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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
Published on: May 26, 2022
Renin angiotensin system blockade ameliorates lead nephropathy
Hwee-Yeong Ng1, You-Lin Tain, Yueh-Ting Lee
1Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Biochemical and Biophysical Research Communications
|July 31, 2013
Summary
Lead exposure activates the intrarenal renin-angiotensin system (RAS), causing kidney damage and hypertension. Blocking this system with captopril or losartan effectively protected against lead-induced kidney injury and lowered blood pressure.
Area of Science:
- Nephrology
- Toxicology
- Cardiovascular Research
Background:
- Lead intoxication is a significant public health concern, often leading to insidious complications like kidney damage and hypertension.
- The specific role of the intrarenal renin-angiotensin system (RAS) in the pathogenesis of lead-induced nephropathy remains largely unexplored.
Purpose of the Study:
- To investigate the involvement of the intrarenal RAS in lead-induced kidney injury.
- To evaluate the therapeutic potential of RAS blockade in mitigating lead-associated nephropathy and hypertension.
Main Methods:
- Adult male Sprague-Dawley rats were exposed to lead acetate (250ppm) or deionized water for 4 weeks.
- Two groups received intraperitoneal captopril (ACE inhibitor) or losartan (angiotensin II receptor blocker) after 2 weeks of lead exposure.
- Protein levels of intrarenal RAS components and transforming growth factor-beta (TGF-β) were analyzed using immunoblotting.
Main Results:
- Lead exposure significantly increased proteinuria, serum creatinine, and decreased glomerular filtration rate (GFR).
- Intrarenal angiotensin converting enzyme (ACE), angiotensin II (ANG II), angiotensin II type 1 receptor (AT1R), and TGF-β were upregulated in lead-exposed rats.
- Captopril and losartan treatments reduced proteinuria, improved renal function markers (creatinine and GFR), and lowered systolic blood pressure.
Conclusions:
- Lead exposure activates the intrarenal RAS, contributing to proteinuria and impaired renal function.
- RAS blockade effectively alleviates lead-induced kidney injury and hypertension.
- Targeting the intrarenal RAS presents a promising therapeutic strategy for lead-associated nephropathy.
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