Abstract
We investigated whether exposure to small concentrations of lead alters blood pressure and vascular reactivity. Male Wistar rats were sorted randomly into the following two groups: control (Ct) and treatment with 100 ppm of lead (Pb), which was added to drinking water, for 30 days. Systolic blood pressure (BP) was measured weekly. Following treatment, aortic ring vascular reactivity was assessed. Tissue samples were properly stored for further biochemical investigation. The lead concentration in the blood reached approximately 8 μg/dL. Treatment increased blood pressure and decreased the contractile responses of the aortic rings to phenylephrine (1 nM–100 mM). Following N-nitro-L arginine methyl ester (L-NAME) administration, contractile responses increased in both groups but did not differ significantly between them. Lead effects on Rmax were decreased compared to control subjects following superoxide dismutase (SOD) administration. Catalase, diethyldithiocarbamic acid (DETCA), and apocynin increased the vasoconstrictor response induced by phenylephrine in the aortas of lead-treated rats but did not increase the vasoconstrictor response in the aortas of untreated rats. Tetraethylammonium (TEA) potentiated the vasoconstrictor response induced by phenylephrine in aortic segments in both groups, but these effects were greater in lead-treated rats. The co-incubation of TEA and catalase abolished the vasodilatory effect noted in the lead group. The present study is the first to demonstrate that blood lead concentrations well below the values established by international legislation increased blood pressure and decreased phenylephrine-induced vascular reactivity. The latter effect was associated with oxidative stress, specifically oxidative stress induced via increases in hydrogen peroxide levels and the subsequent effects of hydrogen peroxide on potassium channels.
Highlights
Lead is a common industrial and environmental pollutant that exerts a variety of acute and chronic toxic effects [1]
We performed incubation with diethyldithiocarbamic acid (DETCA) (0.5 mM), an inhibitor of Cu/Zn superoxide dismutase that increased both vasoconstrictor responses and phenylephrine sensitivity in the aortic rings of animals treated with lead (Fig. 6). These results suggest that superoxide anion levels and endogenous Cu/Zn SOD activity are both increased in lead-treated animals, which may contribute to increased hydrogen peroxide levels
The major findings of this study indicate that chronic treatment with low concentrations of lead increases systolic arterial blood pressure and decreases the contractile responses induced by phenylephrine in rat aortas
Summary
Lead is a common industrial and environmental pollutant that exerts a variety of acute and chronic toxic effects [1]. The manufacturing and recycling of these products may result in sufficient lead exposure to cause the development of acute and chronic health problems [3]. Chronic lead exposure may trigger a cascade of events that culminates in the development of hypertension and cardiovascular disease [1]. Navas-Acien and collaborators (2007) [4] reviewed the link between lead exposure and cardiovascular events in several population studies, highlighting the elevation of arterial pressure. The cardiovascular effects of lead are not limited to increases in blood pressure. Several reports have indicated that lead treatment can either increase or decrease aortic ring vascular reactivity to phenylephrine in response to different conditions and stimuli [5,6,7,8]
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