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Effects of AT(1A) receptor deletion on blood pressure and sodium excretion during altered dietary salt intake.

The present study was performed to investigate the role of type 1A ANG II (AT(1A)) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT(1A) receptor-deficient (-/-) mice. Groups of AT(1A) (-/-) and wild-type mice were placed on a low (LS)-, normal (NS)-, or high-salt (HS) diet for 3 wk. AT(1A) (-/-) mice on an LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On an HS diet, (-/-) mice demonstrated significant diuresis, yet blood pressure increased to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure-natriuresis relationship in AT(1A) (-/-) mice demonstrated a shift to the left and a decreased slope compared with wild-type littermates. These studies demonstrate that mice lacking the AT(1A) receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.