Effects of nitric oxide synthase blockade on esophageal peristalsis and the lower esophageal sphincter in the cat.

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The present study explores the role of nitric oxide (NO) in control of esophageal peristalsis and lower esophageal sphincter (LES) function in the cat. Studies were performed on 20 ketamine-anesthetized cats with manometric recording at the LES, 0, 2, 4, and 6 cm above the LES (smooth muscle section), and 12 and (or) 14 cm above the LES (striated muscle section). L-Ng-Nitro-arginine (L-NNA, 10(-6)-10(-4) mol/kg) was given intravenously, and the effects on swallow-induced esophageal peristalsis were assessed. (i) L-NNA increased the velocity of swallow-induced peristalsis in the smooth muscle esophagus; the effect was dose dependent, more prominent distally, and completely reversed by L-arginine (10(-3) mol/kg). (ii) L-NNA decreased the amplitude of peristaltic contraction in the very distal esophagus; the decrease also was dose dependent but not returned to normal by L-arginine. (iii) L-NNA inhibited LES relaxation (reversed by L-arginine) and decreased the LES "after-contraction" amplitude (unaffected by L-arginine). (iv) L-NNA was associated with the appearance of repetitive contractions. Basal LES tone was unaffected by L-NNA. In conclusion, NO is an important mediator for the timing of peristalsis in the distal smooth muscle esophagus and for LES relaxation in the cat, a species whose contraction amplitude is largely determined by cholinergic excitation. The role of NO in controlling esophageal body and LES contraction amplitude, and in preventing repetitive contractions, requires further study.