ABSTRACT
Lead (Pb(2+)) exposure is related to increased blood pressure or hypertension of human or animals. Abnormal vascular relaxant responses of low level Pb(2+) exposed animals were reported by several studies. However, it is difficult to tell whether these effects were induced directly by Pb(2+) or not. In this study we hypothesized that Pb(2+) can directly affect the relaxation of vessels. Male Wistar rat aortae were removed and cultured in PMRI 1640 with 1 ppm Pb(2+) (4.8 microM lead acetate) for 0.5, 6, 12 and 24h, and then their responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were examined. After incubated for 24h, the relaxation induced by ACh was significantly decreased in Pb(2+) exposed aortic rings. However, there was not significant difference in relaxation induced by SNP between Pb(2+) exposed and control group. The nitrite in the culture media of aortic rings cultured for 24h, measured with Griess method, was significantly decreased in the Pb(2+) exposed group. The expression of endothelial NOS (eNOS) and isoform NOS (iNOS) in the homogenate of aortic rings cultured for 24h was measured by Western blot. The expression of eNOS of the Pb(2+) exposed group was significantly upregulated compared with that of the control group. However, there was no significant difference in the expression of iNOS in control and Pb(2+) exposed group. In conclusion, Pb(2+) was able to directly affect the relaxation of rat aorta. This effect may have some relation with the lower level of NO in the media, though the expression of eNOS was upregulated.
