Murine Hypertension Model
Murine Hypertension Model - Related Videos
09:20
Intracellular Staining and Flow Cytometry to Identify Lymphocyte Subsets within Murine Aorta, Kidney and Lymph Nodes in a Model of Hypertension
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Cited by 8 •
2017
This article provides detailed methodology to identify and quantify functional T lymphocyte subsets present within murine kidney, aorta and lymph nodes by intracellular staining and flow cytometry. The model of angiotensin II induced hypertension was chosen to explain, step-by-step, the procedures and fundamental principles of flow cytometry and intracellular staining.
06:34
Laser-Induced Chronic Ocular Hypertension Model on SD Rats
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Cited by 26 •
2007
Glaucoma is one of the major causes of blindness in the world. Elevated intraocular pressure is a major risk factor. Laser photocoagulation induced ocular hypertension is one of the well established animal models. This video demonstrates how to induce ocular hypertension by Argon laser photocoagulation in rat.
09:40
Hemodynamic Characterization of Rodent Models of Pulmonary Arterial Hypertension
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Cited by 35 •
2016
Pulmonary arterial hypertension (PAH) is a disease of pulmonary arterioles that leads to their obliteration and the development of right ventricular failure. Rodent models of PAH are critical in understanding the pathophysiology of PAH. Here we demonstrate hemodynamic characterization, with right heart catheterization and echocardiography, in the mouse and rat.
08:27
Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.
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Cited by 13 •
2015
We describe a method for creating a reliable model of cerebral venous hypertension in the adult mouse. This model has been widely described and tested in the rat. This new counterpart in the mice opens the possibility of using genetic modified animals and thereby broadens the applications of the model.
04:35
Murine Ileal Resection Model: Studying Ileectomy-Induced Bile Metabolism in Murine Model
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2023
This video describes the detailed protocol for intestinal resection in a murine model. This technique provides insights into ileectomy-induced bile malabsorption, overaccumulation, and toxicity in the mouse intestine.
FAQs
Genetic backgrounds, excess dietary salt, pharmacological activation of the renin–angiotensin–aldosterone system, and vascular or renal interventions create hypertension through different biological routes. These approaches allow investigators to distinguish mechanisms driven primarily by inherited susceptibility, salt-related changes, neurohormonal signaling, vascular resistance, or kidney dysfunction. Comparing models helps link a blood-pressure phenotype with its underlying pathophysiology.
Blood pressure elevation can reflect interacting changes rather than a single abnormality. Increased vascular resistance alters the force opposing blood flow, while kidney dysfunction can affect fluid and pressure regulation. Neurohormonal pathways, including the renin–angiotensin–aldosterone system, provide another regulatory influence. Studying these components together helps explain how hypertension is maintained and why organ injury may develop.
Genetic models can reveal how inherited biological backgrounds influence susceptibility to sustained pressure elevation, whereas dietary, pharmacological, vascular, or renal interventions test defined causal influences. Their comparison separates effects associated with predisposition from those produced by a specific experimental challenge. This distinction is useful when interpreting disease progression, mechanisms, and responses to biological interventions.
Models that differ in their initiating cause can be examined for how hypertension progresses and how injury develops in affected organs. Relating the initiating strategy to changes in vascular function, kidney function, and neurohormonal regulation helps investigators determine whether damage is associated with a particular hypertensive mechanism. The resulting comparisons support more precise biological interpretation of organ outcomes.
A study begins by selecting a suitable mouse background or choosing an intervention such as excess dietary salt, pharmacological activation of the renin–angiotensin–aldosterone system, or a vascular or renal manipulation. Investigators then examine sustained arterial pressure, disease progression, and target-organ injury under controlled conditions. The same framework can be used to compare mechanisms or evaluate an intervention.
Model selection depends on the biological question. A genetic background is useful for examining inherited susceptibility, whereas dietary salt can address salt-related mechanisms. Pharmacological activation emphasizes renin–angiotensin–aldosterone signaling, while vascular or renal interventions focus attention on those systems. Choosing the model that matches the proposed mechanism improves the relevance of subsequent disease and treatment analyses.
The system can support assessment of whether an intervention affects sustained arterial pressure, disease progression, or target-organ injury. Because hypertension can be produced through several mechanisms, treatment responses can also be compared across models with different genetic, dietary, neurohormonal, vascular, or renal drivers. This provides biological context for interpreting how broadly or selectively an intervention acts.