The Effect of Prazosin Therapy on Platelet Activation in Essential Hypertension

Abstract

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.

Pharmacological Modulation of Platelet Function in Hypertension

“…58 -60 Table 2 also shows the variability in effects reported by different groups, some of whom studied purified platelets ex vivo. [61][62][63][64][65][66][67][68][69][70][71][72] There appears to be little consensus of an effect on aggregation, although other pathophysiologic mechanisms (such as fibrinolysis 51,73 ) might be influenced by these classes of drugs. Gleerup et al 70 showed that treatment with both atenolol and isradipine was associated with reduced plasminogen activator inhibitor, a molecule involved in fibrinolysis that is known to be present in platelets as well as other cells.…”

Diltiazem Inhibits the Spontaneous Platelet Aggregation in Essential Hypertension

“…Our previous report has indicated that the increased platelet aggregation and in vivo platelet activation in essential hyper tension need not be restored to normal after effective decrease in blood pressure by pra zosin [3], Since a positive correlation of the elevated platelet free cytosolic calcium con tent with the arterial blood pressure in essen tial hypertension was observed [15], both antihypertensive and antiplatelet properties of the calcium channel blocker diltiazem could be supposed. However, the effect of diltiazem on platelet functions in essential hypertension was not studied.…”

“…The increased platelet aggregation and in vivo activation in essential hypertension were observed by many authors [1][2][3]. The interaction of activated platelets with the vessel wall may be one of the factors of the endothelial damage and, theoretically, of the acceleration of atherosclerosis [4,5].…”