Urapidil treatment decreases plasma fibrinogen concentration in essential hypertension☆

Abstract 

The effects of antihypertensive drugs on cardiovascular metabolic risk factors were monitored in 42 patients with essential hypertension (diastolic blood pressure [DBP] >95 mm Hg). In a double-blind randomized parallel-group study, they were treated with atenolol 50 mg once per day (n = 25) or urapidil 60 mg twice per day (n = 17), a peripheral α₁-receptor blocker with an additional central serotonin 1A (5HT1A) receptor agonistic effect, for 12 weeks. Plasma fibrinogen concentration decreased by 24% (P < .0001) during urapidil treatment and by 9% (P = .05) during atenolol treatment, with the effects of the two drugs differing significantly. Plasminogen activator inhibitor (PAI) activity tended to increase by 17% (nonsignificant [NS]) in the atenolol-treated group and to decrease by 4% (NS) in the urapidil group. Differences between the effects of the two drugs on very—low-density lipoprotein (VLDL) triglycerides (TG) and on total TG were significant. During urapidil medication, these two parameters were reduced by 22% and 13%, respectively, but the changes were nonsignificant (P = .11 and P = .14, respectively). In contrast, atenolol treatment caused a significant increase in both VLDL TG and total TG of 31% and 21%, respectively. Hemoglobin A_1c (HbA_1c) increased by 4% (P = .06) during atenolol treatment, but was unaffected by urapidil. There were no significant changes within or between atenolol- and urapidil-treated groups regarding glucose disposal on an oral glucose tolerance test (OGTT) or the insulin sensitivity index on a hyperinsulinemic-euglycemic clamp test. In conclusion, urapidil treatment was characterized by neutral or favorable effects on several variables associated with the metabolic syndrome. Atenolol treatment had neutral properties in some metabolic aspects, but deleterious effects on lipid status.

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