Katzman P L, Hulthén U L, Hökfelt B
Department of Endocrinology, Lund University Clinics, General Hospital, Malmö, Sweden.
Acta Med Scand. 1988;223(2):125-31. doi: 10.1111/j.0954-6820.1988.tb15776.x.
Studies were performed in 10 male patients with untreated essential hypertension, WHO grade I-II, aged 25-62 years, to explore the acute (single dose) and long-term (8 weeks) effects of felodipine on sympathetic activity--evaluated by plasma and urinary catecholamines--as related to blood pressure, heart rate and the activity in the renin-angiotensin-aldosterone system. The patients were hospitalized for 8 (acute) and 6 (long-term) days and were maintained on a standardized daily intake of sodium (150 mmol), potassium (75 mmol) and water (2,500 ml). Acute felodipine administration (10 mg) significantly reduced blood pressure and increased heart rate. Plasma and urinary noradrenaline, plasma renin activity and angiotensin II increased, whereas plasma and urinary adrenaline, dopamine, aldosterone and plasma vasopressin were unaltered. Long-term felodipine treatment, 10 mg twice daily, reduced blood pressure to a similar extent as acute felodipine administration, but heart rate was not significantly changed. Plasma noradrenaline 3 and 12 hours after the last dose and urinary noradrenaline were increased, whereas plasma and urinary adrenaline and dopamine were unchanged. Plasma renin activity and angiotensin II were increased 3 hours, but unchanged 12 hours after the last dose. Plasma aldosterone was unchanged but urinary aldosterone increased. Plasma vasopressin was unchanged. The changes in plasma noradrenaline as related to blood pressure, heart rate, plasma renin activity and angiotensin II during long-term felodipine treatment may reflect decreased cardiac and renal beta-adrenoceptor-mediated responses. Increased renal clearance of aldosterone could partly explain the unaltered plasma aldosterone level in spite of increased plasma angiotensin II following long-term felodipine treatment.
对10名未经治疗的原发性高血压男性患者（年龄25 - 62岁，WHO分级为I - II级）进行了研究，以探讨非洛地平对交感神经活性的急性（单剂量）和长期（8周）影响——通过血浆和尿儿茶酚胺评估——及其与血压、心率和肾素 - 血管紧张素 - 醛固酮系统活性的关系。患者住院8天（急性研究）和6天（长期研究），并维持标准化的每日钠（150 mmol）、钾（75 mmol）和水（2500 ml）摄入量。急性给予非洛地平（10 mg）可显著降低血压并增加心率。血浆和尿去甲肾上腺素、血浆肾素活性和血管紧张素II升高，而血浆和尿肾上腺素、多巴胺、醛固酮和血浆血管加压素未改变。长期非洛地平治疗，每日两次，每次10 mg，血压降低程度与急性给予非洛地平相似，但心率无显著变化。末次给药后3小时和12小时的血浆去甲肾上腺素及尿去甲肾上腺素升高，而血浆和尿肾上腺素及多巴胺未改变。末次给药后3小时血浆肾素活性和血管紧张素II升高，但12小时后未改变。血浆醛固酮未改变，但尿醛固酮增加。血浆血管加压素未改变。长期非洛地平治疗期间血浆去甲肾上腺素与血压、心率、血浆肾素活性和血管紧张素II的变化可能反映了心脏和肾脏β - 肾上腺素能受体介导反应的降低。醛固酮肾清除率增加可部分解释长期非洛地平治疗后尽管血浆血管紧张素II升高但血浆醛固酮水平未改变的原因。
