Young M A, Watson R D, Littler W A
J Hypertens. 1985 Oct;3(5):481-3.
Intra-arterial blood pressure (IABP), baroreflex sensitivity and set point were measured in nine patients with essential hypertension during a control period and then after acute (4 h after a 12 mg oral dose) and chronic (after 3 months) treatment with the loop diuretic piretanide, mean dose 10 mg. Acutely, there was a fall in mean systolic IABP (P less than 0.05) associated with a reduction in pulse interval (P less than 0.01). Chronically, mean systolic IABP remained significantly reduced (P less than 0.01) but pulse interval returned to control values. There were no significant changes in baroreflex sensitivity, either acutely or chronically. These results demonstrate acute deactivation of the vagal efferent limb of the baroreflex followed by a chronic resetting of the baroreflex-heart rate mechanism. We conclude that changes in baroreflex sensitivity are not responsible for the hypotensive effects of this drug and that resetting of the reflex arc is likely to be due to physiological adaptation rather than to any direct drug effect.
对9例原发性高血压患者在对照期以及口服12mg剂量的髓袢利尿剂吡咯他尼(平均剂量10mg)后急性(口服后4小时)和慢性(3个月后)治疗期间测量动脉内血压(IABP)、压力感受器反射敏感性和调定点。急性治疗后,平均收缩期IABP下降(P<0.05),同时脉搏间期缩短(P<0.01)。慢性治疗后,平均收缩期IABP仍显著降低(P<0.01),但脉搏间期恢复至对照值。急性或慢性治疗期间压力感受器反射敏感性均无显著变化。这些结果表明压力感受器反射的迷走传出支急性失活,随后压力感受器反射-心率机制发生慢性重置。我们得出结论,压力感受器反射敏感性的变化并非该药物降压作用的原因,反射弧的重置可能是由于生理适应而非药物的任何直接作用。