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Updated: Dec 1, 2025
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Mohammad Saleem1, Pierina Barturen-Larrea1, Luz Saavedra1
1Department of Medicine/Clinical Pharmacology Division, Vanderbilt University Medical Center.
Abstract:
Renal artery stenosis is a common condition in patients with coronary or peripheral vascular disease where the renin angiotensin aldosterone system (RAAS) is overactivated. In this context, there is a narrowing of the renal arteries that stimulate an increase in the expression and release of renin, the rate-limiting protease in RAAS. The resulting rise in renin expression is a known driver of renovascular hypertension, frequently associated with kidney injury and end organ damage. Thus, there is a great interest in developing novel treatments for this condition. The molecular and cellular mechanism of renin control in renal artery stenosis is not fully understood and warrants further investigation. To induce renal artery stenosis in mice, a modified 2 kidney 1 clip (2K1C) Goldblatt mouse model was developed. The right kidney was stenosed in wild type mice and sham operated mice were used as control. After renal artery stenosis, we determined renin expression and kidney injury. Kidneys were harvested, and fresh cortices were used to determine protein and mRNA expression of renin. This animal model is reproducible and can be used to study pathophysiological responses, molecular and cellular pathways involved in renovascular hypertension and kidney injury.
Insights
Renal artery stenosis, a condition linked to high blood pressure, involves overactivation of the renin angiotensin aldosterone system (RAAS). This study developed a mouse model to investigate renin control in renovascular hypertension.
Area of Science:
- Cardiovascular Science
- Nephrology
- Endocrinology
Background:
- Renal artery stenosis is common in patients with vascular disease, often leading to overactivated renin angiotensin aldosterone system (RAAS).
- Increased renin expression due to renal artery narrowing drives renovascular hypertension, kidney injury, and end-organ damage.
- Understanding renin control mechanisms in renal artery stenosis is crucial for developing new treatments.
Purpose of the Study:
- To investigate the molecular and cellular mechanisms of renin control in renal artery stenosis.
- To establish and validate a reproducible mouse model for studying renovascular hypertension and kidney injury.
Main Methods:
- A modified 2 kidney 1 clip (2K1C) Goldblatt mouse model was used to induce renal artery stenosis.
- Wild-type mice underwent renal artery stenosis, with sham-operated mice serving as controls.
- Renin expression and kidney injury markers were assessed in harvested kidney tissues.
Main Results:
- The study successfully established a reproducible 2K1C Goldblatt mouse model for renal artery stenosis.
- The model allows for the determination of renin expression and kidney injury following stenosis.
- This model is suitable for studying the pathophysiology of renovascular hypertension.
Conclusions:
- The developed 2K1C Goldblatt mouse model is effective for investigating renin regulation in renovascular hypertension.
- This model can be utilized to explore molecular and cellular pathways underlying kidney injury in this condition.
- Further research using this model may lead to novel therapeutic strategies for renal artery stenosis.
