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Low-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortas.

Fiorim J, Ribeiro Júnior RF, Silveira EA, Padilha AS, Vescovi MV, de Jesus HC, Stefanon I, Salaices M, Vassallo DV - PLoS ONE (2011)

Bottom Line: Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 µM) or sodium nitroprusside (0.01 nM-0.3 µM).This effect is accompanied by increased p-eNOS, iNOS protein expression and Na(+)/K(+)-ATPase functional activity.These factors might be a compensatory mechanism to the increase in SBP.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espírito Santo, Brazil.

ABSTRACT
Chronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 µg/100 g, subsequent dose 0.05 µg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 µg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 µM) or sodium nitroprusside (0.01 nM-0.3 µM). Endothelium removal, N(G)-nitro-L-arginine methyl ester (100 µM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 µM) increased but losartan (10 µM) and enalapril (10 µM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na(+)/K(+)-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na(+)/K(+)-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na(+)/K(+)-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBP.

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The effects of seven-day exposure to lead acetate on the concentration-response curves to phenylephrine (A), acetylcholine (B) and sodium nitroprusside (NSP; C) treatment in aortic rings.*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.
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pone-0017117-g001: The effects of seven-day exposure to lead acetate on the concentration-response curves to phenylephrine (A), acetylcholine (B) and sodium nitroprusside (NSP; C) treatment in aortic rings.*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.

Mentions: Lead treatment did not affect the response to KCl (untreated: 3.48±0.08 g, n = 39; lead-treated: 3.52±0.09 g, n = 40; P>0.05), but it decreased the contractile responses induced by phenylephrine in rat aortas (Figure 1 A). It also decreased Rmax but not sensibility to phenylephrine (Table 1).


Low-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortas.

Fiorim J, Ribeiro Júnior RF, Silveira EA, Padilha AS, Vescovi MV, de Jesus HC, Stefanon I, Salaices M, Vassallo DV - PLoS ONE (2011)

The effects of seven-day exposure to lead acetate on the concentration-response curves to phenylephrine (A), acetylcholine (B) and sodium nitroprusside (NSP; C) treatment in aortic rings.*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3045404&req=5

pone-0017117-g001: The effects of seven-day exposure to lead acetate on the concentration-response curves to phenylephrine (A), acetylcholine (B) and sodium nitroprusside (NSP; C) treatment in aortic rings.*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.
Mentions: Lead treatment did not affect the response to KCl (untreated: 3.48±0.08 g, n = 39; lead-treated: 3.52±0.09 g, n = 40; P>0.05), but it decreased the contractile responses induced by phenylephrine in rat aortas (Figure 1 A). It also decreased Rmax but not sensibility to phenylephrine (Table 1).

Bottom Line: Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 µM) or sodium nitroprusside (0.01 nM-0.3 µM).This effect is accompanied by increased p-eNOS, iNOS protein expression and Na(+)/K(+)-ATPase functional activity.These factors might be a compensatory mechanism to the increase in SBP.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espírito Santo, Brazil.

ABSTRACT
Chronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 µg/100 g, subsequent dose 0.05 µg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 µg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 µM) or sodium nitroprusside (0.01 nM-0.3 µM). Endothelium removal, N(G)-nitro-L-arginine methyl ester (100 µM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 µM) increased but losartan (10 µM) and enalapril (10 µM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na(+)/K(+)-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na(+)/K(+)-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na(+)/K(+)-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBP.

Show MeSH
Related in: MedlinePlus