Journal
TRENDS IN CARDIOVASCULAR MEDICINE
Volume 19, Issue 4, Pages 111-118Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2009.07.001
Keywords
-
Categories
Funding
- National Institutes of Health [HL-81526, HL-64724]
- American Heart Association [0735084N]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL030077, R01HL064724, R01HL081562] Funding Source: NIH RePORTER
Ask authors/readers for more resources
During activation of the sympathetic nervous system, cardiac performance is increased as part of the fight-or-flight stress response. The increase in contractility with sympathetic stimulation is an orchestrated combination of intrinsic inotropic, lusitropic, and chronotropic effects, mediated in part by activation of P-adrenergic receptors and protein kinase A. This causes phosphorylation of several Ca cycling proteins in cardiac myocytes (increasing Ca entry via L-type Ca channels, sarcoplasmic reticulum Ca pumping, and the dissociation rate of Ca from the myofilaments). Here, we discuss how stimulation of the Na/K-ATPase, mediated by phosphorylation of phospholemman (a small sarcolemmal protein that associates with and modulates Na/K-ATPase), is an additional important player in the sympathetic fight-or-flight response. Enhancement of Na/K-ATPase activity limits the rise in [Na](i) caused by the higher level of Na influx and by doing so limits the rise in cellular and sarcoplasmic reticulum Ca load by favoring Ca extrusion via the Na/Ca exchanger Thus, phospholemman-mediated activation of the Na/K-ATPase may prevent Ca. overload and triggered arrhythmias during stress. (Trends Cardiovasc Med 2009; 19:111-118) (C) 2009, Elsevier Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available