Cell membrane changes after in vivo acute Na+ load in normotensive and spontaneously hypertensive rats

Clin Exp Hypertens A. 1984;6(9):1559-74. doi: 10.3109/10641968409044069.

Abstract

Our previous observation of a greater increase in erythrocyte Na+ in SHR than in WKY after an acute Na+ load may result either from a genetic membrane property or from a specific plasma influence. In order to elucidate this question, membrane characteristics were compared with or without an acute Na+ load. Na+ transport was measured in Ringer and in plasma on Na+ enriched and K+ depleted red cells. Platelet microviscosity was measured as an index of membrane structural changes. After acute Na+ load a similar reduction of net Na+ extrusion and of K+ influx was observed in both strains. This indicates an inhibition of the Na+,K+-pump. Platelet microviscosity was similarly increased in SHR and WKY. Thus an acute Na+ load induced alterations of membrane properties in both SHR and WKY. The higher erythrocyte Na+ content in SHR stems rather from their intrinsic membrane properties than from a plasma factor.

MeSH terms

  • Animals
  • Blood Platelets / drug effects*
  • Blood Viscosity / drug effects
  • Cell Membrane / drug effects*
  • Cell Membrane Permeability / drug effects
  • Erythrocyte Membrane / drug effects*
  • Hemoglobinometry
  • Hypertension / blood*
  • Ion Channels / drug effects*
  • Male
  • Platelet Aggregation / drug effects
  • Potassium / blood
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred Strains
  • Rats, Inbred WKY
  • Sodium / blood
  • Sodium Chloride / pharmacology*

Substances

  • Ion Channels
  • Sodium Chloride
  • Sodium
  • Potassium