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J Appl Physiol 103: 600-607, 2007. First published May 24, 2007; doi:10.1152/japplphysiol.01286.2006
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Airway mechanoreceptor deactivation

J. Guardiola,1 M. Proctor,1 H. Li,1 R. Punnakkattu,1 S. Lin,1 and J. Yu1,2

Departments of 1Medicine, and 2Physiology and Biophysics, University of Louisville, Louisville, Kentucky

Submitted 14 November 2006 ; accepted in final form 28 April 2007

Airway sensors play an important role in control of breathing. Recently, it was found that pulmonary slowly adapting stretch receptors (SARs) cease after a brief excitation following sodium pump blockade by ouabain. This deactivation can be explained by overexcitation. If this is true, mechanical stimulation of the SARs should also lead to a deactivation. In this study, we recorded unit activity of the SARs in anesthetized, open-chest, and mechanically ventilated rabbits and examined their responses to lung inflation at different constant pressures. Forty-seven of 137 units had a clear deactivation during the lung inflation. The deactivation threshold varied from unit to unit. For a given unit, the higher the inflation pressure, the sooner the deactivation occurs. For example, the SARs deactivated at 3.0 ± 0.3 and 4.8 ± 0.4 s when the lungs were inflated to constant pressures of 30 and 20 cmH2O, respectively (n = 25, P < 0.0001). The units usually ceased after a brief intense discharge. In some units, their activity shifted to a lower level, indicating a pacemaker switching. Our results support the notion that SARs deactivate due to overexcitation.

slowly adapting stretch receptors; lung inflation


Address for reprint requests and other correspondence: J. Yu, Dept. of Medicine (Pulmonary), Univ. of Louisville, Louisville, KY 40292 (e-mail: j0yu0001{at}louisville.edu)






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