Protection of extracellular fluid volume is a fundamental characteristic of fluid and electrolyte homeostasis. The homeostatic mechanisms sense changes in the effective circulating volume(ECV).

ECV is difficult to define because it is not a measurable and distinct body fluid compartment. ECV relates to the”fullness” and pressure within the arterial tree.

Because only 15% of total blood volume is in the arterial compartment, arterial volume can be decreased in relation to the holding capacity of the arterial tree. In most circumstances, with the total extracellular fluid volume, except in certain disorders in which ECV is decreased in the presence of an increased total extracellular fluid volume. In these disorders, the ECV is decreased as a result of either decreased cardiac output vasodilatation, which decreases fullness and pressure in the arterial circulation. The afferent mechanisms sense alterations in the ECV and activate a series of effectors that create an integrated volume response. Two cardinal mechanisms protect the extracellular fluid volume: alterations in systemic hemodynamics and alterations in the external and water balance. Hemodynamic alterations occur within minutes of a perceived volume re duction and are characterized by tachycardia, increased peripheral resistance from arterial vasoconstriction, and decreased venous capacitance from venoconstriction. conservation of salt and water lags behind by 12 to 24 hours and involves release of various hormones.

Stimulation of the extrarenal baroreceptors also results in the release of antidiuretic hormone(ADH), which promotes water retention in the kidney. Vasoconstrictive factors, such as endothelins produced and released by vascular endothelial cells, also play a role in modulating systemic hemodynamics. Alterations in the glomerular hemodynamics, through changes in the peritubular Starling forces, directly modulate sodium and water reabsorption in the proximal tubules.

Furthermore, vasodilator prostaglandins, such as prostaglandin E2, maintain the glomerular filtration rate GFR) by enhancing the renal blood flow in states associated with ECW depletion.