Gadolinium inhibits mechanoelectrical transduction in rabbit carotid baroreceptors. Implication of stretch-activated channels.

G Hajduczok; M W Chapleau; R J Ferlic; H Z Mao; F M Abboud

doi:10.1172/JCI117605

Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

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Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

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Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

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Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

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Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

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Published in Volume 94, Issue 6 on December 1, 1994
J Clin Invest. 1994;94(6):2392–2396. https://doi.org/10.1172/JCI117605.
© 1994 The American Society for Clinical Investigation

Published December 1, 1994 - Version history

Gadolinium (Gd3+) has been shown to prevent mechanoelectrical transduction believed to be mediated through stretch-activated channels. We investigated the possible role of Gd(3+)-sensitive channels in mediating baroreceptor activity in the carotid sinus of rabbits. Baroreceptor activity induced by a ramp increase of carotid sinus pressure was reduced significantly during exposure to Gd3+. The inhibition was dose-related and reversible, and was not associated with alteration of carotid sinus wall mechanics as the pressure-strain relationship was unaffected. Veratrine triggered action potentials from single- and multiple-baroreceptor fibers when their response to pressure was inhibited by Gd3+. This suggests that the effect of Gd3+ on baroreceptors in the isolated carotid sinus was specific to their mechanical activation. The results suggest that stretch-activated ion channels sensitive to Gd3+ may be the mechanoelectrical transducers of rabbit carotid sinus baroreceptors.