Distal convoluted tubule and collecting duct
By the time distal convoluted tubule is reached, only about 10% of the originally filtered NaCl and 25% of the water remain in the tubule. Most reabsorption from this point on depends on the body’s needs at the time and is regulated by hormones (mainly aldosteron for Na+, ADH for water and PTH for Ca2+ . If necessary, nearly all of the water and Na+ reaching these region can be reclaimed.
In the absence of antidiuretic hormone (ADH), the collecting duct are relatively impermeable to water. Reabsorption of more water depends on the presence of ADH, which makes the collecting ducts more permeable to water by inserting aquaporins into the collecting duct luminal membranes.
Aldosteron “fine tunes” reabsorption of the remaining Na+. Decreased blood volume or blood pressure, low extracellular Na+ concentration (hyponatremia), or high extracellular K+ concentration (hyperkalemia) can cause the adrenal cortex to release aldosteron to the blood. Except for the hyperkalemia (which directly stimulate the adrenal cortex to secrete aldosteron), these condition promote the renin-angiotensin mechanism, which in turn prompts the release of aldosteron. Aldosteron targets the principal cells of the collecting ducts and cells of the distal portion of the distal convoluted tubule (prodding them to synthesize and retain more luminal Na+ and K+ channels and more basolateral Na+K+ ATPase). As a result, little or no Na+ leaves the body in urine. In the absence of aldosterone, much less Na+ is reabsorbed by these segments, resulting in Na+ losses of about 2% of Na+ filtered daily, an amount incompatible with life.
Physiology, aldosteron’s role is to increase blood volume, and therefore blood pressure, by enhancing Na+reabsorption. In general, water follows Na+ if it can. Aldosterone also reduces blood K+ concentrations because aldosterone induced reabsorption of Na+ is coupled to K+secretion in the principal cells. That is, as Na+ enters, K+ moves into the lumen.