Abstract
We tested the hypothesis that Kv1.3 channels affect sympathetic neurovascular transmission using margatoxin (MgTX), a specific inhibitor. In isolated rat tail arteries during electrical field stimulation (4 Hz, 60 volts, 1 min) MgTX (10 nM) decreased release of 3H‐norepinephrine (NE) from 5.3+1.1% to 2.7+0.4% (p<0.05, n=6). In superfused cremaster preparations of anesthetized mice, local periarteriolar nerve stimulation (PNS) with a glass microelectrode (2 µm tip) produced constriction (57+3% at 4 Hz, 75+4% at 8 Hz; resting diameter, 43+3 µm) which MgTX perifusion (100 nM, 50 µm pipette tip) reduced (to 37+2 % at 4 Hz and 47+5% at 8 Hz; p<0.05, n=6). Phentolamine (1 µM) inhibited constriction to PNS (n=3) while MgTX had no effect on constriction to 10 nM NE (47+10%; n=3). These findings suggest that MgTX inhibits Kv1.3 channels in perivascular sympathetic nerve terminals. MgTX perifusion also reduced arteriolar diameter (by 16+6%, n = 6; p<0.05 vs. vehicle, n=3). These data indicate that the activation of Kv1.3 channels in perivascular sympathetic nerve terminals enhances neurovascular transmission and suggest that inhibiting Kv1.3 channels in vascular cells increases vasomotor tone. Support: NIH HL076774, NS050623, HL056786, HL086483, AR048523.
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