Factors related to the low resting membrane potentials of diseased human atrial muscles.

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Abstract
We studied the ionic mechanism of low resting potential (RP) of quiescent "diseased" human atrial fibers. The RP was -49.7 .+-. 0.8 mV (n = 179) in normal Tyrode''s solution (5.4mM [K]0, 36.degree.C). The changes in RP measured at various levels of [K]0 appeared to fit the RP-[K]0 relationship predicted by the Goldman-Hodgkin-Katz equation, assuming PNa/PK ratio (.alpha.) to be 0.102 and [K]i to be 131.9 mM. The .alpha. far exceeded the normal value (about 0.01) by a factor of 10. Acetylcholine (ACh, 10 .mu.M) led to marked increases in the RP. An application of tetrodotoxin (TTX, 6 .mu.M) and perfusion with low [Na]0 (10% of the control) media in the presence and absence of ACh produced considerable hyperpolarizations of the RP. These findings indicate that increased .alpha. value is due to a combination of decreased PK and increased PNa. Applications of ouabain (5 .mu.M) and a cooling procedure (12.3.degree.C) depolarized the membrane, whereas epinephrine (1 .mu.M) hyperpolarized it. Transient hyperpolarization, which exceeded the steady state levels of RP at 5.4 mM [K]0, was observed with perfusing of 5.4 mM [K]0 media following perfusion with K-free media. These findings suggest that electrogenic Na pump current plays a significant role in the maintenance of the RP. In conclusion, partial depolarization of "diseased" human atrial fibers was attributed to both decreases in membrane K+ conductance and increases in Na+ conductance. The electrogenic outward pump current seemed to protect the fibers from severe depolarization produced by teh conductance abnormality (increased PNA/PK).