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Related Experiment Video

Updated: Jul 13, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Lead exposure effect on angiotensin II renal vasoconstriction.

Hilda Vargas Robles¹, Eunice Romo, Alicia Sanchez-Mendoza

¹Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), México City, México.

Human & Experimental Toxicology

|August 21, 2007

Summary

Chronic lead exposure in rats increased blood pressure and vascular reactivity, suggesting lead-induced hypertension is linked to an altered nitric oxide (NO) system and oxidative stress.

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Last Updated: Jul 13, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

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Published on: June 7, 2016

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Area of Science:

Environmental Health
Cardiovascular Physiology
Toxicology

Background:

Low-level chronic lead exposure is linked to hypertension and endothelial dysfunction.
These effects may involve oxidative stress and imbalances in vascular tone regulation.
The precise mechanisms of lead's impact on the nitric oxide (NO) system require further investigation.

Purpose of the Study:

To investigate the effect of chronic lead exposure on angiotensin II-induced vasoconstriction in isolated perfused rat kidneys and microvessels.
To assess the role of the NO system and oxidative stress in lead-induced hypertension.

Main Methods:

Male Wistar rats were treated with lead acetate (100 ppm) or water for 12 weeks.
Vascular reactivity to angiotensin II was evaluated in kidneys and microvessels, with and without N(omega)-nitro-L-arginine methyl ester (L-NAME).
Nitrite concentration, 3-nitrotyrosine, endothelial NO synthase (eNOS) expression, and superoxide production (via dihydroethidium) were measured.

Main Results:

Lead exposure significantly increased blood pressure, eNOS expression, oxidative stress, and vascular reactivity to angiotensin II.
L-NAME potentiated angiotensin II response in controls but not in lead-exposed rats.
Lead-exposed rats showed lower renal nitrite release and higher 3-nitrotyrosine levels compared to controls.

Conclusions:

Chronic lead exposure partially causes hypertension through an altered NO system.
Increased oxidative stress and impaired NO bioavailability contribute to lead-induced endothelial dysfunction and vasoconstriction.