Angiotensin II and vasopressin stimulate calcium-activated chloride conductance in rat mesangial cells

J Clin Invest. 1986 Dec;78(6):1443-8. doi: 10.1172/JCI112734.

Abstract

In an attempt to clarify the mechanisms by which angiotensin II (AII) and arginine vasopressin (AVP) regulate mesangial cell function, we examined the membrane potential change of mesangial cells and found that cells contracted and membrane potential depolarized in response to AII and AVP. The depolarization was associated with decreased input resistance. Ca ionophore A23187 caused similar mesangial cell contraction and depolarization. The reversal potential (Vr) of the depolarization response to AII and AVP was -29 +/- 3 and -25 +/- 7 mV (mean +/- SD), respectively. Not only the Vr of the AII-induced depolarization but also Vr of the Ca ionophore-induced response was dependent upon the extracellular Cl- concentration. Further, AII and AVP caused cell contraction and membrane depolarization in Ca++-free medium containing 0.5 mM EGTA. These data suggest the presence of Ca++ -activated Cl- channels in the mesangial cells and that AII and AVP increase Cl- permeability via an elevation of [Ca++]i released from the intracellular organellae.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Arginine Vasopressin / pharmacology*
  • Calcium / physiology*
  • Chlorides / metabolism*
  • Glomerular Mesangium / drug effects
  • Glomerular Mesangium / physiology*
  • Male
  • Membrane Potentials / drug effects
  • Potassium / metabolism
  • Rats
  • Rats, Inbred Strains
  • Tetraethylammonium Compounds / pharmacology

Substances

  • Chlorides
  • Tetraethylammonium Compounds
  • Angiotensin II
  • Arginine Vasopressin
  • Potassium
  • Calcium