Walker B D, Segal S S
John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Conn. 06519, USA.
J Vasc Res. 1998 Nov-Dec;35(6):405-12. doi: 10.1159/000025611.
Vasodilation originating within a muscle is conducted into feed arteries, but the determinants of conduction along feed arteries are undefined. We have investigated the effect of vasomotor tone on conducted vasodilation in feed arteries of the hamster retractor muscle. Unbranched segments (length, 2-3 mm) were isolated, cannulated, and studied in vitro at 37 degreesC while pressurized to 25 mm Hg, 75 mm Hg (in vivo pressure), or 120 mm Hg in the absence and presence of norepinephrine (NE, 10(-7) M + 10(-6) M propanolol). Internal diameter decreased (p < 0.05) as pressure increased (85 +/- 7, 73 +/- 4, 66 +/- 6 microm, respectively), confirming myogenic reactivity. Acetylcholine (ACh, 0.1 M) was delivered (1 microA, 500 ms) from a micropipette; vasomotor responses were recorded at the site of release ('local') and at distances up to 1,500 microm ('conducted') along the vessel. There were no responses to ACh at 25 mm Hg. However, dilations (diameter change, microm) were pronounced at 75 mm Hg (local: 22 +/- 3; conducted: 18 +/- 2, respectively), without further change at 120 mm Hg. NE constricted vessels (p < 0. 05) at each pressure (to 65 +/- 9, 57 +/- 6, and 56 +/- 8 microm, respectively); this enabled both local (14 +/- 2 microm) and conducted (10 +/- 1 microm) vasodilation at 25 mm Hg but was without effect on conduction at 75 or 120 mm Hg. Our findings indicate that conducted responses plateau at a physiological level of myogenic tone. Whereas NE had no effect on conduction under normal or hypertensive conditions, it enabled conduction during hypotension. We conclude that pressure and NE influence the ability of conducted vasodilation to govern muscle blood flow.
