Dominance of longitudinal muscle in propagation of intestinal slow waves.

The purpose of these experiments was to test the hypothesis that circular muscle plays an active role in the propagation of intestinal slow waves, specifically be providing excitatory current through a process of regenerative amplification. With volume-recording techniques and microelectrode recordings we obtained the following results that are not consistent with such a mechanism: 1) slow waves propagated without delay or decrease in amplitude along segments of cat jejunum devoid of a ring of circular muscle up to 3 mm wide, i.e., across a longitudinal muscle bridge more than 4 space constants long (9 of 11 preparations) but did not propagate across a circumferential cut through the longitudinal muscle layer (14 of 14 preparations); 2) the membrane current associated with the slow wave had a pronounced inward component when recorded from either the serosal or the mucosal side of the longitudinal muscle bridge but was entirely outward when recorded from either the mucosal or the serosal side of exposed circular muscle, including those preparations in which various thicknesses of circular muscle were removed from the mucosal side of the recording area; 3) slow-wave amplitudes recorded intracellularly from intact (n = 9) and isolated (n = 8) longitudinal muscle preparations were not significantly different (27.0 +/- 4.3 vs. 25.4 +/- 5.3 (SD) mV); 4) after 30 min in 4.4 X 10(-6) M verapamil, slow-wave amplitude did not significantly decrease, although contractile activity had long since terminated. These results are more consistent with the hypothesis that longitudinal muscle provides most, if not all, of the current required for slow-wave propagation in the small intestine.