It is the excretion of a considerable amount of sodium in the exceptionally salty urine.
Which is similar to diuresis (excretion of a considerable amount of urine). It occurs with some diuretics and in some diseases (such as the adrenal glands), leading the person to a loss of salt, a syndrome characterized by dehydration, vomiting, low blood pressure, and the risk of sudden death.
The natriuresis pressure appears to be the dominant physiological mechanism that connects the changes in systemic blood pressure to the total amount of sodium in the body.
It also acts by increasing the renal excretion of sodium when entering the blood pressure in the kidneys. The mechanism works completely autonomously within the kidneys and independently of the external hormonal regulation mechanisms.
Its importance in connecting renal transport of sodium to blood pressure makes pressure natriuresis the dominant mechanism.
The mechanism of pressure natriuresis is not yet apparent; however, changes in peritubular capillary transport probably underlie its functioning.
As the blood pressure entering the kidneys increases, the hydrostatic pressure within the peritubular capillaries also increases. This causes the Starling force to be reduced due to fluid resorption in the veins from the renal interstitial fluid.
With the diminution of the peritubular capillary resorption of water and salt, a leak appears in the tubule, producing improved urinary sodium excretion.
The relationship between incoming blood pressure and urinary and renal sodium excretion in a solitary kidney is gradual. Therefore pressure natriuresis alone can not explain the accuracy in volume regulation customarily observed.
The renin, angiotensin, and aldosterone (RAAS) system are responsible for providing pressure natriuresis much more sensitive to blood pressure responses.