Key result
Vitamin C prevents lead-induced blood pressure elevation and impaired vascular relaxation in rats.
Why the study?
Low-level lead exposure causes hypertension associated with increased reactive oxygen species and impaired endothelial-dependent vasorelaxation, but its effect on the vascular NO/cGMP system was unclear.
Does vitamin C cotreatment prevent lead-induced hypertension and vascular NO/cGMP system alterations in Wistar rats?
Does vitamin C cotreatment prevent lead-induced hypertension and vascular NO/cGMP system alterations in Wistar rats?
Answers are grounded in this paper and cite their sources.
Vitamin C prevents lead-induced hypertension and restores the NO/cGMP relaxing system in the vascular wall of rats, suggesting reactive oxygen species mediate lead's vascular toxicity.
Low-level lead exposure is a known cause of hypertension that has been associated with increased reactive oxygen species activity and endothelial-dependent vasorelaxation impairment. The effect of lead exposure on the vascular nitric oxide (NO)/cyclic guanocine monophosphate (cGMP) system was analyzed. Wistar rats were exposed to 5 ppm lead acetate in the drinking water during 30 d. Mean arterial BP increased significantly in the lead-treated rats. Relaxation to both acetylcholine and sodium nitroprusside (SNP) was reduced in lead-treated rats; however, the vascular wall of lead-administered rats showed an increased expression of endothelial NO synthase. The expression of both subunits (alpha(1) and beta(1)) of soluble guanylate cyclase (sGC) and the cGMP accumulated in the vascular wall were decreased in lead-treated rats. Cotreatment of lead with vitamin C (3 mmol/L) prevented the increase on mean arterial BP, improved the relaxation to both acetylcholine and sodium nitroprusside, and restored the normal expression of endothelial NO synthase and sGC proteins in the vascular wall. In conclusion, lead exposure altered both the endothelium-dependent and -independent relaxing response and induced a reduced expression of sGC in the vascular wall. These effects were abrogated with the antioxidant vitamin C, which suggests the involvement of reactive oxygen species in the regulation of the NO/cGMP relaxing system in the vascular wall of lead-treated rats.
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Marqués et al. (2001) studied Lead-induced hypertension. Lead acetate vs. Unexposed controls / Vitamin C cotreatment was evaluated on Mean arterial blood pressure and vascular relaxation. Lead exposure increased mean arterial blood pressure and impaired vascular relaxation in rats, effects that were prevented by cotreatment with vitamin C.
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