Captopril reduced portal pressure in cirrhotic patients with low portal venous velocity

Abstract

neuronal pathway is responsible for this signal transmission, or which neurotransmitter in the NTS is involved. Objectives: to clarify if 1) a capsalcin-sensitive neuronal pathway is the relaying signal between increased portal pressure and NTS activation, and 2) if local Fos expression in NTS is related to nitric oxide (NO) production. Hypotheses: 1) Intact vagal innervation is necessary for NTS activation, and 2) NO may co-expressed with Fos in NTS. Methods: Male SD rats at day 5 after portal vein stenosis (PVS) were used in this experiment. For capsaicin treatment, 1% capsaicin or vehicle (10% Tween-80 in olive oil) was applied to the celiac ganglion or vagus for total 30 min and portal vein was stenosed at the same time. Separate groups (PVS and sham-operated) at day 5 were used for NTS Fos and NO staining by standard immunohistochemistry. Results: NTS Fos expression was significantly attenuated by vagal capsaicin treatment (P < 0.01), but not celiac ganglion capsaicin treatment. In the NTS, only a few neurons were double-stained with both Fos and NO; the majority showed only single staining with NO (cytoplasm) or Fos (nucleus). Conclusions: Fos expression in NTS is dependent on intact vagus but not celiac ganglion. Central neuronal activation responsible for hyperdynamic circulation, as judged by Fos expression is not mediated by NO as a neurotransmitter.