Vasomotor control in arterioles of the mouse cremaster muscle

Recent advances in transgenic mouse technology provide novel models to stud y cardiovascular physiology and pathophysiology. In light of these developm ents, 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 superfuse d cremaster muscle preparation of anesthetized C57B16 mice. Spontaneous res ting tone increased with branch order and was enhanced by oxygen. Norepinep hrine and acetylcholine (ACh) caused concentration-dependent vasoconstricti on and vasodilation, respectively, Microiontophoresis of ACh evoked vasodil ation that conducted along arterioles; the local (direct) response was inhi bited by N-w-nitro-L-arginine (LNA), and both local and conducted responses were inhibited by 17-octadecynoic acid (17-ODYA), Microejection of KCI evo ked a biphasic response: a transient conducted vasoconstriction (inhibited by nifedipine), followed by a conducted vasodilation that was insensitive t o LNA, indomethacin, and 17-ODYA, Phenylephrine evoked focal vasoconstricti on that did not conduct. Perivascular sympathetic nerve stimulation evoked constriction along arterioles that was inhibited by tetrodotoxin. These fin dings indicate that for arterioles in the mouse cremaster muscle, nitric ox ide and endothelial-derived hyperpolarizing factor (as shown by LNA and 17- ODYA interventions, respectively) mediate vasodilatory responses to ACh but not to KCI, and that vasomotor responses spread along; arterioles by multi ple pathways of cell-to-cell communication.