Dilation

Why are the endothelial-derived contributors to flow-mediated dilation important to humans with vascular disease? Listen as Associate Editor Debra Diz (Wake Forest School of Medicine) interviews lead author Andreas Beyer (Medical College of Wisconsin) and expert Jennifer Pollock (University of Alabama at Birmingham) about the innovative new work by Beyer et al, which shows that an acute stress response in the human vasculature changes the mechanism of dilation from cardioprotective nitric oxide to pro-atherosclerotic hydrogen peroxide after exposure to increased intraluminal pressure. What do the authors speculate is mediating the “switch” from NO to H2O2, and how do pre-existing conditions, such as systemic hypertension, complicate the stress response mechanism? Listen to find out.


Andreas M. Beyer, Matthew J. Durand, Joseph Hockenberry, T. Clark Gamblin, Shane A. Phillips, David D. Gutterman An acute rise in intraluminal pressure shifts the mediator of flow-mediated dilation from nitric oxide to hydrogen peroxide in human arterioles Am J Physiol Heart Circ Physiol, published December 1, 2014. DOI: 10.1152/ajpheart.00557.2014.

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Circulating FGF23 Levels in Heart Failure

Have Imazu et al discovered a new clinical biomarker for predicting renal dysfunction in heart failure patients? In this engaging podcast Associate Editor Leon De Windt interviews lead author Masafumi Kitakaze (National Cerebral and Cardiovascular Center, Japan) and expert Thomas Thum (Hannover Medical School, Germany) about the pioneering work by Kitakaze and colleagues, which investigated the correlation between circulating FGF23 in non-ischemic patients with early chronic kidney disease and higher incidences of heart failure hospitalization in these patients. How did inflammation, ischemic conditions, gender, age, and other medications influence circulating FGF23 levels? Listen now.


Miki Imazu, Hiroyuki Takahama, Hiroshi Asanuma, Akira Funada, Yasuo Sugano, Takahiro Ohara, Takuya Hasegawa, Masanori Asakura, Hideaki Kanzaki, Toshihisa Anzai, Masafumi Kitakaze Pathophysiological Impact of Serum Fibroblast Growth Factor 23 in Patients with Non-ischemic Cardiac Disease and Early Chronic Kidney Disease Am J Physiol Heart Circ Physiol, published November 15, 2014. DOI: 10.1152/ajpheart.00331.2014.

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Exercise Training Improves Metabo and Mechanoreflex Control in Heart Failure

The so called “exercise pressor reflex” is enhanced in chronic heart failure and drives sympathetic nerve activity during exercise. While exercise training can impact the sensitivity of this reflex, the molecular mechanisms that are at play remain unclear. Listen as Editor-in-Chief Irving H. Zucker interviews lead author Carlos Negrao (University of Sao Paulo) and expert Vaughan Macefield (University of Western Sydney) about the exciting new work by Antunes-Correa et al., who found that exercise training in chronic heart failure patients decreased the muscle mechanoreflex control of sympathetic nerve activity. Did Negrao and colleagues find that molecular abnormalities in skeletal muscle underlie abnormal muscle sympathetic nerve activity in humans with heart failure? Are these effects reversible with exercise training? Listen and learn more.


Ligia M. Antunes-Correa, Thais S. Nobre, Raphaela V. Groehs, Maria-Janieire N.N. Alves, Tiago Fernandes, Gisele K. Couto, Maria Urbana P.B. Rondon, Patricia Alves de Oliveira, Marta Lima, Wilson Mathias Jr., Patricia C. Brum, Charles Mady, Dirceu R. Almeida, Luciana Venturini Rossoni, Edilamar Menezes de Oliveira, Holly R. Middlekauff, Carlos Eduardo Negrao Molecular Basis for the Improvement in Muscle Metaboreflex and Mechanoreflex Control in Exercise-Trained Humans with Chronic Heart Failure Am J Physiol Heart Circ Physiol, published December 1, 2014. DOI: 10.1152/ajpheart.00136.2014.

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