Skip to main content
Log in

Blood pressure relationship to nitric oxide, lipid peroxidation, renal function, and renal blood flow in rats exposed to low lead levels

  • Original Articles
  • Published:
Biological Trace Element Research Aims and scope Submit manuscript

Abstract

The results of experiments designed to show that inhibition of nitric oxide production in rats exposed to low lead levels increases vascular resistance, decreases renal blood flow and glomerular function, and enhances oxidative stress. Forty-five adult male Sprague-Dawley rats were divided into four groups. Group A was used as controls and consisted of rats that received no treatment; group B acted as NO-inhibited controls by receiving l-NAME (N G-nitro-l-arginine methyl ester) as the NO inhibitor; group C was injected intraperitoneally with 8 mg/kg lead acetate for 2 wk; and group D receiving lead acetate plus l-NAME.

Compared to healthy controls, significant elevation of the mean (p<0.01), systolic (p<0.04), and diastolic (p<0.01) blood pressures was found in the lead-treated rats. The renal blood flow was 1550±468 blood per unit (bpu) in the controls, 488±220 bpu in the l-NAME controls, 1050±458 bpu in the lead-treated group, and 878±487 bpu in the Pb plus l-NAME group.

Low-level lead exposure did not change the urinary flow rate, creatinine clearance, and the creatinine, potassium, phosphorus, glucose, and protein excretion in 24-h urine. In the lead plus NO-inhibited rats, a significant decrease in sodium ion excretion was observed (p<0.01). The NO levels of the lead exposed, l-NAME-treated controls, and l-NAME plus lead-exposed groups are significantly lower compared to untreated control:: p<0.002, p<0.001, and p<0.01, respectively. When compared to untreated controls, the plasma malondialdehyde levels were not significantly different in the lead exposed, lead plus l-NAME, and l-NAME control groups.

These results suggest that lead-induced hypertension might be related to a decrease of NO and consequent vasoconstriction, rather than to a decrease of renal blood flow or to decreases in renal sodium.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. W. R. Harlan, The relationship of blood lead levels to blood pressure in the us population, Environ. Health Perspect. 78, 9–13 (1988).

    Article  PubMed  CAS  Google Scholar 

  2. H. C. Gonick, Y. Ding, S. C. Bandy, Z. Ni, and N. D. Varizi, Lead-induced hypertension: interplay of nitric oxide and reactive oxygen species, Hypertension, 30, 1487–1492 (1997).

    PubMed  CAS  Google Scholar 

  3. N. D. Vaziri, Y. Ding, Z. Ni, and H. C. Gonick, Altered nitric oxide metabolism and increased oxygen free radical activity in lead-induced hypertension: effect of lazaroid therapy, Kidney Int., 52, 1042–1046 (1997).

    Article  PubMed  CAS  Google Scholar 

  4. N. D. Vaziri, Y. Ding, Z. Ni, and H. C. Gonick, Nitric oxide synthase expression in course endothelial cells; role of superoxide, Hypertension 34, 558–562 (1999).

    PubMed  CAS  Google Scholar 

  5. N. D. Vaziri, K. Liang, and Y. Ding, Increased nitric oxide inactivation by reactive oxygen species in lead-induced hypertension, Kidney Int. 56, 1492–1498 (1999b).

    Article  PubMed  CAS  Google Scholar 

  6. D. A. Tsao, H. S. Yu, J. T. Cheng, C. K. Ho, and H. R. Chang, The change of beta-adrenergic system in lead-induced hypertension, Toxicol. Appl. Pharmacol., 164, 127–133 (2000).

    Article  PubMed  CAS  Google Scholar 

  7. M. Carmignani, P. Buscolo, A. Poma, and A. R. Volpe, Kininergic system and arterial hypertension following chronic exposure to inorganic lead, Immunopharmacology 44, 105–110 (1999).

    Article  PubMed  CAS  Google Scholar 

  8. F. Khalil-Manesh, H. D. Gonick, E. W. S. Weiler, B. Prins, M. A. Weber, and R. E. Purdy, Lead induced hypertension possibe role of endothelial factors, Am. J. Hypertens, 6, 723–729 (1993).

    PubMed  CAS  Google Scholar 

  9. S. W. Watts, S. Chai, and R. C. Webb, Lead acetate-induced contratcion in rabit, mesenteric artery: interaction with calcium and protein kinase C, Toxicology, 99, 55–56 (1995).

