Limits...
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.

Show MeSH

Related in: MedlinePlus

Angiotensin converting enzyme (ACE) activity (nmol His-Leu/min) in plasma; correlation between systolic arterial blood pressure and ACE activity (nmol His-Leu/min) in plasma of control and lead-treated rats (r = 0.787, P<0.05).*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3045404&req=5

pone-0017117-g004: Angiotensin converting enzyme (ACE) activity (nmol His-Leu/min) in plasma; correlation between systolic arterial blood pressure and ACE activity (nmol His-Leu/min) in plasma of control and lead-treated rats (r = 0.787, P<0.05).*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.

Mentions: To investigate the involvement of the plasma renin-angiotensin system in potentiating the effects of lead exposure, angiotensin converting enzyme activity (ACE) was evaluated. Lead treatment increased plasma ACE activity (Figure 4 A). There was a significant correlation between systolic arterial blood pressure and ACE activity in the plasma of lead-treated rats (r = 0.787, P<0.05; Figure 4 B). These results reinforce the hypothesis that the renin-angiotensin system is involved in the rise in arterial blood pressure in lead-treated rats.


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)

Angiotensin converting enzyme (ACE) activity (nmol His-Leu/min) in plasma; correlation between systolic arterial blood pressure and ACE activity (nmol His-Leu/min) in plasma of control and lead-treated rats (r = 0.787, P<0.05).*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-g004: Angiotensin converting enzyme (ACE) activity (nmol His-Leu/min) in plasma; correlation between systolic arterial blood pressure and ACE activity (nmol His-Leu/min) in plasma of control and lead-treated rats (r = 0.787, P<0.05).*P<0.05 by Student's t-test. Number of animals used is indicated in parentheses.
Mentions: To investigate the involvement of the plasma renin-angiotensin system in potentiating the effects of lead exposure, angiotensin converting enzyme activity (ACE) was evaluated. Lead treatment increased plasma ACE activity (Figure 4 A). There was a significant correlation between systolic arterial blood pressure and ACE activity in the plasma of lead-treated rats (r = 0.787, P<0.05; Figure 4 B). These results reinforce the hypothesis that the renin-angiotensin system is involved in the rise in arterial blood pressure in lead-treated rats.

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