Induction of taurocholate release from isolated rat hepatocytes in suspension by α-adrenergic agents and vasopressin: Implications for control of bile salt secretion

D. A. Gewirtz, J. K. Randolph, I. David Goldman

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Hepatocytes incubated with 25 μM [3H]taurocholate rapidly deplete the extracellular medium of [3H]taurocholate and achieve a steady-state level of intracellular bile salt within 15 min. Exposure of cells at steady state with extracellular taurocholate to the catecholamines norepinephrine or epinephrine results in release of 3H from the cells into the incubation medium; the 3H released represents almost exclusively unmetabolized [3H]taurocholate. The hierarchy of effectiveness of the catecholamines, norepinephrine ≃ epinephrine > phenylephrine >> isoproterenol, is indicative of an α-adrenergic mechanism. Induction of [3H]taurocholate release by norepinephrine is inhibited by the α-antagonists phenoxybenzamine and phentolamine and by chlorpromazine, but is not affected by the β-antagonist propranolol, further supporting an α-adrenergic basis for this phenomenon. Arginine vasopressin, at concentrations of 1 x 10-9 M and greater, also induces bile salt release. Classical α- and β-antagonists have minimal effects on vasopressin induced bile salt release. While the peptide hormones angiotensin and oxytocin are, alone, relatively ineffective inducers of bile salt release, oxytocin potentiates the induction of bile salt release by vasopressin, suggesting complex interactions with membrane receptor function. Further studies assessing the interaction of sympathetic neurotransmitters and peptide hormones with bile salt transport and release in the hepatocyte may provide insight into the regulation of hepatic secretory function in the intact animal.

Original languageEnglish (US)
Pages (from-to)205-212
Number of pages8
JournalHepatology
Volume4
Issue number2
StatePublished - 1984
Externally publishedYes

Fingerprint

Taurocholic Acid
Bile Acids and Salts
Vasopressins
Adrenergic Agents
Hepatocytes
Suspensions
Norepinephrine
Peptide Hormones
Oxytocin
Epinephrine
Catecholamines
Phenoxybenzamine
Arginine Vasopressin
Phentolamine
Chlorpromazine
Angiotensins
Phenylephrine
Isoproterenol
Propranolol
Neurotransmitter Agents

ASJC Scopus subject areas

  • Hepatology

Cite this

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title = "Induction of taurocholate release from isolated rat hepatocytes in suspension by α-adrenergic agents and vasopressin: Implications for control of bile salt secretion",
abstract = "Hepatocytes incubated with 25 μM [3H]taurocholate rapidly deplete the extracellular medium of [3H]taurocholate and achieve a steady-state level of intracellular bile salt within 15 min. Exposure of cells at steady state with extracellular taurocholate to the catecholamines norepinephrine or epinephrine results in release of 3H from the cells into the incubation medium; the 3H released represents almost exclusively unmetabolized [3H]taurocholate. The hierarchy of effectiveness of the catecholamines, norepinephrine ≃ epinephrine > phenylephrine >> isoproterenol, is indicative of an α-adrenergic mechanism. Induction of [3H]taurocholate release by norepinephrine is inhibited by the α-antagonists phenoxybenzamine and phentolamine and by chlorpromazine, but is not affected by the β-antagonist propranolol, further supporting an α-adrenergic basis for this phenomenon. Arginine vasopressin, at concentrations of 1 x 10-9 M and greater, also induces bile salt release. Classical α- and β-antagonists have minimal effects on vasopressin induced bile salt release. While the peptide hormones angiotensin and oxytocin are, alone, relatively ineffective inducers of bile salt release, oxytocin potentiates the induction of bile salt release by vasopressin, suggesting complex interactions with membrane receptor function. Further studies assessing the interaction of sympathetic neurotransmitters and peptide hormones with bile salt transport and release in the hepatocyte may provide insight into the regulation of hepatic secretory function in the intact animal.",
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T1 - Induction of taurocholate release from isolated rat hepatocytes in suspension by α-adrenergic agents and vasopressin

T2 - Implications for control of bile salt secretion

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AU - Randolph, J. K.

AU - Goldman, I. David

PY - 1984

Y1 - 1984

N2 - Hepatocytes incubated with 25 μM [3H]taurocholate rapidly deplete the extracellular medium of [3H]taurocholate and achieve a steady-state level of intracellular bile salt within 15 min. Exposure of cells at steady state with extracellular taurocholate to the catecholamines norepinephrine or epinephrine results in release of 3H from the cells into the incubation medium; the 3H released represents almost exclusively unmetabolized [3H]taurocholate. The hierarchy of effectiveness of the catecholamines, norepinephrine ≃ epinephrine > phenylephrine >> isoproterenol, is indicative of an α-adrenergic mechanism. Induction of [3H]taurocholate release by norepinephrine is inhibited by the α-antagonists phenoxybenzamine and phentolamine and by chlorpromazine, but is not affected by the β-antagonist propranolol, further supporting an α-adrenergic basis for this phenomenon. Arginine vasopressin, at concentrations of 1 x 10-9 M and greater, also induces bile salt release. Classical α- and β-antagonists have minimal effects on vasopressin induced bile salt release. While the peptide hormones angiotensin and oxytocin are, alone, relatively ineffective inducers of bile salt release, oxytocin potentiates the induction of bile salt release by vasopressin, suggesting complex interactions with membrane receptor function. Further studies assessing the interaction of sympathetic neurotransmitters and peptide hormones with bile salt transport and release in the hepatocyte may provide insight into the regulation of hepatic secretory function in the intact animal.

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