Peripheral vascular neuroeffector mechanisms in experimental cholestasis

G. Jacob, O. Said, J. Finberg, A. Bomzon

Research output: Contribution to journalArticlepeer-review


Jaundiced patients have systemic hypotension and are more susceptible to hemorrhagic shock than nonjaundiced individuals. We have hypothesized that the mechanism whereby these cardiovascular complications arise is linked to a disturbance of the vascular neuroeffector process in the cardiovascular system. With the use of 3-day bile duct-manipulated (sham-operated) and bile duct-ligated rats, we have evaluated α-adrenoceptor function and amine uptake using in vivo and in vitro techniques. Blunted pressor responsiveness to norepinephrine, electrical stimulation, and the α1-adrenoceptor agonists, methoxamine and phenylephrine, was observed in the bile duct- ligated pithed rats. In contrast, normal responsiveness to BHT-933 and clonidine, the α2-adrenoceptor agonists, was seen in these animals. The uptake1 blocker, cocaine, caused potentiation of equal magnitudes of the pressor responsiveness to electrical stimulation and norepinephrine in the sham-operated and bile duct-ligated pithed rats. In aortic rings prepared from the bile duct-ligated rats, blunted in vitro vascular reactivity to norepinephrine and the same α1-adrenoceptor agonists was seen. Bile duct ligation had no effect on norepinephrine uptake or its kinetics in stressed and unstressed arterial rings and portal veins. We have thus concluded that bile duct ligation induces a defect in the functional expression of cardiovascular α1-adrenoceptors without any effects on the activity of α2-adrenoceptors or norepinephrine uptake.

Original languageEnglish
Pages (from-to)G579-G586
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number3 28-3
StatePublished - 1993
Externally publishedYes


  • cardiovascular system
  • norepinephrine uptake
  • obstructive jaundice
  • pressor reactivity
  • vascular reactivity
  • α-adrenoceptors


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