Vasodilation Vasoconstriction
Vasodilation Vasoconstriction - Related Videos
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Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
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A noninvasive procedure to assess endothelial function is demonstrated using the Endo-PAT 2000.
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Antihypertensive Drugs: Vasodilators
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Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
08:09
Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
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Cited by 1 •
2017
We describe the isolation of cardiac extracellular matrix from C57Bl/6J control mice, tight-skin mice, and tight-skin mice treated with the IRF5 inhibitory peptide. We also describe the vasodilation studies on the isolated vessels from C57Bl/6J, tight-skin mice and tight-skin mice treated with the IRF5 inhibitory peptide.
13:32
Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
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Cited by 29 •
2014
Hypoxic pulmonary vasoconstriction (HPV) is an important physiological phenomenon by which at alveolar hypoxia lung perfusion is matched to ventilation. The major vascular segment contributing to HPV is the intra-acinar artery. Here, we describe our protocol for the analysis of HPV of murine pulmonary vessels with diameters of 20-100 μm.
08:42
Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
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Cited by 42 •
2014
Endothelial dysfunction is associated with numerous disease states and is predictive of adverse cardiovascular events in humans. Flow-mediated vasodilation (FMD) is a non-invasive ultrasound method of evaluating endothelial function. Methodological choices and operator experience may affect results. A systematic approach to FMD in human studies is discussed here.
FAQs
Endothelial cells can release nitric oxide, a signaling molecule that promotes relaxation of nearby vascular smooth muscle. This relaxation changes the vessel’s diameter and can increase blood delivery to downstream tissues. The example illustrates how the vessel lining communicates with muscle in the vessel wall, linking cellular signaling to whole-body control of perfusion.
Sympathetic nerve activity and circulating hormones can stimulate vascular smooth muscle to contract. That contraction narrows the vessel and changes how much blood can pass through a vascular region. Because these signals can act throughout the circulation, they help the cardiovascular system respond when blood pressure or other physiological conditions require adjustment.
The two responses work as a complementary control system rather than as isolated events. Increasing vessel diameter can support tissue perfusion, whereas narrowing can contribute to blood-pressure stabilization. Their opposing effects allow blood-flow distribution to change as physiological demands shift, while keeping circulation responsive to changing conditions throughout the body.
Exercise and temperature changes illustrate why the balance between the responses matters. During exercise, vascular adjustments help modify blood delivery to meet changing tissue needs; during temperature regulation, they help alter circulation in relation to body heat. These examples show that the same vascular machinery can serve different physiological priorities.
Changes in vessel caliber provide a way to reason about whether blood delivery to a tissue is being increased or restricted. In a biology context, examining these responses connects vascular smooth-muscle activity with perfusion, the delivery of blood to tissue. This helps explain how vascular regulation influences cardiovascular physiology.
Together, the responses demonstrate how cardiovascular physiology links cellular events, neural and hormonal signals, and system-level outcomes. Smooth-muscle relaxation or contraction affects vessel diameter, while endothelial signals, sympathetic activity, and circulating hormones provide different routes of control. Studying these links helps explain how blood flow, pressure, and perfusion are regulated together.
Impaired vascular regulation can disrupt the circulation’s ability to adjust blood flow, pressure, and tissue perfusion appropriately. Because vasodilation and vasoconstriction normally help stabilize these variables when conditions change, defective control may be relevant to hypertension and other circulatory disorders. The concept therefore connects normal cardiovascular physiology with disease mechanisms involving abnormal vascular responses.