Corresponding author Joanne S. lngwall, PhD

NMR Laboratory for Physiological Chemistry, Brigham and Women’s Hospital, 221 Longwood Avenue, Room 247, Boston, MA 02115, USA.

Current Hypertension Reports
 2006, 8:457-464

Current Science Inc. ISSN 1522-6417
Copyright© 2006 by Current Science Inc.

Adenosine triphosphate (ATP) and phosphocreatine fall in the failing heart. New insights into the control of ATP synthesis, supply, and utilization, and how this changes in the failing heart, have emerged. In this article, we address four questions: What are the mechanisms explaining loss of ATP and creatine from the failing heart? What are the consequences of these changes? Can metabolism be manipulated to restore a normal ATP supply? Does increasing energy supply have physiologic consequences (ie, does it lead to improved contractile [systolic and/or diastolic] performance)? In part 1 we focus on ATP, in part 2 on creatine, and in part 3 on the relationship between creatine and purine metabolism and purine nucleotide signaling.


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