Semin Thromb Hemost 2014; 40(06): 660-668
DOI: 10.1055/s-0034-1389082
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Aging of Platelet Nitric Oxide Signaling: Pathogenesis, Clinical Implications, and Therapeutics

Nathan E. K. Procter
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
,
Cher-Rin Chong
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
,
Aaron L. Sverdlov
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
,
Wai Ping A. Chan
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
,
Yuliy Y. Chirkov
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
,
John D. Horowitz
1   Department of Cardiology, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
› Author Affiliations
Further Information

Publication History

Publication Date:
31 August 2014 (online)

Abstract

The nitric oxide (NO)/soluble guanylate cyclase (sGC) system is fundamental to endothelial control of vascular tone, but also plays a major role in the negative modulation of platelet aggregation. The phenomenon of platelet NO resistance, or decreased antiaggregatory response to NO, occurs increasingly with advanced age, as well as in the context of cardiovascular disease states such as heart failure, ischemic heart disease, and aortic valve disease. The central causes of NO resistance are “scavenging” of NO and dysfunction of sGC. In the current review, we discuss the roles of several modulators of NO synthesis and of the NO/sGC cascade on changes in platelet physiology with aging, together with potential therapeutic options to reduce associated thrombotic risk.

 
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