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We have previously shown that in the presence of tetraethylammonium (TEA, 6.7-67 mM) phasic mechanical activity and a myogenic response (MR) to quick stretch are produced in normally multi-unit tracheal smooth muscle. The present studies were designed to investigate the electrophysiological basis for these changes in the mechanical properties of the muscle. Intracellular recordings showed that in the presence of TEA the membrane was partially depolarized and trains of small (8-20 mV), decrementally conducted action potentials were produced spontaneously at a frequency of 15-20/min. Action potentials could also be stimulated by external electrodes, and the conduction velocity over short distances was 0.84 plus or minus 0.2 cm/s. Membrane conductance and rectification, as measured by the magnitude of electrotonic potentials in response to external stimulation, were reduced in the presence of TEA. The length constant was increased from 1.6 plus or minus 0.1 to 2.8 plus or minus 0.2 mm. These results are consistent with the notion that TEA produces phasic membrane electrical activity by reducing P-K.

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In multi-unit tracheal smooth muscle (TSM), quick stretches applied at a velocity of 5 times the measured maximum velocity of isotonic shortening of the muscle, of a magnitude 3 times the measured extension of the series-elastic component when the muscle contracts maximally, and at optimal muscle length (L-o) were unable to elicit any myogenic response (MR). Experimental conditions such as hypoxia (P-O2 smaller than 60 mmHg) and acidosis (pH equals 6.8) or the presence of Ba2+ (2 mM), acetylcholine (10-6 M), or high (K+)-o (59 mM) were also unable to elicit the MR. However, tetraethylammonium chloride (TEA, 0.4-67 mM) produces 1) spontaneous phasic contractions and 2) a MR to quick stretch. The ionic basis for these changes was then investigated by studying the Ca and Mg dependence of the response to TEA. The dose-response relationship to TEA was shifted to the left by decreasing external Mg2+ from 2.5 to 0.5 mM. The ability of TSM to produce a MR was absolutely dependent on external Ca, but the threshold concentration required shifted from 2.5 times 10-5 M at normal external Mg (2.5 mM) to 5 times 10-4 M at the reduced external Mg (0.5 mM). The effects of TEA on spontaneity and the MR were abolished by D-600. These results suggest that 1) TEA functionally converts multiunit smooth muscle into a single unit one and leads to the development of a MR and 2) the MR results from a depolarization-activated mobilization of Ca and is inhibited by ionic conditions known to increase membrane permeability.