Initial studies in cat isolated pulmonary arteries (18, 30) showed that HPV was accompanied by membrane depolarization and action potential generation; both were blocked by verapamil. These data substantiated the earlier studies in isolated lung that at least part of the mechanism involved increased Ca2+ conductance. In isolated rat pulmonary artery rings, various K+ channel antagonists mimicked HPV (43). While it was initially believed that Ca2+-activated K+ (K^J channels were responsible, later studies suggest that voltage-gated K+ (Kv) channels had a more dominant role in HPV (3). Whether K+ channel inhibition plays a role in vivo has not been confirmed. To state that K+ channels are the sensors or mediators ofHPV is difficult because it can be argued that the channels, or at least their subunits may be capable ofboth functions. For example, a K+ channel subunit may sense a change in 02 tension and change its conformation to close or open the channel. This would mediate changes in membrane potential and consequently intracellular Ca2+, and culminate in contraction or relaxation. Whether this effect is direct or it is mediated through a change in the redox status of the cell is unknown.
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