TOTAL NA+-FLUXES AND K+-FLUXES IN ERYTHROCYTES OF SPONTANEOUSLY AND ONE-KIDNEY GOLDBLATT HYPERTENSIVE RATS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 253  (1) , 148-153
Abstract
Na+ and K+ net fluxes were determined from Na+-loaded and K+-depleted erythrocytes of 10-wk-old female spontaneously hypertensive rats of the Okamoto/Oaki strain (SHR) and female 1-kidney Goldblatt hypertensive Wistar rats. Net Na+ extrusion was reduced to 5.60 .+-. 0.40 mmol/l cells .times. h (n = 7) in SHR as compared with normotensive Wistar/Kyoto (WKY) controls (7.13 .+-. 0.25 mmol/l cells .times. h, n = 6; P < 0.05). The Na+/K+ net flux ratio was also lower in SHR (2.39 .+-. 0.17) than in WKY (3.93 .+-. 0.45; P < 0.05). No difference was demonstrated between net Na+ extrusion in sham-operated Wistar rats (7.43 .+-. 0.80 mmol/l cells .times. h, n = 7) and renal hypertensive Wistar rats at 2 (9.17 .+-. 1.33 mmol/l cells .times. h, n = 7; P > 0.05) and 4 wk after operation (9.28 .+-. 0.77 mmol/l cells .times. h, n = 11; P > 0.05). In contrast, net Na+ extrusion even showed a tendency to rise in renal hypertensive rats. Na+/K+ net flux ratios were unchanged in the 3 groups (3.81 .+-. 0.42, 3.28 .+-. 0.29, 3.98 .+-. 0.45; P > 0.05), although blood pressure was markedly increased. Decreased net Na+ extrusion and reduced Na+/K+ net flux ratio in female Okamoto SHR are not caused by an increase in blood pressure but may be a determinant of genetic hypertension in this strain.