Abstract
According to the membrane channel hypothesis of carotid body O 2 chemoreception, hypoxia suppresses K + currents leading to cell depolarization, [Ca 2+] i rise, neurosecretion, increased neural discharge from the carotid body. We show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) which suppressed the Ca 2+ sensitive and other K + currents in rat carotid body type I cells, with and without low [Ca 2+] o plus high [Mg 2+] o , did not essentially influence low P O 2 effects on [Ca 2+] 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 +–O 2 current is linked to events in chemoreception is not substantiated. K +–O 2 current is an epiphemenon which is not directly linked with O 2 chemoreception.
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