Adaptation to hypercapnia vs intracellular ph in cat carotid body: responses in vitro. Lahiri, S., R. Iturriaga, A. Mokashi, F. Botr[acute]e, D. Chugh, and S. Osanai. Department of Physiology, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA
APStracts 3:0037A, 1996.
The hypothesis that the chemosensory discharge rate parallels the intracellular pH (pHi) during hypercapnia, and that the initial _pHi is always more than the steady-state _pHi, giving rise to an overshoot and adaptation, were studied using cat carotid body in vitro at 36.5o C, in the absence and presence of methazolamide (MZ, 30-100 mg/l), a carbonic anhydrase (CNA) inhibitor. Incremental acidic hypercapnia was followed by an incremental initial peak response (overshoot), which was followed in turn by a greater magnitude of adaptation. Acidic hypercapnia (Pco2 = 55-65 Torr, pHo = 7.10-7.2) elicited a rapid initial response followed by a slower adaptation to a sustained activity at lower discharge rate. Isohydric hypercapnia (Pco2 = 55-65 Torr, pHo = 7.36-7.40) produced an equally rapid initial response, but one of smaller magnitude, and the discharge activity rapidly returned to near baseline level. Alkaline hypercapnia (Pco2 = 55 - 65 Torr, pHo = 7.55 - 7.70) induced the same rapid peak response, but one of still smaller magnitude; the activity then decreased rapidly to a value less than the initial baseline activity. Thus, at a given hypercapnia, increasing pHo not only reduced the peak response but also increased the extent and speed of adaptation. The miminization of initial discharge activity during hypercapnia at the same pHo showed that the initial _pHi which was associated with adaptation was managed by active transport. CNA inhibition by MZ eliminated the initial overshoot which also suggested involvment of the initial rapid pHi in the overshoot. HEPES decreased the baseline and steady-state activities but an overshoot and subsequent adaptation still persisted. These results are consistent with rapid intracellular CO2 hydration and acid formation, mediated by CNA, and the subsequent pHi redistribution by active transport, giving rise to adaptation. Increasing pHo, however, decreased the final steady-state activity in parallel with but presumably alkaline to the electrochemical gradients, and pHi is nearly a unique function of pHo. 

Received 31 January 1994; accepted in final form 7 November 1995.
APS Manuscript Number A97-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 January 96