Abstract
Hemodynamic studies (using radiocardiography) were performed before and 9 weeks after oral administration of prazosin (av. 8.0mg/day), and 5 weeks afterthat of ecarazine (av. 115 mg/day), metoprolol (av. 195mg/day) or pindolol (av. 27mg/day) in 61 outpatients with essential hypertension (av. 46.2 yrs., WHO I-II). Metoprolol reduced mean arterial pressure (MAP) from 132± 5mmHg to 115±4 mmHg (P< 0.01). The cardiac index (CI) fell from 4.10±0.24 1/min/m2 to 3.30±0.221/min/m2 (P<0.01) without any change in the total peripheral resistanceindex (TPRI). Pindolol reduced MAP from 130±3 mmHg to 116±2 mmHg (P <0.01).TPRI fell from 2, 781±136 dyne·sec·cm-5·m2 to 2, 442±156 dyne·sec·cm-5·m2, although the decrease was not significant. However, there was a significant correlation between the changes in TPRI and MAP in the pindolol-treated group (n=23, r=0.716, P<0.005). Both prazosin and ecarazine reduced MAP (prazosin, from 128 ± 3mmHg to 116±3mmHg, P<0.025; ecarazine, from 130±3mmHg to117±4 mmHg, P<0.005). Both of these vasodilators induced a small and insignifi-cant decrease in TPRI (prazosin, from 3, 062±231 dyne·sec·cm-5·m2 to 2, 837±287dyne·sec·cm-5·m2; ecarazine, from 2, 655±175 dyne·sec·cm-5·m2) without any change in CI.The addition of prazosin or ecarazine to the pretreated group with metoprolol tended to lead to a further decrease in MAP and a reduction in TPRI (from av. 3, 315dyne·sec·cm-5·m2 to av. 2, 743 dyne·sec·cm-5·m2, not significant) with aslight increase in CI. These changes were similar to those observed with the use of prazosin or ecarazine alone. In contrast, the addition of metoprolol to the vasodi-lator therapy induced a decrease in CI, although statistically insignificant. After pretreatment with pindolol, the addition of prazosin or ecarazine induced a re-duction in MAP and a further decrease in TPRI without a concomitant increase in CI. When pindolol was given to patients pretreated with ecarazine, MAP and TPRI tended to decrease further, but not significantly.Increased peripheral resistance has been considered the hemodynamic hallmark in most cases of essential hypertension, and the antihypertensive action of some beta-adrenergic blockers may be attributed mainly to a decrease in vascular re-sistance as observed in the pindolol therapy in this study. This study revealed that the beta-adrenergic blockers induced less reduction in TPRI in the non-responders than in the responders. These results suggest that vasodilators such as prazosin and ecarazine may induce a further reduction in TPRI in the beta-blocker-treated patients, and so the vasodilators may be useful as adjuncts to beta-blockade in the treatment of essential hypertension.
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