Impaired renal autoregulation in susceptible models of renal disease
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Updated: May 7, 2026

An Effective Mouse Model of Unilateral Renal Ischemia-Reperfusion Injury
Published on: July 15, 2021
Sydney Murphy, Jan M Williams1
1Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA. jmwilliams5@umc.edu.
Abstract:
One of the major functions of the kidney is to maintain constant renal blood flow and glomerular filtration rate in response to increases in renal perfusion pressure. This phenomenon is referred to autoregulation and involves two independent mechanisms: tubular glomerular feedback and myogenic response. The latter, the renal myogenic response, involves constriction of the preglomerular vasculature to increases in transmural pressure. Over the last three decades, there has been substantial evidence that demonstrates that the myogenic response plays an important role in protecting the kidney from hypertension-induced renal injury. Furthermore, impairment of the renal myogenic response allows the transmission of systemic pressures to the glomerular capillaries leading to the development of glomerular injury and progressive proteinuria during hypertension. This review article discusses the role of the myogenic response in the pathogenesis of renal disease in various genetic and experimental rodent models that develop hypertension-induced renal injury.
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