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 ϭ 12) or a control diet (zinc content 30 mg/kg; n ϭ 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. Moderate and marginal zinc deficiency is by far more common than severe deficiency, especially in infants, children, and pregnant women in developing and developed countries, as a result of imbalances between intake and increased requirements (1,2). Zinc is an essential trace element required by all living organisms for many physiologic functions, including growth, development, and reproduction (3). Zinc has been documented to act as an antioxidant, to have membranestabilizing properties, to block apoptotic cell death, and to be essential for endothelial integrity (4 -6). Intracellular zinc is associated with proteins, primarily via complex interactions with cysteines, acting as an integral component of numerous metalloenzymes, structural proteins, and transcription factors (1,7).There is increasing interest in possible involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases (8). Many enzymes that are involved in the regulation of arterial blood pressure (BP), such as nitric oxide (NO) synthase (NOS), angiotensin-converting enzyme, and neutral endopeptidases, contain zinc in their structure (9 -11). The NOSs are a family of enzymes that catalyze the synthesis of NO and L-citrulline from L-arginine in the presence of NADPH and O 2 . The NOS family consists of three isoforms that are expressed in many tissues, including endothelium and vascular
