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Related Experiment Videos

Potentiation of regulatory volume decrease by P2U purinoceptors in HSG-PA cells

H D Kim1, J W Bowen, M R James-Kracke

  • 1Department of Pharmacology, School of Medicine, University of Missouri, Columbia 65212, USA.

The American Journal of Physiology
|January 1, 1996
PubMed
Summary

Human salivary gland cells show altered regulatory volume decrease (RVD) with changing osmolarity. UTP enhances RVD, indicating receptor-mediated control over this cellular process.

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Area of Science:

  • Cell biology
  • Physiology
  • Molecular mechanisms

Background:

  • Human salivary gland (HSG-PA) cells display regulatory volume decrease (RVD) when exposed to hypotonic stress.
  • The P2U purinoceptor agonist UTP modulates RVD, with varying effects depending on medium osmolarity.

Purpose of the Study:

  • To investigate the mechanisms underlying UTP-mediated potentiation of RVD in HSG-PA cells.
  • To elucidate the roles of ion fluxes, membrane potential, and anion conductance in RVD.

Main Methods:

  • Measurement of cell volume changes in response to osmotic stress.
  • Assessment of ion fluxes (K+ and Cl-) and membrane potential.
  • Use of gramicidin to abolish membrane potential and study anion transport.
  • Tracer flux studies to confirm chloride efflux.

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Main Results:

  • UTP exposure induced Ca2+ mobilization, hyperpolarization, and K+ efflux, suggesting involvement of Ca(2+)-activated K+ channels.
  • Gramicidin-treated cells showed secondary swelling in 180 mosM but not 220 mosM medium, indicating spontaneous RVD via anion conductance.
  • In 180 mosM, increased anion conductance facilitated RVD, while in 220 mosM, it was marginal.
  • UTP-activated RVD involved hyperpolarization driving net Cl- efflux.

Conclusions:

  • HSG-PA cells exhibit spontaneous RVD mediated by anion conductance, particularly in lower osmolarity.
  • UTP potentiates RVD through mechanisms involving ion channel activity and membrane potential changes.
  • Cellular RVD is not an autonomous process but is subject to extracellular, receptor-mediated regulation.