
pmid: 17525293
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.
Pulmonary Stretch Receptors, Action Potentials, Animals, Muscle, Smooth, Rabbits, Lung, Mechanoreceptors, Mechanotransduction, Cellular
Pulmonary Stretch Receptors, Action Potentials, Animals, Muscle, Smooth, Rabbits, Lung, Mechanoreceptors, Mechanotransduction, Cellular
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