    Article  PubMed  CAS  Google Scholar 

  10. H. C. Gonick, Y. Ding, and N D. Vaziri, Effect of low lead exposure on eicosanoid excretion in rats, Prostaglandins Other Lipid Mediat. 55, 77–82 (1998).

    CAS  Google Scholar 

  11. M. Carmignani, P. Boscolo, A. Poma, and A. R. Volpe, Catchomamine and nitric oxide systems as targets of chronic lead exposure in inducing selective functional impairmen, Life Sci. 68, 401–415 (2000).

    Article  PubMed  CAS  Google Scholar 

  12. Y. Ding, N. D. Vaziri, and H. C. Gonick, Lead-induced hypertension. II. Response to seguential of l-arginine, superoxide dismutase and nitroprusside, Environ. Res., 76, 107–113 (1998).

    Article  PubMed  CAS  Google Scholar 

  13. L. T. Dijkhorst-Oei and H. A. Koomans, Effects of a nitric oxide synthesis inhibitor on renal sodium handling and diluting capacity in humans, Nephrol. Dial. Transplant. 13, 587–593 (1998).

    Article  PubMed  CAS  Google Scholar 

  14. S. Harada, S. Tokunaga, M. Momohara, et al., Inhibition of nitric oxide formation in the nucleus tractus solitarius increases renal sympathetic nerve activity in rabbits, Circ. Res. 72, 511–516 (1993).

    PubMed  CAS  Google Scholar 

  15. B. Halliwell, What nitrates tyrosine? Is nitrotyrosine specific as a biomarker of peroxynitrite formation in vivo? FEBS Lett. 411, 157–160 (1997).

    Article  PubMed  CAS  Google Scholar 

  16. H. H. Draper and M. Hadley, Malondialdehyde determination as on index of lipid peroxidation. Methods Enzymol. 186, 421–431 (1990).

    Article  PubMed  CAS  Google Scholar 

  17. K. Arto and T. Sandra, The calcium dependent nitric oxide production of human vascular endothelial cell in preeclamsia, Am. J. Obstet. Gynecol. 174, 1056–1060 (1996).

    Article  Google Scholar 

  18. V. D. Vaziri, Y. Ding, and Z. Ni, Compensatory upregulation of nitric oxide synthase isoforms in lead induced hypertension; reversal by a superoxide dismutase-imetic drug, J. Pharmacol. Exp. Ther., 298, 679–685 (2001).

    PubMed  CAS  Google Scholar 

  19. R. Kim, D. Sparrow, S. Weiss, C. Wager, and H. Hu, A longitudinal study of low-level exposure and impairment of renal function. The Normative Aging Study, JAMA 275, 1177–1781 (1996).

    Article  PubMed  CAS  Google Scholar 

  20. J. Staessen, Low-level lead exposure, renal function and blood pressure, Verh. K. Acad. Genesskd. Belg. 57(6), 527–574 (1995).

    CAS  Google Scholar 

  21. Y. Ding, H. C. Gonick, N. D. Vaziri, K. Liang, and L. Wei, Lead induced hypertension. III Increased hidroxyl radical production, Am. J. Hypertens. 14, 169–173 (2001).

    Article  PubMed  CAS  Google Scholar 

  22. Y. Ding, C. Harvey, H. C. Gonick, and N. D. Vazin, Lead promotes hydroxyl radical generation and lipid peroxidation in caltured aortic endothelial cell, Am. J. Hypertens, 13, 552–555 (2000).

    Article  PubMed  CAS  Google Scholar 

  23. N. Dursun and A. Tutu, Chronic occupational lead exposure and thyroid function, J. Trace Elements Exp. Med., 12(1), 45–49 (1999).

    Article  Google Scholar 

  24. N. Dursun and R. Saraymen, Chronic occupational lead exposure and testicular function, Trace. Elements Electrolytes, 54(2), 64–68 (2001).

    Google Scholar 

  25. N. Dursun, P. Dogan, and H. Donmez, Plasma and erythrocyte lipid peroxide levels in workers with occupational exposure to lead, Biol. Trace Element Res 82(1–3), 29–34 (2001).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Dursun, N., Arifoglu, C., Süer, C. et al. Blood pressure relationship to nitric oxide, lipid peroxidation, renal function, and renal blood flow in rats exposed to low lead levels. Biol Trace Elem Res 104, 141–149 (2005). https://doi.org/10.1385/BTER:104:2:141

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1385/BTER:104:2:141

Index Entries

Navigation