Pressure natriuresis is a process whereby increases in renal perfusion pressure result in enhanced Na excretion.
A number of paracrine and/or autocrine factors have been suggested as mediators of pressure natriuresis, including Nitric oxide.
The site of action of NO in mediating pressure natriuresis is not clear. Originally, pressure natriuresis was thought to be due to inhibition of sodium transport in the distal nephron. This theory was supported by data showing that amiloride, an inhibitor of collecting duct sodium absorption, could prevent pressure natriuresis.
However, recent data indicate that pressure natriuresis may be due to inhibition of sodium absorption by the proximal tubule. Acute increases in renal perfusion pressure have been shown to inhibit Na/H exchange activity in this nephron segment.
BP is the product of cardiac output and total peripheral resistance, with cardiac output itself the product of heart rate and stroke volume. BP is influenced primarily by effective intravascular volume.
Effective intravascular volume is influenced by vascular tone and also by extracellular fluid volume (ECFV), the latter determined by sodium balance. If BP rises, so too does renal arterial pressure (RAP) and the kidney responds by increasing sodium excretion and reducing ECFV; the converse applies if blood pressure falls. This renal response to changes in RAP is called the acute pressure natriuresis response.

Reference:
Ivy JR, Bailey MA. Pressure natriuresis and the renal control of arterial blood pressure. J Physiol. 2014;592(18):3955-3967. doi:10.1113/jphysiol.2014.271676

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