Blood Pressure Decreases Following Lead Treatment Cessation: Highest NO Bioavailability Involved.

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.

journal_name

Biol Trace Elem Res

authors

Broseghini-Filho GB,Almenara CC,Vassallo DV,Padilha AS

doi

10.1007/s12011-015-0497-y

subject

Has Abstract

pub_date

2016-04-01 00:00:00

pages

410-4

issue

2

eissn

0163-4984

issn

1559-0720

pii

10.1007/s12011-015-0497-y

journal_volume

170

pub_type

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