INTERACTION BETWEEN CONDUCTED VASODILATION AND SYMPATHETIC-NERVE ACTIVATION IN ARTERIOLES OF HAMSTER STRIATED-MUSCLE

We 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 mu m) fi lled with acetylcholine (ACh, 1 mol/L) were positioned adjacent to the wall of second-order (2A) or third-order (3A) arterioles approximate to 1 mm distal to their origin to induce local and conducted vasodilat ion; diameter responses were recorded at the micropipette tip and at v essel origins, respectively. For 2A and 3A arterioles (resting diamete rs, 15 to 54 and 9 to 30 mu m, respectively), vasoconstriction with PN S was frequency dependent (0.5 to 32 Hz); this was attenuated by 65% ( P>.05) with cr-adrenoceptor blockade (phentolamine, 1 mu mol/L). Condu cted vasodilation was attenuated by >40% during 16-Hz PNS (P<.05); thi s effect was reversed by phentolamine. In a reciprocal fashion, conduc ted vasodilation diminished PNS-induced vasoconstriction by approximat e to 50% (P<.05). Elevating oxy ,gen (from 0% to 10%) in the superfusi on solution induced vasoconstriction similar to that with 16-Hz PNS ye t had no effect on conduction. Neural blockade with tetrodotoxin (1 mu mol/L) eliminated PNS-induced vasoconstriction and enhanced (P<.05) c onducted vasodilation. These findings indicate that perivascular nerve s in striated muscle can influence cell-to-cell communication along th e arteriolar wall both at rest and during enhanced sympathetic activit y. The attenuation of sympathetic vasoconstriction by conducted vasodi lation suggests a novel explanation for functional sympatholysis.