4.6 Tubular reabsorption  (Page 8/18)

Regulation of urine volume and osmolarity are major functions of the collecting ducts. By varying the amount of water that is recovered, the collecting ducts play a major role in maintaining the body’s normal osmolarity. If the blood becomes hyperosmotic, the collecting ducts recover more water to dilute the blood; if the blood becomes hyposmotic, the collecting ducts recover less of the water, leading to concentration of the blood. Another way of saying this is: If plasma osmolarity rises, more water is recovered and urine volume decreases; if plasma osmolarity decreases, less water is recovered and urine volume increases. This function is regulated by the posterior pituitary hormone ADH (vasopressin). With mild dehydration, plasma osmolarity rises slightly. This increase is detected by osmoreceptors in the hypothalamus, which stimulates the release of ADH from the posterior pituitary. If plasma osmolarity decreases slightly, the opposite occurs.

When stimulated by ADH, aquaporin channels are inserted into the apical membrane of principal cells, which line the collecting ducts. As the ducts descend through the medulla, the osmolarity surrounding them increases (due to the countercurrent mechanisms described above). If aquaporin water channels are present, water will be osmotically pulled from the collecting duct into the surrounding interstitial space and into the peritubular capillaries. Therefore, the final urine will be more concentrated. If less ADH is secreted, fewer aquaporin channels are inserted and less water is recovered, resulting in dilute urine. By altering the number of aquaporin channels, the volume of water recovered or lost is altered. This, in turn, regulates the blood osmolarity, blood pressure, and osmolarity of the urine.

As Na ⁺ is pumped from the forming urine, water is passively recaptured for the circulation; this preservation of vascular volume is critically important for the maintenance of a normal blood pressure. Aldosterone is secreted by the adrenal cortex in response to angiotensin II stimulation. As an extremely potent vasoconstrictor, angiotensin II functions immediately to increase blood pressure. By also stimulating aldosterone production, it provides a longer-lasting mechanism to support blood pressure by maintaining vascular volume (water recovery).

In addition to receptors for ADH, principal cells have receptors for the steroid hormone aldosterone. While ADH is primarily involved in the regulation of water recovery, aldosterone regulates Na ⁺ recovery. Aldosterone stimulates principal cells to manufacture luminal Na ⁺ and K ⁺ channels as well as Na ⁺ /K ⁺ ATPase pumps on the basal membrane of the cells. When aldosterone output increases, more Na ⁺ is recovered from the forming urine and water follows the Na ⁺ passively. As the pump recovers Na ⁺ for the body, it is also pumping K ⁺ into the forming urine, since the pump moves K ⁺ in the opposite direction. When aldosterone decreases, more Na ⁺ remains in the forming urine and more K ⁺ is recovered in the circulation. Symport channels move Na ⁺ and Cl ^– together. Still other channels in the principal cells secrete K ⁺ into the collecting duct in direct proportion to the recovery of Na ⁺ .

Intercalated cells play significant roles in regulating blood pH. Intercalated cells reabsorb K ⁺ and HCO ₃ ^– while secreting H ⁺ . This function lowers the acidity of the plasma while increasing the acidity of the urine.

Chapter review

The kidney regulates water recovery and blood pressure by producing the enzyme renin. It is renin that starts a series of reactions, leading to the production of the vasoconstrictor angiotensin II and the salt-retaining steroid aldosterone. Water recovery is also powerfully and directly influenced by the hormone ADH. Even so, it only influences the last 10 percent of water available for recovery after filtration at the glomerulus, because 90 percent of water is recovered before reaching the collecting ducts. Depending on the body’s fluid status at any given time, the collecting ducts can recover none or almost all of the water reaching them.

Mechanisms of solute recovery include active transport, simple diffusion, and facilitated diffusion. Most filtered substances are reabsorbed. Urea, NH ₃ , creatinine, and some drugs are filtered or secreted as wastes. H ⁺ and HCO ₃ ^– are secreted or reabsorbed as needed to maintain acid–base balance. Movement of water from the glomerulus is primarily due to pressure, whereas that of peritubular capillaries and vasa recta is due to osmolarity and concentration gradients. The PCT is the most metabolically active part of the nephron and uses a wide array of protein micromachines to maintain homeostasis—symporters, antiporters, and ATPase active transporters—in conjunction with diffusion, both simple and facilitated. Almost 100 percent of glucose, amino acids, and vitamins are recovered in the PCT. Bicarbonate (HCO ₃ ^– ) is recovered using the same enzyme, carbonic anhydrase (CA), found in erythrocytes. The recovery of solutes creates an osmotic gradient to promote the recovery of water. The descending loop of the juxtaglomerular nephrons reaches an osmolarity of up to 1200 mOsmol/kg, promoting the recovery of water. The ascending loop is impervious to water but actively recovers Na ⁺ , reducing filtrate osmolarity to 50–100 mOsmol/kg. The descending and ascending loop and vasa recta form a countercurrent multiplier system to increase Na ⁺ concentration in the kidney medulla. The collecting ducts actively pump urea into the medulla, further contributing to the high osmotic environment. The vasa recta recover the solute and water in the medulla, returning them to the circulation. Nearly 90 percent of water is recovered before the forming urine reaches the DCT, which will recover another 10 percent. Calcium recovery in the DCT is influenced by PTH and active vitamin D. In the collecting ducts, ADH stimulates aquaporin channel insertion to increase water recovery and thereby regulate osmolarity of the blood. Aldosterone stimulates Na ⁺ recovery by the collecting duct.