Pharmacological modulation of platelet function in hypertension.
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.
Blann
Andrew D
AD
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK.
Nadar
Sunil
S
Lip
Gregory Y H
GY
D000959:Antihypertensive Agents / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008955:Models, Cardiovascular; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use
D000959:Antihypertensive Agents; D010975:Platelet Aggregation Inhibitors