Cell membrane changes after in vivo acute Na+ load in normotensive and spontaneously hypertensive rats.
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.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects*; D001809:Blood Viscosity / Q000187:drug effects; D002462:Cell Membrane / Q000187:drug effects*; D002463:Cell Membrane Permeability / Q000187:drug effects; D004910:Erythrocyte Membrane / Q000187:drug effects*; D006452:Hemoglobinometry; D006973:Hypertension / Q000097:blood*; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D011188:Potassium / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D011921:Rats, Inbred WKY; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000494:pharmacology*
D007473:Ion Channels; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium