Abstract
Activation of intrinsic nonadrenergic noncholinergic (NANC) esophageal nerves during peristalsis or by electrical field stimulation (EFS) in vitro produces a hyperpolarization followed by a depolarization of the circular smooth muscle of the opossum esophagus. N(ω)-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase, and nitric oxide (NO) were used to test the hypothesis that NO or a NO-containing compound is a mediator of this NANC nerve-induced hyperpolarization of circular esophageal smooth muscle. The transmembrane potential difference of esophageal circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated membrane responses were evoked by single electrical pulses of 0.5 ms duration and 50 V amplitude. L-NNA abolished the initial hyperpolarization and reduced the amplitude of and the time to maximal depolarization. L-Arginine (1 mM), the substrate for NO synthase, antagonized the effect of L-NNA. Exogenous NO produced hyperpolarization of the smooth muscle membrane potential and attenuated the amplitudes of EFS-induced hyperpolarization and depolarization. The effect of NO was blocked neither by L-NNA nor by tetrodotoxin (1 μM). The data support the hypothesis that NO or a NO-containing compound mediates NANC nerve-induced responses of the esophageal smooth muscle membrane.
Original language | English (US) |
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Pages (from-to) | G1012-G1016 |
Journal | American Journal of Physiology - Gastrointestinal and Liver Physiology |
Volume | 261 |
Issue number | 6 24-6 |
DOIs | |
State | Published - 1991 |
Keywords
- Endothelium-derived relaxing factor
- Enteric nervous system
- Gastrointestinal motility
ASJC Scopus subject areas
- Physiology
- Hepatology
- Gastroenterology
- Physiology (medical)