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Platelets exhibit membrane receptor proteins the structure of which has adapted, in the course of evolution, to halt hemorrhage. These receptors are also implicated in thrombosis, and their structural variability is likely able to account for part of the variability in intraindividual susceptibility to thrombotic events. This review offers a summary of current knowledge on the molecular structure and function of platelet membrane receptors, here studied also in relation to the variability of platelet function in the general population, with the aim of discussing possible implications for the atherothrombotic risk.

The renin-angiotensin system (RAS) plays a central role in cardiovascular homeostasis. Angiotensin is the key peptide of the RAS, and exerts its influence on the heart and blood vessels both through its haemodynamic effects (via its influence on after-load and pre-load and determining coronary vasoconstriction) and through its direct cellular effects (via its actions on cell proliferation). Numerous studies in the past 10 years have demonstrated that the pharmacological inhibition of angiotensin converting enzyme (ACE), one of the two critical enzymes of the RAS, improves the outcome in patients with several cardiovascular disorders (hypertension, heart failure, ischaemic heart disease). These studies suggest a role of the RAS as a major determinant of cardiovascular risk. Recent data suggest that genetics may in turn contribute to modulating the effects of angiotensin on coronary vascular biology and ischaemia. This paper reviews the physiologic characteristics of the RAS and recent research developments related to angiotensin cell biology and pathobiology in heart disease. In particular, this review will cover the genetic aspects of RAS and their implications in cardiovascular disease.