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Research ArticleCARDIOVASCULAR

Vascular Reactivity of Isolated Thoracic Aorta of the C57BL/6J Mouse

Amber Russell and Stephanie Watts
Journal of Pharmacology and Experimental Therapeutics August 2000, 294 (2) 598-604;
Amber Russell
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Stephanie Watts
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Abstract

We characterized the thoracic aorta from the C57BL/6J mouse, a strain used commonly in the generation of genetically altered mice, in response to vasoactive substances. Strips of aorta were mounted in tissue baths for measurement of isometric contractile force. Cumulative concentration-response curves to agonists were generated to observe contraction, or relaxation in tissues contracted with phenylephrine or prostaglandin F2α (PGF2α). In endothelium-denuded strips, the order of agonist contractile potency (−log EC50 [M]) was norepinephrine > phenylephrine = 5-hydroxytryptamine > dopamine > PGF2α > isoproterenol > KCl. Angiotensin II and endothelin-1 were weakly efficacious (15% of maximum phenylephrine contraction), as were UK14,304, clonidine, histamine, and adenosine. In endothelium-intact strips, agonists still caused contraction and both angiotensin II and endothelin-1 remained ineffective. In experiments focusing on angiotensin II, angiotensin II-induced contraction was abolished by the AT1 receptor antagonist losartan (1 μM) but was not enhanced in the presence of the AT2 receptor antagonist PD123319 (0.1 μM), tyrosine phosphatase inhibitor orthovanadate (1 μM) or when angiotensin II was given noncumulatively. Prazosin abolished isoproterenol-induced contraction and did not unmask isoproterenol-induced relaxation. Angiotensin II and endothelin-1 did not cause endothelium-dependent or -independent relaxation in phenylephrine- or PGF2α-contracted tissues. Acetylcholine but not histamine, dopamine, or adenosine caused an endothelium-dependent vascular relaxation. These experiments provide information as to the vascular reactivity of the normal mouse thoracic aorta and demonstrate that the mouse aorta differs substantially from rat aorta in response to isoproterenol, angiotensin II, endothelin-1, histamine, and adenosine.

Footnotes

  • Send reprint requests to: Stephanie W. Watts, Ph.D., B445 Life Sciences Bldg., Department of Pharmacology & Toxicology, Michigan State University, East Lansing, MI 48824-1317. E-mail:wattss{at}msu.edu

  • ↵1 This study was supported in part by Grant HL58489 from the National Institutes of Health.

  • Abbreviations:
    PG
    prostaglandin
    5-HT
    5-hydroxytryptamine
    AT
    angiotensin
    SNAP
    S-nitroso-N-acetylpenicillamine
    • Received January 18, 2000.
    • Accepted April 6, 2000.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 294 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 294, Issue 2
1 Aug 2000
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Research ArticleCARDIOVASCULAR

Vascular Reactivity of Isolated Thoracic Aorta of the C57BL/6J Mouse

Amber Russell and Stephanie Watts
Journal of Pharmacology and Experimental Therapeutics August 1, 2000, 294 (2) 598-604;

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Research ArticleCARDIOVASCULAR

Vascular Reactivity of Isolated Thoracic Aorta of the C57BL/6J Mouse

Amber Russell and Stephanie Watts
Journal of Pharmacology and Experimental Therapeutics August 1, 2000, 294 (2) 598-604;
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