Abstract
To clarify the long-term effects of α-adrenergic blockade on blood pressure, glucose, and lipid metabolism, a slective α 1-adrenergic inhibitor (prazosin, 1.0 to 2.0 mg/day in divided doses) was administered as a single antihypertensive agent to 10 (four men and six women, aged 52 to 76 years) hypertensive patients (systolic blood pressure [SBP] ≥ 150 mm Hg or diastolic blood pressure [DBP] ≥ 90 mm Hg) with non-insulin-dependent diabetes mellitus (NIDDM) for up to 20 weeks. Blood pressure, glucose tolerance and immunoreactive insulin (IRI) response to 75 gm oral glucose load, hemoglobin A 1 (Hb A 1), serum lipid profile, and serum apolipoprotein were examined before and after treatment. SBP and DBP were significantly reduced at 20 weeks after treatment with the selective α 1-adrenergic inhibitor (SBP 167 ± 6 mm Hg versus 152 ± 7 mm Hg; DBP 81 ± 3 mm Hg versus 76 ± 3 mm Hg, ( p < 0.05 and p < 0.01), respectively). Glucose tolerance and IRI response to glucose load were not significantly changed at 4 and 12 to 20 weeks after selective α 1-inhibitor treatment compared with the baseline data before treatment; the level of Hb A 1 was not significantly changed at 4 and 20 weeks after treatment. Total cholesterol and free fatty acid (FFA) concentrations were significantly reduced at 20 weeks (total cholesterol 213 ± 13 mg/dl versus 196 ± 10 mg/dl [5.52 ± 0.34 mmol/L versus 5.08 ± 0.26 mmol/L], FFA 0.67 ± 0.11 mEq/L versus 0.48 ± 0.11 mEq/L; p < 0.05 and p < 0.01, respectively). High-density lipoprotein (HDL) cholesterol and the ratio of HDL: total cholesterol were significantly increased at 20 weeks after treatment (HDL cholesterol 46 ± 3 mg/dl versus 48 ± 3 mg/dl [1.19 ± 0.08 mmol/L versus 1.24 ± 0.08 mmol/L], HDL cholesterol: total cholesterol 0.22 ± 0.02 mg/dl versus 0.25 ± 0.02 mg/dl, p < 0.05, respectively). No significant change in the levels of triglyceride or apolipoprotein A 1, B, C 2, C 3, and E was observed during treatment. These data suggest that treatment with a selective α 1-adrenergic inhibitor elicits a favorable effect on blood pressure and lipid metabolism without causing a deterioration in blood glucose control in hypertensive NIDDM patients.
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