Hypertension Induction
Hypertension Induction - Related Videos
07:10
Induction and Characterization of Pulmonary Hypertension in Mice using the Hypoxia/SU5416 Model
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Cited by 7 •
2020
This protocol describes the induction of pulmonary hypertension (PH) in mice based on the exposure to hypoxia and the injection of a VEGF receptor antagonist. The animals develop PH and right ventricular (RV) hypertrophy 3 weeks after the initiation of the protocol. The functional and morphometrical characterization of the model is also presented.
11:33
Inductance
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2023
Source: Yong P. Chen, PhD, Department of Physics & Astronomy, College of Science, Purdue University, West Lafayette, IN This experiment will use inductive coils to demonstrate the concept of inductor and inductance. Magnetic induction will be demonstrated using a rod magnet inserted into or extracted away from the core of a coil to induce a transient electromotive force (emf) voltage in the coil, measured by a voltmeter. This experiment will also demonstrate the mutual inductance between...
07:00
A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects
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Cited by 26 •
2013
Chronic ocular hypertension is induced using laser photocoagulation of the trabecular meshwork in mouse eyes. The intraocular pressure (IOP) is elevated for several months after laser treatment. The decrease of visual acuity and contrast sensitivity of experimental animals are monitored using the optomotor test.
09:26
A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice
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Cited by 71 •
2016
Here, we present a protocol to induce ocular hypertension in the murine eye that results in the loss of retinal ganglion cells as observed in glaucoma. Magnetic microbeads are injected into the anterior chamber and attracted to the iridocorneal angle using a magnet to block the outflow of aqueous humour.
07:41
Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
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Cited by 2 •
2022
We present a protocol to induce and phenotype an acute right heart failure in a large animal model with chronic pulmonary hypertension. This model can be used to test therapeutic interventions, to develop right heart metrics or to improve the understanding of acute right heart failure pathophysiology.
FAQs
Angiotensin II and mineralocorticoid treatments are used, often with increased salt intake, to produce physiological changes that maintain elevated pressure. Their relevance is that they act through complementary dimensions of blood-pressure regulation: vascular tone, fluid balance, and neurohumoral control. This combination gives investigators an experimental model for examining how cardiovascular stress becomes linked to neurological consequences.
In these models, increased salt intake is paired with angiotensin II or mineralocorticoid treatment rather than treated as an isolated detail. The combination helps investigators examine hypertension in the context of altered fluid balance and neurohumoral regulation, while the accompanying vascular changes provide a basis for studying downstream effects on the brain and its circulation.
Experimental elevation of blood pressure provides a way to investigate whether cardiovascular changes are accompanied by altered cerebral blood flow and blood-brain barrier function. These measurements connect systemic hypertension with the brain’s vascular interface, helping researchers determine how changes outside the nervous system may influence relationships between the circulation and neural tissue.
Neuroinflammation and neuronal function extend the analysis beyond blood pressure itself. Including them allows investigators to examine whether induced hypertension is associated with inflammatory brain responses or changes in how neurons function. Together with stroke risk assessment, these endpoints help characterize neurological consequences and clarify which aspects of brain health may be vulnerable to sustained cardiovascular stress.
A study can combine an experimental blood-pressure-elevating approach with observation of brain-related outcomes. The source describes angiotensin II or mineralocorticoid treatment, increased salt intake, and assessment of cerebral blood flow, the blood-brain barrier, neuroinflammation, neuronal function, or stroke risk. The combination depends on whether the investigation emphasizes mechanism, disease consequences, or treatment evaluation.
Researchers can link a cardiovascular change to specific neurological outcomes rather than considering the two systems separately. Measurements may reveal relationships among elevated pressure, cerebral blood flow, blood-brain barrier changes, inflammatory activity, neuronal function, and stroke risk. This integrated information supports analysis of neurovascular disease and helps identify brain-related effects that should be targeted or monitored.
Investigators use these models when they need to test whether an intervention can reduce or protect against neurological effects associated with hypertension. Because the approach produces linked cardiovascular and brain outcomes, researchers can examine potential treatments in relation to cerebral blood flow, blood-brain barrier changes, neuroinflammation, neuronal function, or stroke risk. The model therefore supports interventions aimed at protecting neurological health.