How do β-adrenergic receptor subtypes regulate immune function in the heart? In this unique episode of The AJP-Heart and Circ Podcast, Consulting Editor Dr. Kristine DeLeon-Pennell (Medical University of South Carolina) interviews two authors about their two articles published recently in AJP-Heart and Circulatory Physiology. Dr. Laurel Grisanti (University of Missouri, Columbia) discussed her study (Tanner et al.) on the important role for β2-adrenergic receptor expression on immune cells in the development of heart failure in response to chronic catecholamine elevation. Using a chronic isoproterenol infusion model of heart failure, Dr. Grisanti and co-authors concluded that the immune cell expression of β2-adrenergic receptor is an important contributor to the detrimental responses seen with chronic elevations in catecholamine. The macrophage populations lacking β2-adrenergic receptor largely retained their reparative phenotype and failed to illicit pro-inflammatory macrophage recruitment. Dr. Petra Eder-Negrin (University Hospital, Würzburg) discussed her work (Cellini et al.) in context of Dr. Grisanti's study, underscoring the mechanistic link between sodium potassium -ATPase and β-adrenergic stimulation in the post-MI heart. Eder-Negrin and co-authors found that sodium potassium ATPase alpha 2 overexpressing cardiomyocytes are a crucial adaption, providing an important functional reserve for the heart to cope with chronic stress more efficiently. Sodium potassium ATPase alpha 2 overexpression could be an alteration to attenuate heart failure. How do these research studies connect? Listen now.

Miles A. Tanner, Charles A. Maitz, and Laurel A. Grisanti Immune cell β2-adrenergic receptors contribute to the development of heart failure Am J Physiol Heart Circ Physiol, published September 15, 2021. DOI: 10.1152/ajpheart.00243.2021

Antonella Cellini, Dorina Höfler, Paula A. Arias-Loza, Sandra Bandleon, Tanja Langsenlehner, Michael Kohlhaas, Christoph Maack, Wolfgang R. Bauer, and Petra Eder-Negrin The α2-isoform of the Na+/K+-ATPase protects against pathological remodeling and β-adrenergic desensitization after myocardial infarction Am J Physiol Heart Circ Physiol, published September 15, 2021. DOI: 10.1152/ajpheart.00808.2020