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nephron.  Cortical nephrons have short loops, those near the corticomedullary junction have longer loops.  All nephrons filter, absorb and secrete, but corticomedullary ones (less numerous) also establish and maintain the medulla’s gradient.  

Very important for maintaining the salt gradient is the thick ascending limb that actively pumps out NaCl.  Cells have lots of mito along the long axis for this, like PCT, except here there is no brush border (rather small stubby microvilli).  As the thick ascending limb returns to the cortex, it contacts the vascular pole of the renal corpuscle, forming the macula densa.  

The macula densa:  Where thee DCT contacts the glomerulus.  The cells in the DCT wall are narrow and columnar with nuclei close together.  Macula densa cells sense the ionic content and water volume of the tubular fluid.  Then, they influence the GFR, blood pressure (via stimulating renin secretion) and can cause vasodilation by NO synthesis.  Macula desna cells are near the afferent arteriole.

DCT:  continuation of the thick ascending limb in the cortex.  Lined by cuboidal epithelium.  Cells here are responsive to aldosterone, resulting in ion exchance.  Na is absorbed and K excreted.   Helps maintain acid and base balance by secreting hydrogen and ammonium ions.  DCT cells have lots of mito parallel to the long axis of the cell (typical of a salt pumping cell), and lack a brush border.  

Collecting ducts:  Collecting tubules continuous with the DCT, and empty into cortical collecting ducts.  Cells here are columnar with distinct lateral cell boundaries.  They have no brush borders and sparse mitochondria.  When several of these ducts run together and drain toward the medulla, they form medullary rays.  Larger ducts in the medulla are called ducts of Bellini.  Epithelium in collecting ducts includes principal cells (have ADH receptors, which respond by bringing aquaporin to the cell surface) and intercalated cells (secrete or resorb protons as needed).  

Diseases of kidney tubules and interstitium:


2 major causes of damage are bacterial infection (pyelonephritis) or injury due to toxic drugs or metabolic disorders (intersitital nephritis).  Ibuprofen and NSAIDS can cause kidney damage.

JGA contains a group of structures at the vascular pole of the glomerulus.  It’s important for BP control.  It includes juxtaglomerular cells, macula densa, and extragolmerular mesengial cells (Lacis cells).  JG cells are in the wall of the afferent arteriole.  They are modified smooth muscle, and store renin in cytoplasmic granules.  With decreased BP, they release renin.  JG cells are adjacent to macula densa cells, and communicate with them by gap junctions.  Macula densa cells are in the DCT wall (more numerous and columnar), where it contacts its mother glomerulus.  Macula densa cells are in close proximity to afferent arteriole, and communicate with its JG cells.  Macula densa cells sense osmolarity and volume changes of tubular fluid, and can influence GFR and renin secretion.  Macula densa cells themselves make NO, and can cause vasodilation.  Lacis cells (aka extraglomerular mesengial cells) are outside the glomerulus, near the macula densa.  They play a role in BP control, though it’s not well understood.

BP control by the JGA:  Response to a drop in blood pressure -  Decreased BP in the afferent arteriole stimulates JG cells there to secrete renin.  Renin converts angiotensinogen in the blood to angiotensin I (inactive).  This goes to the lungs’ endothelium, where ACE converts it to angiotensin II (very active octapeptide).  Angiotensin II raises BP by stimulating pituitary to release ADH (increasing water reabsorption from collecting ducts and blood volume and BP).  Angiotensin II also constricts arteriole walls to increase BP.  Angiotensin

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