Aims: 

The neurohypophysal peptide vasopressin (AVP) is involved in diverse function, including smooth muscle contraction, stimulation of liver glycogenesis, modulation of ACTH release, inhibition of diuresis. However, the role of this peptide in the regulation of bile formation is not clear yet.

Methods: 

Biliary duct cannulated rats were used in acute experiment. Desmopressin (1-Desamino-8D-arginin vasopressin, dDAVP) (1 ng/100 g b.w.) and antagonist of V1_a vasopressin receptors ([b-Mercaptob, bcyclop entamethylenepropionyl1, O-me-Tyr2, Arg8]-Vasopressin) (1mg/100 g b.w.) were administered i.v. Secreted bile volume was measured. The quantitative content of bile acid in each probe taken was determined using the thin-layer chromatography method.

Results: 

Obtained data demonstrate that dDAVP considerably increases volume of bile secretion. Moreover, absolute content of conjugated bile acids in bile, such as taurocholates (+65.7%, p < 0.01), glycocholates (+49.0%, p < 0.05) was significantly increased. Administration of V1 _a vasopressin receptors antagonist was followed by the slow increase bile secretion rate. V1 _a antagonist caused very similar to dDAVP injective effects alterations of taurocholates (+46.6%, p < 0.05), glycocholates (+58.1%, p < 0.01) output. Interestingly that during blockade of V1_a recepors by V1_a vasopressin receptors antagonist dDAVP do not show fully the choleretic action and total content of bile acids was decreased respectively, taurocholates (-27.3%, p < 0.01) and glycocholates (–20.1%, p > 0.05) as compared to dDAVP effect.

Conclusion: 

These results demonstrated that dDAVP elevates bile flow and absolute content of conjugated bile acid in bile drowing V1_a vasopressin receptors.