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* The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519, USA; and
Department of Pharmacology, Yale University School of Medicine, Boyer Center for Molecular Medicine, New Haven, Connecticut 06536, USA
2Correspondence: The John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Ave., New Haven, CT 06519, USA. E-mail: sssegal{at}jbpierce.org
Recent advances in transgenic mouse technology provide novel models to
study cardiovascular physiology and pathophysiology. In light of these
developments, there is an increasing need for understanding
cardiovascular function and blood flow control in normal mice. To this
end we have used intravital microscopy to investigate vasomotor control
in arterioles of the superfused cremaster muscle preparation of
anesthetized C57Bl6 mice. Spontaneous resting tone increased with
branch order and was enhanced by oxygen. Norepinephrine and
acetylcholine (ACh) caused concentration-dependent vasoconstriction and
vasodilation, respectively. Microiontophoresis of ACh evoked
vasodilation that conducted along arterioles; the local (direct)
response was inhibited by N
-nitro-L-arginine (LNA), and
both local and conducted responses were inhibited by 17-octadecynoic
acid (17-ODYA). Microejection of KCl evoked a biphasic response: a
transient conducted vasoconstriction (inhibited by nifedipine),
followed by a conducted vasodilation that was insensitive to LNA,
indomethacin, and 17-ODYA. Phenylephrine evoked focal vasoconstriction
that did not conduct. Perivascular sympathetic nerve stimulation evoked
constriction along arterioles that was inhibited by tetrodotoxin. These
findings indicate that for arterioles in the mouse cremaster muscle,
nitric oxide and endothelial-derived hyperpolarizing factor (as shown
by LNA and 17-ODYA interventions, respectively) mediate vasodilatory
responses to ACh but not to KCl, and that vasomotor responses spread
along arterioles by multiple pathways of cell-to-cell communication.
Hungerford, J. E., Sessa, W. C., Segal, S. S. Vasomotor
control in arterioles of the mouse cremaster muscle.
Key Words: microcirculation • vasodilation • vasoconstriction • conduction
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