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Subcutaneous Resistance Arteries 

Human resistance arteries are our most frequently used blood vessel to predict the effects of test drugs on peripheral vascular resistance and hence systemic blood pressure. Resistance arteries are the primary way by which organ-specific blood flow is regulated and, due to the high number of small resistance arteries and their ability to markedly dilate and constrict, they are key to the overall vascular control of systemic blood pressure. Our expert scientists can isolate resistance arteries from human or animal subcutaneous tissues to assess drug-mediated vasoconstriction and vasodilatation.

  • Assess whether your test articles cause vasoconstriction/dilatation to measure the effect on blood pressure
  • Compare with reference vasodilators and vasoconstrictors
  • Option for studies to be conducted in accordance with GLP regulations
  • Customized protocols are also available 

Image: One of our scientists dissecting subcutaneous resistance arteries.

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Vasoconstriction in subcutaneous resistance arteries

These assays determine whether your test articles cause vasoconstriction in human subcutaneous resistance arteries using phenylephrine, 5-HT or U46619 (thromboxane A2 mimetic) as reference compounds.

Phenylephrine model
This assay uses subcutaneous resistance arteries to assess the effect of your test article on vasoconstriction via adrenoceptors.

5-HT (serotonin) model
This assay uses subcutaneous resistance arteries to assess the effect of your test article on vasoconstriction via 5-HT (serotonin) receptors.

U46619 (thromboxane A2) model
This assay uses subcutaneous resistance arteries to assess the effect of your test article on vasoconstriction via prostanoid (thromboxane) receptors.

Vasodilation in subcutaneous resistance arteries

These assays determine whether your test articles cause vasodilatation (vasodilation) in human subcutaneous resistance arteries. Several reference compounds are available, including acetylcholine, desmopressin, bradykinin, milrinone, or sodium nitroprusside.

Vasodilation via ACh receptors
This assay uses subcutaneous resistance arteries to assess the ability of your test article to induce vasodilation via endothelium-dependent mechanisms and provides a comparison with known vasodilators such as acetylcholine.

Vasodilation via NO donors
This assay assesses the effect of your test article to induce vasodilation via endothelium-independent mechanisms and provides a comparison with the effects of a direct nitric oxide (NO) donor such as SNP.

Vasodilation via ACh receptors
This assay uses subcutaneous resistance arteries to assess the ability of your test article to induce vasodilation via endothelium-dependent mechanisms and provides a comparison with known vasodilators such as acetylcholine.

Vasodilation via PDE3 receptors
This assay uses subcutaneous resistance arteries to assess the effect of your test article on vasodilation via PDE3 receptors.

Desmopressin model
This assay uses subcutaneous resistance arteries to assess the effect of your test article on vasodilation via vasopressin & oxytocin receptors.

Diseased arteries

These assays use ischemic subcutaneous resistance or muscular arteries to determine the effects of your test article ex vivo. For ischemic arteries, bradykinin or sodium nitroprusside (SNP) can be used as reference compounds. PDA-angiotensin 1 can be used for atherosclerotic arteries. 

Ischemic bradykinin model
This assay uses ischemic resistance arteries to assess the effect of your test article on vasodilation via bradykinin receptors.

Ischemic SNP model
This assay uses ischemic resistance arteries to assess the effect of your test article on vasodilation via nitric oxide (NO) donors.

Atherosclerotic PDA-angiotensin 1 model
This assay uses atherosclerotic resistance arteries to assess the effect of your test article on vasoconstriction via angiotensin receptors.