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Cyclic adenosine monophosphate acutely inhibits and chronically stimulates Na/H antiporter in OKP cells

A Cano1, P Preisig, R J Alpern

  • 1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8856.

The Journal of Clinical Investigation
|October 1, 1993
PubMed

Insights

Chronic increases in cyclic AMP (cAMP) paradoxically activate the renal Na/H antiporter, impacting sodium excretion. Acute inhibition by cAMP differs from its long-term stimulatory effects, requiring protein synthesis.

Area of Science:

  • Nephrology
  • Cellular Physiology
  • Molecular Biology

Background:

  • Parathyroid hormone, dopamine, and angiotensin II influence renal sodium (Na) excretion.
  • These hormones modulate proximal tubule Na/H antiporter activity via cyclic adenosine monophosphate (cAMP).
  • Acute cAMP signaling typically inhibits Na/H antiporter activity.

Purpose of the Study:

  • To investigate the impact of chronic cyclic adenosine monophosphate (cAMP) increases on proximal tubule Na/H antiporter activity.
  • To determine if prolonged cAMP exposure alters Na/H antiporter function in kidney cells.

Main Methods:

  • OKP cells were treated with 8-bromo cAMP, forskolin, or forskolin + 3-isobutyl-1-methylxanthine for 6 hours.
  • Na/H antiporter activity was measured 16-20 hours after cAMP removal.
  • Protein synthesis inhibition was assessed using cycloheximide.
  • Cellular pH changes were monitored.

Main Results:

  • Chronic 6-hour exposure to 8-bromo cAMP increased Na/H antiporter activity by 24%.
  • This persistent activation required over 2 hours of exposure and was mimicked by forskolin.
  • Protein synthesis inhibition prevented the cAMP-induced stimulation.
  • Antiporter stimulation was independent of cell acidification.

Conclusions:

  • While acute cAMP inhibits the Na/H antiporter, chronic exposure leads to persistent activation.
  • This chronic activation necessitates protein synthesis and is independent of acute cell pH changes.
  • Hormonal effects on renal Na excretion via cAMP may differ significantly between acute and chronic signaling pathways.

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