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The kidney and hypertension: lessons from mouse models
1Division of Nephrology, Department of Medicine, Duke University, Durham, NC 27710, USA.
Insights
The kidney plays a crucial role in regulating blood pressure and hypertension. Genetically modified mouse models reveal how kidney defects, particularly in solute transport, contribute to high blood pressure.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Genetics
Background:
- Hypertension pathogenesis is multifactorial, involving vasculature, kidneys, nervous system, and hormones.
- The kidney is increasingly recognized as a primary determinant of chronic blood pressure levels.
- Human genetic studies highlight the kidney's role in blood pressure homeostasis.
Purpose of the Study:
- To review recent research on the kidney's role in hypertension using genetically modified mouse models.
- To investigate molecular defects in nephron function affecting blood pressure.
- To understand the link between kidney solute transport and hypertension.
Main Methods:
- Analysis of genetically modified mouse models.
- Review of human genetic studies on Mendelian disorders affecting blood pressure.
- Focus on genes impacting kidney solute transport.
Main Results:
- Human genetic studies identified genes affecting kidney solute transport as causal in blood pressure disorders.
- Genetically modified mouse models are instrumental in studying kidney function in hypertension.
- Specific molecular defects in nephron function alter blood pressure.
Conclusions:
- The kidney is a key determinant in the pathogenesis of hypertension.
- Understanding kidney solute transport mechanisms is vital for hypertension research.
- Genetically modified mouse models provide critical insights into kidney-related hypertension.
Abstract:
The pathogenesis of hypertension is multi-factorial, involving many of the systems contributing to blood pressure homeostasis including the vasculature, kidneys, central, and sympathetic nervous systems, along with various hormonal regulators. However, over the years, many studies have indicated a predominant importance of the kidney in blood pressure homeostasis and hypertension. This work has established the notion that the kidney is a key determinant of the chronic level of intra-arterial pressure playing a major role in the pathogenesis of hypertension. Therefore, this review will focus on recent work using genetically modified mouse models addressing the role of the kidney in hypertension. In particular, human genetic studies of Mendelian disorders with major impact on blood pressure homeostasis have provided powerful evidence for a role of the kidney in hypertension. Of the approximately 20 genes identified as causal in these disorders, virtually all have an effect on the control of solute transport in the kidney. As such, we have especially focused on generation of mouse models addressing the nature of these specific molecular defects in nephron function that produce an alteration in blood pressure.
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