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Vol. 294, Issue 2, 598-604, August 2000
Department of Pharmacology and Toxicology, Michigan State
University, East Lansing, Michigan
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 F2
(PGF2). In
endothelium-denuded strips, the order of agonist contractile potency
(
log EC50 [M]) was norepinephrine > phenylephrine = 5-hydroxytryptamine > dopamine > PGF2 > 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 PGF2-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.
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