AJP-Heart and Circulatory Physiology Podcast

Nerve induced EC Ca2+ signals oppose vasoconstriction

Our latest podcast takes us into the realm of calcium pulsars. Associate Editor Nancy Kanagy talks with senior author Mark Nelson (University of Vermont) and leading expert Michael Hill (University of Missouri) about how the work of Nausch et al challenges the traditional view that the sympathetic nervous system regulates vascular tone independent of the endothelium. This work by Nelson and colleagues shows that the endothelium is dynamically engaged during neurovascular coupling through transcellular negative feedback which limits vasoconstriction. Listen as we explore how the vascular smooth muscle communicates with the endothelium, and the potential significance of this EDH mechanism to oppose sympathetically-mediated constriction.

Lydia W. M. Nausch, Adrian D. Bonev, Thomas J. Heppner, Yvonne Tallini, Michael I. Kotlikoff, Mark T. Nelson. Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries Am J Physiol Heart Circ Physiol, published ahead of print December 2, 2011, doi:10.1152/ajpheart.00773.2011.

In pursuit of scientific excellence - sex matters

Sex and gender matter in physiology, but are frequently ignored in scientific publications. In our latest podcast, Editor in Chief William Stanley has a lively conversation with leading experts Virginia Miller (Mayo Clinic) and Jane Reckelhoff (University of Mississippi) about the importance of sex and gender differences in physiology research and publications. Clear sex differences are apparent at the molecular, cellular and whole organ levels, prompting a new editorial policy for the American Physiological Society publications which requires reporting of the sex and/or gender of animals and humans, as well as all derived materials. Learn about how to approach this important issue in your work, and the surprising effects of sex on physiology from the molecular level on up.

Virginia M. Miller. In pursuit of scientific excellence - sex matters Am J Physiol Heart Circ Physiol, published ahead of print February 10, 2012, doi: 10.1152/ajpheart.00073.2012.

Fructose diet-induced cardiomyocyte Ca2+ cycling abnormality

In our latest podcast we explore the cardiac-specific effects of a high fructose diet. An inventive new study by Mellor et al investigates excitation contraction coupling changes in myocytes isolated from an experimental mouse model. These studies reveal, upon high fructose feeding, marked alterations in myocyte Ca2+ handling, but with maintained contractile function. Associate Editor Meredith Bond and leading expert Susan Howlett (Dalhousie University) interview senior author Lea Delbridge (University of Melbourne) about her exciting new work on diabetic cardiomyopathy.

Kimberley M Mellor, Igor R Wendt, Rebecca H Ritchie, and Lea M.D. Delbridge. Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca2+ handling and myofilament responsiveness Am J Physiol Heart Circ Physiol, published ahead of print December 23, 2011, doi:10.1152/ajpheart.00797.2011.

Molecular mechanisms linking salt to hypertension

It is well known that there is no single cause of hypertension, but many of the factors that contribute to hypertension are known. Our latest podcast spotlights an elegant new Review article by Blaustein and colleagues which focuses on the interplay of salt and the secretion and action of endogenous ouabain. Associate Editor Irving Zucker interviews senior author, and fellow Associate Editor, Mordecai Blaustein (University of Maryland), along with leading expert John Osborn (University of Minnesota) about how endogenous ouabain might contribute to salt-sensitive hypertension and plays a central role in the alterations in the central nervous system, kidney and vasculature which contribute to chronic hypertension.

Mordecai P. Blaustein, Frans HH Leenen, Ling Chen, Vera A. Golovina, John M Hamlyn, Thomas L Pallone, James W. Van Huysse, Jin Zhang, Withrow Gil Wier. How NaCl raises blood pressure: A new paradigm for the pathogenesis of salt-dependent hypertension Am J Physiol Heart Circ Physiol, published ahead of print November 4, 2011, doi:10.1152/ajpheart.00899.2011.

BH4 and Vascular Function in Women

What's the problem with arterial function following menopause? Listen as Editor in Chief William Stanley, senior author Kerrie Moreau (University of Colorado Denver), and leading women’s health expert Virginia Miller (Mayo Clinic) engage in a lively conversation about the latest clinical study by Moreau et al on the role of estrogen and uncoupled nitric oxide synthase in arterial stiffening in post-menopausal women. Can early intervention with estrogen combat accelerated vascular aging after menopause?

