Effects of hypoxia on the intracellular K+ of clustered and isolated glomus cells of mice and rats.

Carotid bodies of rats and mice were used to measure the intracellular potassium activity, ai(K), of clustered and isolated glomus cells normally oxygenated (pO2 102-139 Torr), and during hypoxia (pO2 2-82 Torr) induced by Na-dithionite. ai(K) was measured with intracellular ion-selective microelectrodes, and the resting potential (EM) with KCl-filled micropipettes. Under normoxia, the ai(K) of clustered cells in both species was higher than that of isolated cells. This resulted in more negative potassium equilibrium potentials (EK's). There was no correlation between ai(K) and EM in clustered cells, but this correlation was significant in isolated cells. Hypoxia significantly decreased ai(K) in clustered and single mouse cells, and in clustered rat cells, although its effects on single rat cells were variable. ai(K) decreases were accompanied by cell depolarization and positive shifts in EK. During hypoxia, there were significant correlations between ai(K) and EM in all cells. It is suggested that ai(K) did not influence the EM of clustered cells under normoxia because of interference by K+ pumping mechanisms toward glomus cells from surrounding sustentacular processes. This hindrance is not present when glomus cells are isolated. During hypoxia K+ pumping from sustentacular cells is disrupted, allowing the EM of clustered glomus cells to follow their ai(K) and behave like isolated cells. The different effects of hypoxia on isolated rat and mouse cells may be due to activation of different types of glomus cells.