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Blood Pressure Decreases Following Lead Treatment Cessation: Highest NO Bioavailability Involved
Gilson B Broseghini-Filho1, Camila C Pereira Almenara2, Dalton V Vassallo2,3
1Department of Physiological Sciences, Federal University of Espirito Santo, Marechal Campos Ave, 1468, Maruípe, 29040-091, Vitória, ES, Brazil. gilsonbras@hotmail.com.
Insights
Lead exposure increases blood pressure, but this effect reverses after stopping lead treatment. Vascular function also normalizes, suggesting nitric oxide (NO) plays a compensatory role in reducing blood pressure post-lead exposure.
Area of Science:
- Toxicology
- Cardiovascular Physiology
- Environmental Health
Background:
- Lead exposure is a known cause of arterial hypertension and vascular damage.
- The long-term effects of lead cessation on blood pressure and vascular function remain unclear.
- Understanding these effects is crucial for public health and clinical management of lead poisoning.
Purpose of the Study:
- To investigate the reversibility of lead-induced hypertension after lead exposure cessation.
- To evaluate changes in vascular function following lead treatment discontinuation.
- To explore the role of nitric oxide (NO) in mediating vascular responses after lead exposure.
Main Methods:
- Rats were exposed to lead acetate in drinking water for 14 days.
- Systolic blood pressure (SBP) was measured weekly using tail plethysmography.
- Vascular reactivity to phenylephrine in isolated aortic rings was assessed, with and without L-NAME (a nitric oxide synthase inhibitor).
Main Results:
- Lead exposure increased SBP, which reversed upon cessation of exposure.
- Vascular vasoconstrictor response to phenylephrine was reduced after lead cessation.
- L-NAME potentiated phenylephrine response more in the lead-exposed group, indicating altered NO modulation.
Conclusions:
- The increase in systolic blood pressure induced by lead is reversible after exposure cessation.
- Nitric oxide (NO) modulation of vascular contractile responses may act as a compensatory mechanism to lower blood pressure post-lead exposure.
- These findings highlight the dynamic nature of lead's cardiovascular effects and the body's adaptive responses.
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.
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