Effects of aspirin on intra-platelet vascular endothelial growth factor, angiopoietin-1, and p-selectin levels in hypertensive patients.
BACKGROUND
Although aspirin is useful in reducing platelet activation and cardiovascular events, its effects on platelet levels of angiogenic factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), and markers of platelet activation in hypertension are unknown. The aim of this study was to study the effects of aspirin on the platelet morphology, plasma and platelet levels of VEGF (sVEGF and pVEGF respectively), Ang-1 (sAng-1 and pAng-1 respectively), and P-selectin (sPsel and pPsel respectively) in patients with well controlled hypertension.


METHODS
A total of 35 aspirin-naive, hypertensive patients (29 male and six female; mean age 64 years) were compared with 30 (23 male, seven female, mean age 59 years) normotensive control subjects. Blood was collected for plasma VEGF, P-selectin, and Ang-1 (enzyme-linked immunoassay), intra-platelet levels of VEGF, Ang-1, and P-selectin, and platelet volume and mass. Research indices in hypertensive patients were studied before and after 3 months treatment with aspirin 75 mg daily.


RESULTS
Hypertensive patients had significantly higher plasma levels of VEGF (P=.04), Ang-1 (P<.001), as well as pVEGF (P=.008), pAng-1(P=.001), sPsel (P=.02), pPsel (P<.001), and mean platelet mass (P=.01) when compared with control subjects. After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1. Neither pVEGF nor pAng-1 correlated with blood pressure or with their respective plasma levels.


CONCLUSIONS
The use of aspirin in high-risk hypertensive patients leads to a reduction in intra-platelet angiogenic growth factors and platelet activation. This may have implications for the use of aspirin in conditions (such as vascular disease) that have been associated with an increase in angiogenesis and platelet activation.
Nadar
Sunil
S
Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England.
Blann
Andrew D
AD
Lip
Gregory Y H
GY
D000368:Aged; D042683:Angiopoietin-1 / Q000097:blood*; D001241:Aspirin / Q000494:pharmacology* / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D016022:Case-Control Studies; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D004739:England; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood / Q000187:drug effects*; D015539:Platelet Activation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D010976:Platelet Count; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000187:drug effects*
D042683:Angiopoietin-1; D015415:Biomarkers; D016861:Cyclooxygenase Inhibitors; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D042461:Vascular Endothelial Growth Factor A; D001241:Aspirin