K+-current modulated by PO2 in type I cells in rat carotid body is not a chemosensor.
According to the membrane channel hypothesis of carotid body O2 chemoreception, hypoxia suppresses K+ currents leading to cell depolarization, [Ca2+]i rise, neurosecretion, increased neural discharge from the carotid body. We show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) which suppressed the Ca2+ sensitive and other K+ currents in rat carotid body type I cells, with and without low [Ca2+]o plus high [Mg2+]o, did not essentially influence low PO2 effects on [Ca2+]i and chemosensory discharge. Thus, hypoxia may suppress the K+ currents in glomus cells but K+ current suppression of itself does not lead to chemosensory excitation. Therefore, the hypothesis that K+-O2 current is linked to events in chemoreception is not substantiated. K+-O2 current is an epiphemenon which is not directly linked with O2 chemoreception.
Lahiri
S
S
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6085, USA.
Roy
A
A
Rozanov
C
C
Mokashi
A
A
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002344:Carotid Body / Q000166:cytology / Q000187:drug effects*; D002628:Chemoreceptor Cells / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D010100:Oxygen / Q000494:pharmacology*; D010313:Partial Pressure; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D019789:Tetraethylammonium / Q000494:pharmacology
D015221:Potassium Channels; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D010100:Oxygen