Pharmacological modulation of platelet function in hypertension

Andrew D. Blann, Sunil Nadar, Gregory Y.H. Lip*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

80 Citations (Scopus)


Platelets exert a considerable influence on human morbidity and mortality. The rationale for their study in hypertension follows the observation that the major consequences of hypertension are stroke and myocardial infarction. However, the etiology of these consequences in hypertension is, paradoxically, not hemorrhagic (as might be expected from the effects of high blood pressure), but occlusive, with thrombus being the culprit lesion. Mechanisms of platelet activation include high shear force, activation of the renin-angiotensin system, endothelial changes, and the presence of comorbidity, such as atrial fibrillation. The treatment of high blood pressure brings about a reversal of the changes seen in the cell. This could be in part due to the direct effect of the drug on the megakaryocyte and/or the platelets themselves, or it might simply be due to the reduction in blood pressure. Some drugs, such as calcium channel antagonists and angiotensin II receptor blockers, however, might have direct effects on platelet biochemistry other than reducing blood pressure. Finally, antiplatelet drugs are becoming an important part of the management of high-risk hypertensives, which aim to minimize vascular complications.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
Issue number1
Publication statusPublished - Jul 1 2003


  • Antihypertensive therapy
  • Chronic
  • Hypertension
  • Platelet activation

ASJC Scopus subject areas

  • Internal Medicine


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