• colon motility;
  • iNOS;
  • NF-κB;
  • nitric oxide;
  • nNOS;
  • vasopressin


Background  Arginine vasopressin (AVP) is widely used in the treatment of critical diseases with hypotension, but the reports about its effect on gastrointestinal motility are controversial. The purpose of this study was to characterize the role of AVP in the regulation of colonic motility and the underlying mechanism.

Methods  The contraction of the circular muscle strips (CM) of colon in male rats was monitored by a polygraph. The expressions of cytoplasmic inducible nitric oxide synthase (iNOS), I-κB, and the nuclear P65 in proximal colon were measured by Western blot. The V1 receptors (V1Rs) and iNOS were localized by immunohistochemistry. The content of nitric oxide (NO) in the colon was measured by Griess reagent at the absorbance of 560 nm.

Key Results  Arginine vasopressin (10−10–10−6 mol L−1) caused a concentration-dependent inhibition on CM contraction. Pretreatment with one of the following chemicals, including V-1880 (10−7 mol L−1), TTX (10−5 mol L−1), l-NAME (10−4 mol L−1), NPLA (10−7 mol L−1), SMT (10−3 mol L−1), and PDTC (10−3 mol L−1), attenuated the inhibitory effect of AVP on CM contraction. Arginine vasopressin increased the expression of iNOS and the content of NO in proximal colon. These effects were attenuated by pretreatment with PDTC (10−3 mol L−1). Following AVP administration, the amount of cytoplasmic I-κB decreased, but that of nuclear P65 increased. Double immunofluorescence labeling revealed that V1Rs and iNOS were co-localized on the cells of myenteric plexus in proximal colon.

Conclusions & Inferences  Arginine vasopressin inhibited the contraction of CM in proximal colon. This effect was mediated by NO produced from NF-κB–iNOS pathway and neuronal NOS activation in myenteric plexus.