Knorr A
Arch Int Pharmacodyn Ther. 1981 Sep;253(1):148-53.
Na(+) and K(+) net fluxes were determined from Na(+)-loaded and K(+)-depleted erythrocytes of 10 weeks old female spontaneously hypertensive rats of the Okamoto/Oaki strain (SHR) and female one-kidney Goldblatt hypertensive Wistar rats. Net Na(+) extrusion was reduced to 5.60 + 0.40 mmol/l cells x hr (n=7) in SHR as compared with normotensive Wistar/Kyoto (WKY) controls (7.13+ 0.25 mmol/l cells x hr, n=6; P less than 0.05). The na(+)/K(+) net flux ratio was also lower in SHR (2.39 +0.17) than in WKY (3.39 +0.45; P less than 0.05). On the other hand, no difference could be demonstrated between net Na(+) extrusion in sham-operated Wistar rats (7.43 +0.80 mmol/l cells x hr, n=7; P less than 0.05) and four weeks after operation (9.28 +0.77 mmol/l cells x hr, n=11; P greater than 0.05). In contrast ne Na(+) extrusion even showed a tendency to rise in renal hypertensive rats. Na(+)/K(+) net flux ratios were unchanged in the three groups (3.81 +0.42, 3.28 +0.29, 3.98 +0.45; P greater than 0.05), although blood pressure was markedly increased. It is concluded that decreased net Na(+) extrusion and reduced Na(+)/K(+) net flux ratio in female Okamoto SHR are not caused by increase in blood pressure, but may be a determinant of genetic hypertension in this strain.