Thromb Haemost 2000; 83(05): 752-758
DOI: 10.1055/s-0037-1613904
Review Article
Schattauer GmbH

Influence of SIN-1 on Platelet Ca2+ Handling in Patients with Suspected Coronary Artery Disease: Ex Vivo and In Vitro Studies

Kim-Hanh Le Quan Sang
,
Claude Le Feuvre
1   Clinique Cardiologique, Hôpital Necker-Enfants Malades, Paris, France
,
Annie Brunet
,
Thuc Do Pham
,
Jean-Philippe Metzger
1   Clinique Cardiologique, Hôpital Necker-Enfants Malades, Paris, France
,
André Vacheron
1   Clinique Cardiologique, Hôpital Necker-Enfants Malades, Paris, France
,
Marie-Aude Devynck
› Author Affiliations
This study was partially supported by a research grant from the Fédération Française de Cardiologie, Paris (France). The kind participation of Liliane FOUQUE in the practical organization of the study is gratefully acknowledged.
Further Information

Publication History

Received 08 September 1999

Accepted after resubmission 10 January 2000

Publication Date:
08 December 2017 (online)

Summary

The 3-morpholinosydnonimine (SIN-1) generates both nitric oxide (NO) and superoxide anion (O2−). It elicits dose-dependent vasodilation in vivo, in spite of the opposite effects of its breakdown products on vascular tone and platelet aggregation.

This study was designed to investigate the influence of intravenous SIN-1 injection on platelet Ca2+ handling in patients undergoing coronary angiography. SIN-1 administration reduced cytosolic [Ca2+] in unstimulated platelets by decreasing Ca2+ influx. It attenuated Ca2+ mobilization from internal stores evoked by thrombin or thapsigargin.

In vitro studies were used as an approach to investigate how simultaneous productions of NO and O2− from SIN-1 modify thrombin- or thapsigargin-induced platelet Ca2+ mobilization. Superoxide dismutase, the O2− scavenger, enhanced the capacity of SIN-1 to inhibit Ca2+ mobilization but catalase had no effect.

This suggests that the effects of SIN-1 on platelet Ca2+ handling resemble those of NO, but are modulated by simultaneous O2− release, independently of H2O2 formation.

 
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