Kerrie L Moreau, Amie Meditz, Kevin Deane, Wendy M. Kohrt. Tetrahydrobiopterin Improves Endothelial Function and Decreases Arterial Stiffness in Estrogen-Deficient Postmenopausal Women Am J Physiol Heart Circ Physiol, published ahead of print January 13, 2012, doi:10.1152/ajpheart.01065.2011.

Obesity and orthopedic trauma

The obesity epidemic in the United States shows no signs of abating, which is why our latest podcast is particularly insightful. Associate Editor Nancy Kanagy talks with author Lusha Xiang (University of Mississippi) and leading expert Jeff Frisbee (West Virginia University) about the study by Xiang and colleagues, which suggests the mechanism behind the poor prognosis for obese trauma victims and provides insight into a new therapeutic intervention to improve recovery of obese victims of traumatic injury.

Lusha Xiang, Silu Lu, William Fuller, Arun Aneja, George V Russell, Louis B Jones, and Robert L. Hester. Impaired blood pressure recovery to hemorrhage in obese Zucker rats with orthopedic trauma. Am J Physiol Heart Circ Physiol, published ahead of print October 14, 2011, doi: 10.1152/ajpheart.00439.2011.

Muscle oxygen transport and utilization in heart failure

A well-known problem for heart failure patients is the inability, or markedly decreased ability, to exercise. When even low levels of daily activity are impaired, the quality of life for heart failure patients suffers considerably. The mechanisms for exercise intolerance are very complicated and extend far beyond impaired cardiac performance. Listen in as Associate Editor Irving Zucker, senior author David Poole (Kansas State University) and leading expert Peter Wagner (University of California, San Diego) discuss the new Review article by Poole and colleagues, which tackles the mechanisms of muscle dysfunction in heart failure at the oxygen transport and microcirculatory levels.

David C. Poole, Daniel M. Hirai, Steven W. Copp, and Timothy I. Musch. Muscle Oxygen Transport and Utilization in Heart Failure: Implications for Exercise (In)tolerance Am J Physiol Heart Circ Physiol, published ahead of print November 18, 2011, doi:10.1152/ajpheart.00943.2011.

Interstitial Volume Modulates the Conduction Velocity- Gap Junction Relationship

What are the parameters which modulate conduction under normal and disease conditions in the heart? This age-old debate has pitted two distinct schools of thought against each other—ephaptic conduction vs. gap junctions. Can changes in interstitial volume by pharmacological means dramatically change conduction velocity? In our latest podcast on the article by Veeraraghavan et al, Associate Editor Igor Efimov, leading expert Craig Henriquez (Duke University) and senior author Steven Poelzing (University of Utah) wade into the debate.

Rengasayee Veeraraghavan, Mohamed E. Salama, and Steven Poelzing. Interstitial volume modulates the conduction velocity-gap junction relationship. Am J Physiol Heart Circ Physiol, published ahead of print October 21, 2011, doi: 10.1152/ajpheart.00868.2011.

Mitofusin-1 Deficiency in the Heart

Our latest podcast focuses on mitochondrial dynamics, as senior author Ken Walsh (Boston University) and expert Elizabeth “Tish” Murphy (NHLBI) join Consulting Editor Michael Wolin to discuss the recent study by Papanicolau et al, showing surprising effects of cardiac deletion of the key mitochondrial membrane protein mitofusin-1. Listen in as we uncover the unexpected impact of mitofusin-1 and mitofusin-2 on mitochondrial size and resistance to stress.

Kyriakos N. Papanicolaou, Gladys A. Ngoh, Errine R Dabkowski, Kelly A O'Connell, Rogerio F. Ribeiro, William C. Stanley, and Kenneth Walsh. Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell death. Am J Physiol Heart Circ Physiol, published ahead of print October 28, 2011, doi: 10.1152/ajpheart.00833.2011.

SIRT3 and cardiac mitochondria

Post-translational modification through acetylation by the NAD+-dependent deacetylase sirtuin-3, or SIRT3, has recently emerged as a key player in regulating mitochondrial function. What is SIRT3 doing in cardiac mitochondria? How does it impact cardiac physiology and pathophysiology? Listen as Editor in Chief William Stanley and Associate Editor Junichi Sadoshima talk with the author Michael Sack (National Heart, Lung and Blood Institute, NIH) about his just-published Review article which tackles these very questions.

Michael N. Sack. Emerging characterization of the role of SIRT3 mediated mitochondrial protein deacetylation in the heart. Am J Physiol Heart Circ Physiol, published ahead of print October 7, 2011, doi:10.1152/ajpheart.00199.2011.