ABSTRACT
The concentration of these salts normally is regulated very tightly through the appropriate intake of water and renal regulation of water excretion, processes which demand an intact thirst mechanism and the modulation of vasopressin release and its hydro-osmotic effect, respectively. The increase in sodium excretion with decreases in hematocrit were also associated with a concomitant rise in solute-free water reabsorption and potassium excretion. Sodium is largely confined to the extracellular fluid (EFC) compartment, where its salts constitute virtually all of the extracellular fluid volume (ECFV). The process whereby the kidney is able to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) over a wide range of renal perfusion pressures is known as renal autoregulation. The mechanism underlying this tubuloglomerular feedback remains unclear. Though the entire tubular apparatus is involved in the regulation of sodium reabsorption, the term glomerulotubular balance (GTB) is popularly applied to the contribution of the proximal tubule to this regulatory process.
