Figure 11. Effect of varying time constant τ_SE of the sodium intake–natriuresis mechanism on the system's response to the elevated sodium intake and AngII input.

Neurally driven resistance responses are independent of renal control and thus TPR, R_as and R_ar remain same for any τ_SE and contribute equally to the rise in arterial pressure. Larger time constants lead to a delay in sodium excretion response and thus additional accumulation of blood volume. Volume expansion leads to an additional elevation in arterial pressure. The slope of the pressure–natriuresis relationship diminishes with increasing τ_SE which is consistent with experimental observations of volume-loading hypertension.