Simon G, Snyder D K
Clin Pharmacol Ther. 1984 Sep;36(3):315-9. doi: 10.1038/clpt.1984.181.
The effect of long-term treatment with nitrendipine on systemic pressor responses to norepinephrine (NE) and angiotensin II (AII) was evaluated in 11 subjects with mild, uncomplicated hypertension. Pressor responses to NE and AII were measured at the end of a 4-wk placebo period and after 5 wk treatment with nitrendipine (final dose 16 mg twice daily; range 5 to 20 mg/day) or placebo. In subjects who received nitrendipine, clinic supine blood pressure was reduced from 152 +/- 12/96 +/- 4 mm Hg to 134 +/- 11/84 +/- 5 mm Hg and pressor responses to NE but not to AII were attenuated. Endogenous plasma levels of NE and renin activity were not changed by nitrendipine. Data suggest that noradrenergic blood pressure control mechanisms depend more on cellular calcium transport than do AII-mediated ones and may help explain the greater effectiveness of calcium entry blockers in the treatment of low-renin hypertension.
在11例轻度、无并发症的高血压患者中，评估了硝苯地平长期治疗对去甲肾上腺素（NE）和血管紧张素II（AII）引起的全身升压反应的影响。在4周安慰剂期结束时以及使用硝苯地平（最终剂量为每日两次16mg；范围为5至20mg/天）或安慰剂治疗5周后，测量对NE和AII的升压反应。在接受硝苯地平治疗的患者中，临床仰卧位血压从152±12/96±4mmHg降至134±11/84±5mmHg，对NE的升压反应减弱，但对AII的升压反应未减弱。硝苯地平未改变内源性血浆NE水平和肾素活性。数据表明，去甲肾上腺素能血压控制机制比AII介导的机制更依赖于细胞钙转运，这可能有助于解释钙通道阻滞剂在低肾素性高血压治疗中更有效的原因。
