Abstract
In anesthetized, artificially ventilated rabbits with vagus nerve section, release from 10 consecutive hyperinflations (inflation volume = 3 tidal volume) caused an inhibition of the slowly adapting pulmonary stretch receptor (SAR) activity for 16–22 sec. Intravenous administration of tetraethylammonium (TEA, 10 and 20 mg/kg), a K + channel blocker, did not significantly alter either basal SAR discharge or tracheal pressure (P T). Although TEA treatment at 10.0 mg/kg had no significant effect on the magnitude and duration of inhibited SAR activity seen after release from hyperinflation, the increasing dose of this K + channel blocker up to 20 mg/kg inhibited these effects of the receptor activity but this inhibition was small. The Na +-K + ATPase inhibitor ouabain (5 and 10 μg/kg) that had no significant effect on SAR activity and P T in the control abolished or attenuated the inhibitory action of SARs in a dose-dependent manner. Furthermore, the changes in dynamic lung compliance (Cdyn) and P T in response to post-hyperinflation were not significantly influenced by pretreatment with either TEA or ouabain. These results suggest that the inhibitory action of receptors seen during post-hyperinflation corresponded with the induction of slow afterhyperpolarization (sAHP), and that the mechanism of generating the sAHP of SARs is mainly mediated by the activation of Na +-K + pump activity.
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