Barrios Vivencio, Calderón Alberto, Navarro-Cid Josefa, Lahera Vicente, Ruilope Luis M
Department of Cardiology, Hospital Ramón y Cajal, Madrid, Spain.
Blood Press. 2002;11(4):235-9. doi: 10.1080/08037050213760.
Sulfhydryl group donors, such as N-acetylcysteine (NAC), may enhance the antihypertensive effect of some drugs through a nitric oxide (NO) mechanism. It has been observed that the hypotensive effect of angiotensin-converting enzyme inhibitors (ACEIs) is, at least partially, mediated by NO. We performed a within patient crossover study with the aim to investigate the potential effect of NAC on the ACEI antihypertensive action, via an NO-dependent mechanism. We studied 18 smoker (> 10 years of habit and > 10 cigarettes daily) hypertensive patients (15 males and three females, aged 69 +/- 5 years) on ACEI therapy (11 captopril and seven enalapril). Patients were randomly allocated to two treatment arms. In one arm, the patients (n = 10) initially received the addition of NAC (600 mg t.i.d.) to the ACEI regimen. In the other group (n = 8), the patients remained only on ACEI. After 21 days, the therapeutic patterns were crossed. The first group received only ACEI, and the second group received ACEI and NAC and completed other 21-day treatment period. We evaluate the effect of NAC on each patient by ambulatory blood pressure monitoring (ABPM), performed at the end of each therapeutic regimen. A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p < 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01). DtBP: 149.7 +/- 5.6 vs 141 +/- 3.7 and 92.1 +/- 4 vs 86 +/- 3.2 (both, p < 0.05). No significant difference was observed in night-time BP (ntBP). The NAC effect was not statistically different for the two ACEIs. In conclusion, the addition of NAC to an ACEI potentiates its antihypertensive effect during 24hBP and dtBP in smoker hypertensives. This effect may be mediated by an NO-dependent mechanism, probably through the protective effect of NAC on NO oxidation.
巯基供体，如N - 乙酰半胱氨酸（NAC），可能通过一氧化氮（NO）机制增强某些药物的降压作用。据观察，血管紧张素转换酶抑制剂（ACEI）的降压作用至少部分是由NO介导的。我们进行了一项患者自身交叉研究，旨在通过NO依赖性机制研究NAC对ACEI降压作用的潜在影响。我们研究了18例接受ACEI治疗（11例卡托普利和7例依那普利）的吸烟（吸烟习惯> 10年且每日> 10支香烟）高血压患者（15例男性和3例女性，年龄69±5岁）。患者被随机分配到两个治疗组。在一组中，患者（n = 10）最初在ACEI治疗方案中加用NAC（600 mg，每日三次）。在另一组（n = 8）中，患者仅继续使用ACEI。21天后，治疗方案交叉。第一组仅接受ACEI，第二组接受ACEI加NAC并完成另外21天的治疗期。我们通过在每个治疗方案结束时进行的动态血压监测（ABPM）评估NAC对每位患者的影响。与仅使用ACEI的时期相比，ACEI与NAC联合使用（ACEI + NAC）时，24小时收缩压和舒张压（24 hBP）以及日间血压（dtBP）显著降低：24 hBP = 146.1±4.2 vs 137±3.1（p < 0.05），89.2±2.8 vs 83.5±3.7mmHg（p = 0.01）。dtBP：149.7±5.6 vs 141±3.7以及92.1±4 vs 86±3.2（均p < 0.05）。夜间血压（ntBP）未观察到显著差异。两种ACEI的NAC效应在统计学上无差异。总之，在ACEI基础上加用NAC可增强其在吸烟高血压患者24 hBP和dtBP期间的降压作用。这种效应可能由NO依赖性机制介导，可能是通过NAC对NO氧化的保护作用。
