title: Erythrocyte sodium ion transport system in DOC-salt, Goldblatt, and spontaneously hypertensive rats.
abstract: Altered erythrocyte Na+ transport has been observed in relation to the pathogenesis of essential hypertension. In the present study, intracellular Na+ and K+ levels, Na(+)-K+ pump activity, Na(+)-K+ cotransport, and Na+ passive permeability were measured in erythrocytes of DOC-salt hypertensive (DSH) rats, two-kidney, one clip Goldblatt hypertensive (2KH) rats, and spontaneously hypertensive rats (SHR). The results were as follows: 1. In comparison with the control groups, no change in the erythrocyte Na+ level was noted in the DSH and 2KH groups, whereas a significant increase was seen in the SHR group. 2. Although no change was noted in the erythrocyte K+ level in the 2KH and SHR groups when compared with the control groups, a significant decrease was seen in the DSH group. 3. Na(+)-K+ pump activity of erythrocytes was not changed in the DSH and 2KH groups when compared with the control group, but a significant increase was noted in the SHR group. 4. Na(+)-K+ cotransport of erythrocytes was not changed in any hypertensive rats when compared with the controls. 5. Na+ passive permeability in the erythrocyte membrane was not changed in the DSH and 2KH groups when compared with the control groups, but a significant increase was noted in the SHR group. These findings suggest that increased erythrocyte Na+ levels in SHR are due to increased Na+ passive permeability of the erythrocyte membrane, and increased Na(+)-K+ pump activity may be compensating for the increased intracellular Na+ concentration in erythrocytes. Furthermore, the increase in Na+ passive permeability observed in SHR might not result from hypertension itself but from abnormalities in the erythrocyte cell membrane, because no increase in Na+ passive permeability was noted in either DSH or 2KH rats.
authors.affiliation: Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yokomatsu
authors.forename: K
authors.initials: K
authors.lastname: Fujito
authors.forename: H
authors.initials: H
authors.lastname: Numahata
authors.forename: H
authors.initials: H
authors.lastname: Koide
mesh_terms: D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism*; D006973:Hypertension / Q000097:blood*; D006978:Hypertension, Renovascular / Q000097:blood*; D017136:Ion Transport; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017208:Rats, Wistar; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase
chemical_list: D002034:Bumetanide; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium