Nitric Oxide Regulates Basal But Not Capsaicin-, CGRP-, or Bile Salt-Stimulated Rabbit Esophageal Mucosal Blood Flow

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Abstract
Esophageal mucosal blood flow is a dynamic phenomenon that is altered by luminal content that probably represents an important intrinsic method of defense. This study investigated the role played by endogenous nitric oxide in the regulation of esophageal mucosal blood flow at rest and in response to luminal capsaicin, a specific stimulant for visceral afferent nerves, as well as calcitonin gene-related peptide, and the bile salt deoxycholate. The L-arginine analog L-NAME was used to block nitric oxide synthesis. Radiolabeled microspheres were used to measure blood flow in a well-characterized rabbit model. Phenylephrine was used to mimic the hemodynamic effects of L-NAME to show the specificity of positive findings. Administration of L-NAME led to a significant reduction in mucosal blood flow at rest, an effect that was not shared by phenylephrine. The blood flow responses to luminal capsaicin, intra-arterial calcitonin gene-related peptide (CGRP), and luminal deoxycholate, however, were not diminished in the presence of L-NAME. Although nitric oxide may play a role in the maintenance of normal resting esophageal mucosal blood flow, the reactive responses to luminal capsaicin, luminal deoxycholate, and intra-arterial CGRP are not nitric oxide dependent.

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