Endothelial Dysfunction
Endothelial Dysfunction - Related Videos
12:43
On-Chip Endothelial Inflammatory Phenotyping
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Cited by 3 •
2012
Microfluidic flow chambers etched by photolithography and fabricated from PDMS are applied to probe functional outcomes associated with EC dysfunction and inflammation. In a representative experiment, the ability of differential shear stress to modulate monocytic cell adhesion to cytokine activated EC monolayers is demonstrated.
09:23
Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
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Cited by 20 •
2013
We present a preparation for visualizing and manipulating calcium signaling in native, intact microvascular endothelium. Endothelial tubes freshly isolated from mouse resistance arteries supplying skeletal muscle retain in vivo morphology and dynamic signaling within and between neighboring cells. Endothelial tubes can be prepared from microvessels of other tissues and organs.
10:15
Isolation and Culture Expansion of Tumor-specific Endothelial Cells
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Cited by 20 •
2015
We report a reliable method to isolate and culture primary tumor-specific endothelial cells from genetically engineered mouse models.
11:04
Isolation of Valvular Endothelial Cells
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Cited by 82 •
2010
We provide a method for isolating and culturing pure populations of heart valve endothelial cells (VEC). VEC can be isolated from either side of the cusp or leaflet and immediately following, underlying interstitial cell (VIC) isolation is straightforward.
07:46
Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
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Cited by 165 •
2010
A noninvasive procedure to assess endothelial function is demonstrated using the Endo-PAT 2000.
FAQs
Reduced nitric oxide availability weakens the signals that normally support vascular relaxation and balanced vessel control. As this protective influence declines, vascular behavior shifts toward constriction, which can contribute to increased blood pressure and impaired regulation of blood flow. In pharmacology, nitric oxide pathways therefore provide an important target for evaluating vascular effects of cardiovascular drugs.
Oxidative stress can disturb the balance that maintains endothelial function and further reduce nitric oxide bioavailability. This creates conditions that favor abnormal vascular responses rather than effective vessel regulation. Studying oxidative balance helps pharmacologists assess whether a treatment may protect endothelial activity, improve vascular control, or limit processes associated with cardiovascular disease.
Inflammatory signaling can shift the endothelium toward greater leukocyte adhesion, linking vascular dysfunction with inflammatory activity in the vessel wall. This change is important because it may support progression toward atherosclerotic disease and related vascular complications. Pharmacological investigations can therefore examine endothelial inflammation alongside nitric oxide signaling and vascular tone.
Key pharmacological areas include nitric oxide signaling, oxidative balance, blood pressure regulation, and vascular inflammation. Examining these pathways helps determine how cardiovascular drugs influence endothelial responses rather than focusing only on downstream blood pressure values. The approach can also reveal whether a treatment preserves vascular function while addressing conditions associated with endothelial injury.
Researchers can use measurements of endothelial responses to evaluate vascular function, estimate disease risk, and examine therapeutic effects. These assessments are especially useful when comparing how treatments influence vessel control, nitric oxide-related activity, oxidative balance, or vascular inflammation. The resulting information can support drug development and help distinguish beneficial vascular effects from limited control of related risk factors.
Endothelial dysfunction is relevant to studies of hypertension, atherosclerosis, diabetes, and coronary artery disease. In these settings, endothelial measurements can help connect altered vascular regulation with disease risk and can provide evidence about treatment effects. This makes the concept useful for linking pharmacological mechanisms to clinically important outcomes involving blood pressure and vascular inflammation.