Abstract
Although lead is known to induce arterial hypertension and vascular damage, it is not clear if after cessation of lead treatment, the increase of blood pressure is sustained and the vascular function is different from untreated rats. Therefore, we aimed to evaluate the systolic blood pressure during and following lead-treatment discontinuance and the possible vascular alterations involved with it. Rats received lead acetate (100 mg/L) in the drinking water or distilled water for 14 days. After 14 days, lead acetate solution was substituted by water distilled for more 28 days, as control group. Systolic blood pressure (SBP) was measured weekly by tail plethysmography, and the vascular reactivity to phenylephrine in isolated aortic rings was evaluated at end of treatment time. The increase in SBP induced by lead was reversed after stopping exposure, and it was accompanied by a reduction on vasoconstrictor response to phenylephrine. L-NAME treatment increased the phenylephrine response in both groups, but its effect was greater in lead group. Our findings provide evidence that the increased modulation by NO on contractile response to phenylephrine could be a compensatory mechanism that might contribute to decrease blood pressure after lead treatment cessation.
References
Healey N (2009) Lead toxicity, vulnerable subpopulations and emergency preparedness. Radiat Prot Dosimetry 134:143–151. doi:10.1093/rpd/ncp068
Gharaibeh MY, Alzoubi KH, Khabour OF et al (2014) Lead exposure among five distinct occupational groups: a comparative study. Pak J Pharm Sci 27:39–43
Newman N, Jones C, Page E et al (2015) Investigation of childhood lead poisoning from parental take-home exposure from an electronic scrap recycling facility—Ohio, 2012. MMWR Morb Mortal Wkly Rep 64:743–745
Mohmand J, Eqani SAMAS, Fasola M et al (2015) Human exposure to toxic metals via contaminated dust: bio-accumulation trends and their potential risk estimation. Chemosphere 132:142–151. doi:10.1016/j.chemosphere.2015.03.004
Zheng N, Liu J, Wang Q, Liang Z (2010) Health risk assessment of heavy metal exposure to street dust in the zinc smelting district, Northeast of China. Sci Total Environ 408:726–733. doi:10.1016/j.scitotenv.2009.10.075
Fioresi M, Simões MR, Furieri LB et al (2014) Chronic lead exposure increases blood pressure and myocardial contractility in rats. PLoS One 9, e96900
Li M-M, Cao J, Gao Z-Y et al (2015) The trend of lead poisoning rate in Chinese population aged 0-18 years old: a meta-analysis. BMC Public Health 15:756. doi:10.1186/s12889-015-2103-9
[ATSDR] (2007) Registry, Agency for Toxic Substances and Disease. Toxicological Profile for Lead. US Dep. Heal. Hum. Serv. Public Heal. Serv. Agency Toxic Subst. Dis. Regist. Atlanta
Blood lead levels in children aged 1–5 years—United States, 1999–2010.
Silveira EA, Siman FDM, de Oliveira FT et al (2014) Low-dose chronic lead exposure increases systolic arterial pressure and vascular reactivity of rat aortas. Free Radic Biol Med 67:366–376
Fiorim J, Ribeiro RF, Silveira EA et al (2011) Low-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortas. PLoS One. doi:10.1371/journal.pone.0017117
Simões MR, Ribeiro Júnior RF, Vescovi MVA et al (2011) Acute lead exposure increases arterial pressure: role of the renin-angiotensin system. PLoS One 6, e18730. doi:10.1371/journal.pone.0018730
Vassallo DV, Lebarch EC, Moreira CM et al (2008) Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium. Brazilian J Med Biol Res 41:789–795
Vaziri ND, Liang K, Ding Y (1999) Increased nitric oxide inactivation by reactive oxygen species in lead-induced hypertension. Kidney Int 56:1492–1498. doi:10.1046/j.1523-1755.1999.00670.x
Vaziri ND, Ding Y, Ni Z (1999) Nitric oxide synthase expression in the course of lead-induced hypertension. Hypertension 34:558–562. doi:10.1161/01.HYP.34.4.558
Lustberg M, Silbergeld E (2002) Blood lead levels and mortality. Arch Intern Med 162:2443–2449. doi:10.1001/archinte.162.21.2443
Nakade UP, Garg SK, Sharma A, Choudhury S, Rajkumar Singh Yadav KG, Sood N (2015) Lead-induced adverse effects on the reproductive system of rats with particular reference to histopathological changes in uterus. Indian J Pharmacol 47:22–26
Grizzo LT, Cordellini S (2008) Perinatal lead exposure affects nitric oxide and cyclooxygenase pathways in aorta of weaned rats. Toxicol Sci 103:207–214. doi:10.1093/toxsci/kfn018
Weiler E, Khalil-Manesh F, Gonick H (1988) Effects of lead and natriuretic hormone on kinetics of sodium-potassium-activated adenosine triphosphatase: possible relevance to hypertension. Environ Health Perspect 78:113–115. doi:10.1289/ehp.8878113
Piccinini F, Favalli L, Chiari MC (1977) Experimental investigations on the contraction induced by lead in arterial smooth muscle. Toxicology 8:43–51. doi:10.1016/0300-483X(77)90022-1
Chang HR, Chen SS, Tsao DA et al (1997) Reduced vascular β-adrenergic receptors and catecholamine response in rats with lead induced hypertension. Arch Toxicol 71:778–781. doi:10.1007/s002040050460
Fiorim J, Ribeiro Júnior RF, Azevedo BF et al (2012) Activation of K+ channels and Na+/K+ ATPase prevents aortic endothelial dysfunction in 7-day lead-treated rats. Toxicol Appl Pharmacol 262:22–31. doi:10.1016/j.taap.2012.04.015
Félétou M, Vanhoutte PM (2006) Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture). Am J Physiol Heart Circ Physiol 291:H985–H1002. doi:10.1152/ajpheart.00292.2006
Pueyo ME, Arnal JF, Rami J, Michel JB (1998) Angiotensin II stimulates the production of NO and peroxynitrite in endothelial cells. Am J Physiol 274:C214–C220
Acknowledgments
This project was supported by CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior) and CNPq/FAPES (Conselho Nacional de Desenvolvimento Científico e Tecnológico and Fundação de Amparo à Pesquisa do Espírito Santo) (54668662/2011). The funders had no role in the study’s design, data collection nor analysis, nor were they involved in the manuscript’s preparation or the decision to publish it.
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Broseghini-Filho, G.B., Almenara, C.C.P., Vassallo, D.V. et al. Blood Pressure Decreases Following Lead Treatment Cessation: Highest NO Bioavailability Involved. Biol Trace Elem Res 170, 410–414 (2016). https://doi.org/10.1007/s12011-015-0497-y
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DOI: https://doi.org/10.1007/s12011-015-0497-y