Erythrocyte Na(+)-K+ ATPase activity in the genesis of reducing renal mass in hypertensive rats.

Abstract

To study the relationship between natriuretic factor and experimental low renin hypertension, the erythrocyte Na+-K+ ATPase activities in the genesis of reducing renal mass in hypertensive rats were measured. The results were as follows : The fractional excretion of Na in hypertensive, reduced renal mass rats (saline-drinking) was higher than that of normotensive, reduced renal mass rats (water-drinking) (p<.001). The plasma renin activities in the hypertensive group were markedly lower than those of the normotensive group (p<.001).The total ATPase activities of rat erythrocyte membrane in the hypertensive group were lower than in those of the normal and the normotensive groups (p<.001, p<.02).The Mg++-ATPase activities of rat erythrocyte membrane in the normotensive group tended to decrease significantly (p<.001), but the differences between the normotensive and hypertensive group were not significant.The Na+-K+ ATPase activities of rat erythrocyte membrane in the hypertensive group were lower than those of the normal and the normotensive group (p<.001). However, the difference between the normal and the normotensive groups was not significant.When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from normotensive rats, the total ATPase activities of erythrocyte membrane were not different from those of hypertensive rats.When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from normotensive rats, the Mg++ ATPase activities of erythrocyte membrane were lower than those of hypertensive rats (p<.01).When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from hypertensive rats, the Na+-K+ ATPase activities of erythrocyte membrane were lower than those of normotensive rats (p<.01).Based on the above findings, it is suggested that the pathogenesis of low renin, reduced renal mass hypertension is primarily mediated by a natriuretic factor (or an ouabain-like factor, inhibitor of Na+-K+ ATPase) produced by extracellular fluid volume expansion.