Hypoxia-induced cell membrane depolarization

It is now widely accepted that the rise in type I cell [Ca ] induced by hypoxia is due to cell membrane depolarization and the resulting Ca influx via voltage-gated... 

Ky currents in vascular smooth muscle cells have diverse properties. The existence of multiple Ky currents within a given artery, or of the differential distribution between different vascular beds, is unknown. More understanding of the properties and distribution of individual Ky channels may shed some light on their physiological role, and remains an important goal for future research. Inhibition of Ky channels may be involved in hypoxia and vasoconstrictor-induced membrane depolarization. The predicted modulation of Ky channels by vasodilators and vasoconstrictors will also be an important area of future investigation. 

Figure 3 Effects of various stimuli and mitochondrial inhibitors on the resting membrane potential of quiescent chromaffin cells. A typical example of hypoxia-induced membrane depolarization is shown in (a), using nystatin perforated-patch whole-cell recording. In (b), bicuculline (100 pM), a reversible inhibitor of small-conductance Ca +-dependent K+ channels (SK), also caused membrane depolarization similar to hypoxia. The mitochondrial inhibitors 2,4-drnitrophenol (DNP) and cyanide (CN) did not mimic the h poxia-mduced membrane depolarization seen in (c) and (d), respectively in fact, in (d), CN caused membrane h3q)erpolarization, though in most cases no change in membrane potential was observed. Both DNP and CN were usually without effect even after perfusing the drug for >10 min. In (e), the hyperpolarizing effect of CN was reversed in the presence of 200 pM glibenclamide, a blocker of Katp channels.

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