Interaction Between Conducted Vasodilation and Sympathetic Nerve Activation in Arterioles of Hamster Striated Muscle

Abstract

AbstractWe tested the hypothesis that sympathetic nerve activity can influence the conduction of vasodilation along the arteriolar wall. Arterioles in the superfused cremaster muscle of anesthetized male hamsters (n=21, 109±4 g) were studied. Microelectrodes were positioned adjacent to the distal end of primary arterioles to stimulate sympathetic nerves throughout arteriolar networks (perivascular nerve stimulation [PNS]). Microiontophoresis micropipettes (tip outer diameter, 1 to 2 μm) filled with acetylcholine (ACh, 1 mol/L) were positioned adjacent to the wall of second-order (2A) or third-order (3A) arterioles ≈1 mm distal to their origin to induce local and conducted vasodilation; diameter responses were recorded at the micropipette tip and at vessel origins, respectively. For 2A and 3A arterioles (resting diameters, 15 to 54 and 9 to 30 μm, respectively), vasoconstriction with PNS was frequency dependent (0.5 to 32 Hz); this was attenuated by 65% (P<.05) with α-adrenoceptor blockade (phentolamine, 1 μmol/L). Conducted vasodilation was attenuated by >40% during 16-Hz PNS (P<.05); this effect was reversed by phentolamine. In a reciprocal fashion, conducted vasodilation diminished PNS-induced vasoconstriction by ≈50% (P<.05). Elevating oxygen (from 0% to 10%) in the superfusion solution induced vasoconstriction similar to that with 16-Hz PNS yet had no effect on conduction. Neural blockade with tetrodotoxin (1 μmol/L) eliminated PNS-induced vasoconstriction and enhanced (P<.05) conducted vasodilation. These findings indicate that perivascular nerves in striated muscle can influence cell-to-cell communication along the arteriolar wall both at rest and during enhanced sympathetic activity. The attenuation of sympathetic vasoconstriction by conducted vasodilation suggests a novel explanation for functional sympatholysis.