Figure S1. Repolarization of membrane potential in Nω-nitro-L-arginine (L-NNA) does not restore stretch-dependent inhibitory responses. (A) Under control conditions, stretch of circular muscle produces hyperpolarization in membrane potential (dashed line in upper panel) that recovered when stretch was relieved (middle and lower panels). (B) In the presence of L-NNA (100 μmol L−1), stretch did not produce membrane hyperpolarization observed under control conditions. (C) In the continued presence of L-NNA, pinacidil (0.1 μmol L−1) hyperpolarized membrane potential to control levels. Stretch of the circular muscle in the presence of L-NNA and pinacidil, when membrane potential was restored to control levels did not produce membrane hyperpolarization. These data suggest that membrane depolarization alone did not inhibit stretch-dependent inhibitory responses.

Figure S2. Effect of atropine on stretch-dependent responses in the proximal colon. (A) Shows membrane potential hyperpolarization (dashed line) and isometric force recordings (middle panel) in response to a stretch ramp that was delivered at 6 μm s−1 until a 5 mN isometric force was reached (lower panel). In this muscle preparation the 5 mN force was reached in 307 s. (B) Shows changes in membrane potential (dashed line) and isometric force measurement (middle panel) in response to a stretch ramp recorded from the same muscle preparation in the presence of atropine (1 μmol L−1). Atropine had no effect on membrane potential but had a slight but not significant decrease in the frequency of action potential (AP) complexes. Stretch ramps in the presence of atropine caused membrane hyperpolarization and abolished any further AP discharge until the active change in length ramp was ceased. Atropine also increased the compliance of the circular muscle. In the presence of atropine the muscle preparation required 315 s to reach 5 mN of isometric force.

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NMO_12059_sm_Supporting-Methods.docx205KSupporting info item
NMO_12059_sm_TableS1.docx95KSupporting info item

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