Platelet deactivation by 5HT₂receptor blockade parallels the antihypertensive response to ketanserin

Abstract

Serotonin (5HT) has been implicated in thromboembolic complications and blood pressure elevation and both may be reduced with the 5HT₂-receptor blocker ketanserin. In 17 patients with essential hypertension (WHO I and II, diastolic pressure V ≥ 100 mmHg) blood pressure, platelet 5HT uptake, content and release as well as 5HT-induced shape change and aggregation were measured before and immediately after 8 weeks oral ketanserin at 20–40 mg twice daily. During ketanserin therapy, platelet 5HT release, shape change reaction and aggregation to 5HT were significantly reduced by more than 50%. These platelet effects were more pronounced in patients responsive to ketanserin (≥10% decrease of diastolic pretreatment pressure) and the fall in diastolic pressure correlated with the inhibition of 5HT-induced aggregation as well as the change in 5-hydroxy-indoleacetic acid (5HIAA) in platelet-rich plasma (PRP; P < 0.05). Serotonin-receptor-independent platelet events were not affected by ketanserin. Ketanserin corrects 5HT₂-receptor-mediated platelet function along with the reduction of blood pressure.