1. Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or adenosine diphosphate [ADP]) were determined in 26 normotensive subjects and 26 patients with untreated essential hypertension. Groups of 18 essential hypertensive patients and 18 age- and sex-matched normotensives were compared. 2. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measures were repeated in 18 essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline-induced as well as ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on initial and total aggregability. 3. The results confirm increased platelet aggregation and in vivo platelet activation in patients with essential hypertension; however there is a discrepancy with previous reports about those results obtained after prazosin therapy. The results suggest that increased platelet aggregation and in vivo activation need not be restored to normal after effective antihypertensive therapy alone. They give reason for the combination of antihypertensive together with anti-aggregatory therapy in essential hypertension.

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Plasma β-thromboglobulin, initial (spontaneous) and total platelet aggregation, induced by adrenaline or ADP, were determined in 15 patients with essential hypertension before and after 1 week of diltiazem therapy. Diltiazem significantly decreased the spontaneous platelet aggregation in a therapeutic dose of 3 × 60 mg/day. This antiaggregatory effect is the further advantage of the antihypertensive therapy with diltiazem that may be of importance for the inhibition of atherosclerotic and thrombotic complications in essential hypertension.

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The reduction of increased platelet aggregation in essential hypertension is one of the aims of modern antihypertensive therapy. Twenty-one hospitalized patients with non-treated essential hypertension were examined. The platelet function measurements were made before the therapy and after 1 week of celiprolol administration (300 mg/day). Fifteen essentially hypertensive patients were investigated before and after 1 week of placebo administration. Plasma β-thromboglobulin was assayed, and the whole blood platelet aggregation (initial and total – induced by adrenaline and ADP) was measured. A significant decrease in adrenaline-induced (from 19 to 13%, p < 0.02) and ADP-induced aggregation (from 15 to 13%, p < 0.05) was observed after celiprolol administration. This reduction of adrenaline-induced platelet aggregation may be explained by the stimulation effect of celiprolol on platelet β_2- receptors. Thus, some inhibitory effect of celiprolol on platelet aggregation is one of the further advantages of this drug in the therapy of essential hypertension.