Tomat Analía L, Weisstaub Adriana R, Jauregui Agustín, Piñeiro Adriana, Balaszczuk Ana M, Costa María A, Arranz Cristina T
Cátedra de Fisiología, Universidad de Buenos Aires, Argentina.
Pediatr Res. 2005 Oct;58(4):672-6. doi: 10.1203/01.PDR.0000180540.55990.EB.
There is an increasing interest in the involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases. This study was designed to examine whether moderate zinc deficiency during growth influences blood pressure (BP) and vascular nitric oxide (NO) pathway. Three-week-old weaned male Wistar rats were randomly divided into two dietary groups and fed either a moderately zinc-deficient diet (zinc content 9 mg/kg; n = 12) or a control diet (zinc content 30 mg/kg; n = 12) for 60 d. The following were measured: systolic BP, nitrates and nitrites urinary excretion, urinary chemiluminescence intensity, NADPH-diaphorase activity in the thoracic aorta and intestinal arterioles, and NO synthase (NOS) catalytic activity using L-[U14C]-arginine as substrate in the thoracic aorta. Zinc deficiency during growth induced an increase in BP from day 30 of the experimental period, leading to hypertension on day 60. Animals that were fed the zinc-deficient diet had lower urinary excretion levels of nitrates and nitrites and higher intensity of spontaneous luminescence on day 60. At the end of the experiment, zinc-deficient rats showed decreased NADPH diaphorase activity in endothelium and smooth muscle of the thoracic aorta and intestinal arterioles and decreased activity of NOS in thoracic aortic tissue. An imbalance in zinc bioavailability during postnatal and growing periods may be may be a risk factor in development of cardiovascular alterations in adult life. The mechanisms involved may include an impaired vascular NO system as a result of decreased NOS activity and higher systemic oxidative stress.
锌等微量元素在心血管疾病发病机制中的作用越来越受到关注。本研究旨在探讨生长期间中度锌缺乏是否会影响血压(BP)和血管一氧化氮(NO)途径。将3周龄断奶雄性Wistar大鼠随机分为两组,分别给予中度缺锌饮食(锌含量9 mg/kg;n = 12)或对照饮食(锌含量30 mg/kg;n = 12),持续60天。测量以下指标:收缩压、尿硝酸盐和亚硝酸盐排泄量、尿化学发光强度、胸主动脉和肠小动脉中NADPH-黄递酶活性,以及以L-[U14C]-精氨酸为底物在胸主动脉中测量的一氧化氮合酶(NOS)催化活性。生长期间的锌缺乏从实验期第30天开始导致血压升高,在第60天导致高血压。喂食缺锌饮食的动物在第60天尿硝酸盐和亚硝酸盐排泄水平较低,自发发光强度较高。实验结束时,缺锌大鼠胸主动脉和肠小动脉内皮和平滑肌中的NADPH黄递酶活性降低,胸主动脉组织中的NOS活性降低。出生后和生长期间锌生物利用度的失衡可能是成年后心血管改变发生的一个危险因素。涉及的机制可能包括由于NOS活性降低和全身氧化应激增加导致的血管NO系统受损。