High PCO does not alter pHi, but raises [Ca2+]i in cultured rat carotid body glomus cells in the absence and presence of CdC12.
We measured the effect of high PCO (500-550 Torr) on the pHi and [Ca2+]i in cultured glomus cells of adult rat carotid body (CB) as a test of the two models currently proposed for the mechanism of CB chemoreception. The metabolic model postulates that the rise in glomus cell [Ca2+]i, the initiating reaction in the signalling pathway leading to chemosensory neural discharge, is due to [Ca2+] release from intracellular Ca2+ stores. The membrane potential model postulates that the rise in [Ca2+]i comes from influx of extracellular Ca2+ through voltage-dependent Ca2+ channels (VDCC) of the L-type. High PCO did not change pHi at PO2 of 120-135 Torr, showing that CO-induced changes in [Ca2+]i are not due to changes in pHi. High PCO caused a highly significant rise in [Ca2+]i from 90+/-12 nM to 675+/-65 nM, both in the absence and in the presence of 200 microM CdCl2, a potent blocker of L-type VDCCs. This result is fully consistent with release of Ca2+ from glomus cell intracellular stores according to metabolic model, but inconsistent with influx of extracellular Ca2+ through VDCCs according to the membrane potential model.
Mokashi
A
A
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6085, USA.
Roy
A
A
Rozanov
C
C
Osanai
S
S
Storey
B T
BT
Lahiri
S
S
D000818:Animals; D019256:Cadmium Chloride / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002248:Carbon Monoxide / Q000494:pharmacology*; D002344:Carotid Body / Q000166:cytology / Q000187:drug effects*; D002478:Cells, Cultured; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D051381:Rats
D002248:Carbon Monoxide; D019256:Cadmium Chloride; D002118:Calcium