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Urapidil treatment decreases plasma fibrinogen concentration in essential hypertension
Insights
Urapidil favorably impacts cardiovascular metabolic risk factors like fibrinogen and triglycerides in hypertensive patients. Atenolol showed neutral to detrimental effects on lipids and hemoglobin A1c.
Area of Science:
- Cardiology
- Pharmacology
- Metabolic Syndrome Research
Background:
- Essential hypertension management requires monitoring cardiovascular metabolic risk factors.
- Antihypertensive medications can differentially affect metabolic profiles.
Purpose of the Study:
- To compare the effects of urapidil and atenolol on cardiovascular metabolic risk factors in patients with essential hypertension.
Main Methods:
- A 12-week, double-blind, randomized parallel-group study.
- 42 patients with essential hypertension were treated with either urapidil (n=17) or atenolol (n=25).
- Evaluated plasma fibrinogen, PAI activity, VLDL triglycerides, total triglycerides, HbA1c, and glucose metabolism.
Main Results:
- Urapidil significantly decreased plasma fibrinogen (24%) and tended to decrease PAI activity (4%).
- Atenolol showed a smaller decrease in fibrinogen (9%) and a tendency to increase PAI activity (17%).
- Urapidil reduced VLDL triglycerides (22%) and total triglycerides (13%), while atenolol significantly increased them (31% and 21%, respectively).
- HbA1c increased with atenolol (4%) but was unaffected by urapidil.
- No significant differences in glucose disposal or insulin sensitivity were observed between groups.
Conclusions:
- Urapidil demonstrated neutral to favorable effects on metabolic syndrome variables, including lipids and fibrinogen.
- Atenolol exhibited neutral effects in some metabolic aspects but had deleterious effects on lipid status.
- Urapidil may be a preferred option for hypertensive patients with metabolic concerns.
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 alpha1-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 A1c (HbA1c) 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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