The excitatory responses of deflationary slowly adapting pulmonary stretch receptor (SAR) activity to lung deflation ranging from approximately -15 to -25 cm of H_2O for approximately 5 s were examined before and after administration of flecainide, a Na~+ channel blocker, and K~+ channel blockers, such as 4-aminopyridine (4-AP) and tetracethylamonium (TEA). The experiments were performed in anesthetized, artificially ventilated rats after unilateral vagotomy. The deflationary SARs increased their activity during lung deflation and its effect became more pronounced by increasing the degree of negative pressure. During lung deflation the average values for the deflationary SAR adaptation index (Al) were below 40%. Intravenous administration of veratridine (50 #mu#g/kg), an Na~+ channel opener, stimulated deflationary SAR activity: one maintained excitatory activity mainly during deflation and the other receptrors showed a tonic discharge during both deflation and inflation. Despite the difference in deflationary SAR firing patterns after venatridine administration, flecainide treatment (6.0 mg/kg) blocked veratridine-induced deflationary SAR stimulation and also caused strong inhibition of the excitatory responses of deflationary SARs to lung deflation. Under these conditions, the average values for deflation. Under these conditions, the average values for deflationary SAR Al were over 90%. The responses of deflationary SARs deflationary SAR Al to lung deflation were not significantly altered by pretreatment with either 4-AP (0.7 and 2.0 mg/kg) or TEA (2.0 and 6.0 mg/kg). These results suggest that the excitatory effect of lung deflation on deflationary SAR actiivty is mediated by the activation of flecainide-sensitive Na~+ channels on the nerve terminals of deflationary SARs.
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