Muscarinic stimulation of gallbladder epithelium I. Electrophysiology and signaling mechanisms

G. A. Altenberg, M. Subramanyam, J. S. Bergmann, K. M. Johnson, L. Reuss

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


To understand the effects of acetylcholine (ACh) on fluid-absorbing epithelia, we carried out experiments on Necturus gallbladder epithelium. Binding studies with 1-quinuclidinyl[phenyl-4(N)-3H]benzilate (QNB) demonstrated that Necturus gallbladder epithelial cells express high-affinity muscarinic receptors. The effects of ACh and carbachol were exerted from the basolateral surface and consisted of a transient hyperpolarization of both cell membranes and a concomitant decrease in the apparent fractional resistance of the apical membrane. Atropine blocked both effects. ACh also elicited transient elevations of inositol 1,4,5-trisphosphate and intracellular free calcium ([Ca2+](i)) levels, the latter by both release from intracellular stores and basolateral influx. The phospholipase C antagonist U-73122 inhibited the effects of ACh, whereas inhibition of prostaglandin and guanosine 3',5'-cyclic monophosphate synthesis with indomethacin or methylene blue, respectively, had no effect. In conclusion, Necturus gallbladder epithelium expresses muscarinic receptors in the basolateral membrane. Receptor activation stimulates phospholipase C and elevates cellular levels of inositol 1,4,5-trisphosphate and [Ca2+](i). The elevation in [Ca2+](i) activates K+ channels but apparently not Cl- channels.

Original languageEnglish (US)
Pages (from-to)C1604-C1612
JournalAmerican Journal of Physiology - Cell Physiology
Issue number6 34-6
StatePublished - 1993


  • acetylcholine
  • inositol 1,4,5-trisphosphate
  • intracellular calcium
  • maxi potassium channel
  • phospholipase C
  • proximal tubule
  • small intestine

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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