Bb. Herlofson et al., THE EFFECTS OF SODIUM LAURYL SULFATE ON THE PHRENIC-NERVE DIAPHRAGM PREPARATION FROM THE RAT, Pharmacology & toxicology, 79(5), 1996, pp. 217-224
The time period to 50% inhibition of the twitches and compound action
potential of the rat phrenic nerve-diaphragm preparation with sodium l
auryl sulfate (2.5X10(-4)-5.0X10(-3) M) was recorded. The twitch contr
actions during indirect stimulation, the contraction during direct sti
mulation, and the compound action potential of the isolated phrenic ne
rve, were inhibited in that order. Depolarization due to high action p
otential activity induced by tetanic stimulation, veratridine, low Ca2
+- or high K+-solutions, all enhanced the inhibitory effect of sodium
lauryl sulfate (5.0X10(-4) M) during indirect stimulation. Hyperpolari
zation in K+-free solution and membrane stabilization by lidocaine ant
agonized the inhibitory effect of sodium lauryl sulfate. Accordingly,
it probably induced inhibition by depolarization. The depolarization m
ay decrease the influx of Ca2+ and the reuptake of choline(+) as sugge
sted by an observed synergism with tetraethylammonium Cl and hemicholi
nium-3 Br, which antagonize the reuptake of choline(+). On the opposit
e, 3,4-diaminopyridine, which increases the influx of Ca2+, antagonize
d the sodium lauryl sulfate-induced inhibition, and induced a biphasic
contracture. The first phase was probably caused by a depolarization,
and the second phase by release of Ca2+ from the sarcoplasmic reticul
um. The potentiation of the second phase by dantrolene and in low Ca2 solution, was attributed to sodium lauryl sulfate-induced desensitiza
tion.