Adrenergic modulation of intracellular pH in isolated brown fat cells from hamster and rat

S. C. Lee, J. S. Hamilton, T. Trammell, Barbara A Horwitz, P. A. Pappone

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16 Scopus citations


The activity of the uncoupling protein in brown fat mitochondria is enhanced at alkaline pH, leading to the hypothesis that changes in intracellular pH (pH(i)) may modulate the thermogenic response to sympathetic stimulation. We employed ratio imaging of the fluorescent dye 2',7'- bis(carboxyethyl)-5(6)-carboxyfluorescein to measure pH(i) in acutely isolated single brown fat cells from hamster and neonatal rat and in cultured rat cells. Basal pH(i) averaged ~7.2 in HCO3/- media and 0.1-0.15 pH units lower in nominally HCO3/--free media in all cell types. In both HCO3/- and HCO3/--free media, stimulation with norepinephrine (NE) typically caused an alkalinization of ~0.05-0.1 pH units, which was followed by a smaller net acidification occurring primarily after NE was removed. Alkalinization seemed to be mediated predominantly by α-adrenergic stimulation, while acidification most often followed β-adrenergic activation. Similar pH(i) changes were elicited by NE in rat and hamster cells, but responses were more frequent in hamster cells. Assays of recovery from ammonium prepulse-induced acid loads indicated that rat and hamster cells have both Na+-H+ and Na+- and HCO3/--dependent regulatory systems, while hamster cells have, in addition, a Na+-independent recovery mechanism activated at acid pH(i). We conclude that α-adrenergic alkalinization of brown fat may contribute to the control of thermogenesis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Issue number2 36-2
StatePublished - 1994


  • adrenergic receptors
  • amiloride
  • isoproterenol
  • norepinephrine
  • phenylephrine
  • sodium- hydrogen exchange
  • thermogenesis
  • uncoupling protein

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology


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