A rise in arterial pressure increases sodium and water excretion
Expansion
A rise in renal perfusion pressure increases sodium and water excretion, even though autoregulation keeps GFR nearly constant. The mechanism is a fall in tubular reabsorption, mediated by increased medullary blood flow, reduced angiotensin II and locally released nitric oxide.
The relationship is very steep, so small pressure changes produce large changes in sodium output.
Its significance is that it gives the kidney infinite gain in the control of body fluid volume: as long as intake exceeds output, volume and pressure rise until excretion matches intake. Blood pressure therefore settles at whatever value is required to excrete the daily sodium load.
The corollary is that sustained hypertension requires a shift of the pressure natriuresis curve to the right. Every cause of hypertension, from renal artery stenosis to primary hyperaldosteronism to essential hypertension, can be seen as resetting this relationship so that a higher pressure is needed to excrete the same sodium.
It also explains why almost all antihypertensive strategies either promote sodium excretion or reduce the drive to retain it.