Gadolinium and mechanotransduction of rat aortic baroreceptors

The cellular mechanisms enabling baroreceptors to transduce wall distortion into axonal discharge are unknown but might involve stretch- activated ion channels. Gadolinium (Gd³⁺, 10 μM) blocks stretch-activated channels in several preparations. Here we tested Gd³⁺ effects on discharge responses of 15 single-fiber baroreceptors in vitro. We simultaneously measured discharge, pressure, and aortic diameter at Gd³⁺ concentrations from 0.001 to 400 μM. High levels of Gd³⁺ added to a bicarbonate-buffered perfusate (Krebs) slightly shifted the pressure-discharge relation (<4 mmHg, n = 3, P = 0.01) without affecting slope or discharge frequency at threshold. Gd³⁺ in Krebs variably altered the pressure-diameter relation. Because 500 μM Gd³⁺ produced visible precipitate in Krebs, we tested Gd³⁺ in a simpler perfusate using N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Gd³⁺ in HEPES (n = 10) induced minor, but statistically significant, average increases in threshold (less than +5-7%) and no changes in gain. However, prolonged HEPES exposure alone (n = 2) produced similar shifts. Electron microscopy verified that Gd³⁺ diffused from the lumen to reach extracellular locations near baroreceptor endings. We conclude that 1) HEPES perfusate alone reversibly depresses baroreceptor discharge and 2) Gd³⁺ has no direct effects on baroreceptors. Thus it appears that aortic baroreceptor mechanotransduction must utilize a different class of stretch- activated ion channels.