Diethyl pyrocarbonate inhibits rostral ventrolateral medullary H+ sensitivity.
Diethyl pyrocarbonate (DEPC), an acylating agent that reacts with imidazole-histidine in vitro, inhibits CO2 sensitivity when applied by pledget to the rostral chemosensitive area on the ventrolateral medullary (VLM) surface in glomectomized, chloralose-urethan-anesthetized cats. In this study similar application of DEPC inhibits the phrenic nerve response to CO2 expressed as a function of VLM [H+] measured by surface pH electrode. Attempts to evaluate direct chemoreceptor stimulation by HCL-soaked surface pledgets proved difficult, but rostral DEPC did inhibit the response to intravenous infusion of HCl. As previously reported, the CO2 and intravenous H+ responses are not a unique function of the VLM [H+]. DEPC had similar inhibitory effects on both the CO2 and the intravenous H+ responses, suggesting that the difference between them may reflect more the orientation or accessibility of the central chemoreceptor than a different mechanism for sensing CO2 vs. H+. DEPC did not alter the phrenic nerve response to hypoxia, indicating that DEPC effects on central chemoreception are not the result of a generalized inhibitory process. The results support the hypothesis that imidazolehistidine is involved at the rostral area with chemoreception of both CO2 and H+.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood / Q000494:pharmacology; D002415:Cats; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004047:Diethyl Pyrocarbonate / Q000494:pharmacology*; D005260:Female; D005561:Formates / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D010313:Partial Pressure; D010791:Phrenic Nerve / Q000187:drug effects / Q000502:physiology; D012016:Reference Values; D012119:Respiration / Q000187:drug effects*
D005561:Formates; D002245:Carbon Dioxide; D004047:Diethyl Pyrocarbonate