Abstract
We previously demonstrated that 7‐day exposure with a low concentration of lead acetate increases blood pressure (BP) and nitric oxide (NO) bioavailability, which could be a compensatory mechanism in the initial stages of lead exposure.We investigated the involvement angiotensin II and PI3K/AKT pathway in this increased NO bioavailability. Wistar rats were treated with lead (1st dose 4 μg/100g and, subsequent doses 0.05 μg/100g, i.m cover daily loss) or vehicle. After lead treatment, blood levels were of 9.98μg/dL. In aortic rings from lead‐treated rats, phenylephrine (PHE 10‐10‐10‐4M) contractile responses were reduced; L‐NAME (LN‐10µM) increased PHE responses more in lead‐treated rats than untreated rats. Wortmannin (WT‐0,1µM) and PD123319 (PD‐1µM) normalized PHE responses in treated rats, and in presence of either WT, PD or losartan (LOS) that effect of LN on reactivity from lead treated group was blunted. Lead also increased release of NO, which was blocked by LOS, WT and PD. Our results suggest the involvement of angiotensin II and PI3K/AKT pathway in increased NO bioavailability in lead rats. This might be an alternative way to increase the NO bioavailability, as a compensatory mechanism against the increased SBP in the early stages of lead exposure.Grant Funding Source: CAPES, CNPq and FAPES.
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