Juxtaglomerular apparatus

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Juxtaglomerular apparatus
Renal corpuscle.svg
A renal corpuscle, the functional unit of the kidney, shown in blue and pink. The juxtaglomerular apparatus is shown to the left and labelled D.
Anatomical terminology

The juxtaglomerular apparatus is a microscopic structure in the kidney that regulates the function of each nephron, the functional units of the kidney. The juxtaglomerular apparatus is named because it is next to (juxta-[1]) the glomerulus.

The juxtaglomerular apparatus consists of three cells:

  1. the macula densa, a part of the distal convoluted tubule of the same nephron
  2. juxtaglomerular cells, which secrete renin
  3. extraglomerular mesangial cells


The juxtaglomerular apparatus is part of the kidney nephron, next to the glomerulus. It is found between where blood enters a renal corpuscle and the distal convoluted tubule of the same nephron. This location is critical to its function in regulating renal blood flow and glomerular filtration rate.

The juxtaglomerular apparatus consists of three cell types.[2] These are:

  1. the macula densa, a part of the distal convoluted tubule of the same nephron
  2. juxtaglomerular cells, which secrete renin, specialized smooth muscle cells of the afferent arteriole, which supplies blood to the glomerulus
  3. extraglomerular mesangial cells


Juxtaglomerular cells[edit]

The renin-angiotensin system. It is activated when juxtaglomerular cells are poorly perfused.

Renin is produced by Juxtaglomerular cells. These cells are similar to epithelium and are located in the media of the afferent arterioles as they enter the glomeruli.[3] The juxtaglomerular cells secrete renin in response to:

Extraglomerular mesangial cells[edit]

Extraglomerular mesangial cells are located in the junction between the afferent and efferent arterioles, but their significance in this location is unknown. Renin is also found in these cells.[4]

Macula densa[edit]

At the point where the afferent arterioles enter the glomerulus and the efferent arteriole leaves it, the tubule of nephron touches the arterioles of the glomerulus from which it rose. At this location, which marks the start of distal convolution, there is a modified region of tubular epithelium called the Macula densa.[5] Cells in the macular densa respond to changes in the sodium chloride levels in the distal tubule of the kidney.

When there is an increase in the salt concentration, the cells secretes a locally-active vasopressor, which acts on the adjacent afferent arteriole to cause constriction. This decreases the amount of blood filtered by the kidney (the glomerular filtration rate), by decreasing the amount of fluid that enters the renal corpuscule.

This process is called the tubuloglomerular feedback loop. Specifically,

  1. if there is excessive filtration at the glomerulus, or inadequate sodium uptake in the proximal tubule/thick ascending loop of Henle, fluid in the distal convoluted tubule has an abnormally high concentration of sodium.
  2. Apical Na-K-2Cl cotransporters, which are found on the surface of the macular densa cells exposed to the fluid, transport sodium into the cells. The macula densa cells do not have enough Na/K ATPases on their basolateral surface to excrete this added sodium, which results in the cell's osmolarity increases.
  3. Water flows into the cell along the osmotic gradient, causing the cell to swell.
  4. When the cell swells, a stretch-activated non-selective anion channel is opened on the basolateral surface. ATP escapes through this channel and is subsequently converted to adenosine.
  5. Adenosine constricts the afferent arteriole via A1 receptors and dilates (to a lesser degree) efferent arterioles via A2 receptors. This acts to decrease the glomerular filtrate rate. Adenosine also inhibits renin release in juxtaglomerular cells via A1 receptors on JG cells using a Gi pathway. In addition, when macula densa cells detect higher concentrations of Na and Cl, they inhibit nitric oxide synthetase (decreasing renin release) by an unknown pathway.

When there is a decrease in the sodium concentration, less sodium is reabsorbed in the macular densa cells. The cells increase the production of nitric oxide synthetase, which creates nitric oxide and catalyses the formation of prostaglandins. These prostaglandins diffuse to the granular cells and activate a prostaglandin-specific Gs receptor. This receptor activates adenylate cyclase, which increases levels of cAMP. cAMP augments renin release. Prostaglandins and NO also vasodilate the afferent arterioles. Efferent arterioles are spared from this effect by renin release.

Clinical significance[edit]

Excess secretion of renin by the juxtaglomerular cells can lead to excess activity of the renin-angiotensin system, hypertension and an increase in blood volume. This is not responsive to the usual treatment for essential hypertension, namely medications and lifestyle modification.

One cause of this can be increased renin production due to narrowing of the renal artery, or a tumour of juxtaglomerula cells that produces renin. These will lead to secondary hyperaldosteronism, which will cause hypertension, high blood sodium, low blood potassium, and metabolic alkalosis.[citation needed]

See also[edit]


  1. ^ Dictionary.com http://dictionary.reference.com/browse/juxtaposition. Retrieved 11 June 2015.  Missing or empty |title= (help)
  2. ^ Robbins and Cotran Pathologic Basis of Disease 7E
  3. ^ Ganong. Ganong's Review of Medical Physiology. TATA McGRAW HILL. p. 705. ISBN 978-1-25-902753-6. 
  4. ^ Ganong. Ganong's Review of Medical Physiology. TATA McGRAW HILL. p. 705. ISBN 978-1-25-902753-6. 
  5. ^ Ganong. Ganong's Review of Medical Physiology. TATA McGRAW HILL. p. 705. ISBN 978-1-25-902753-6. 

External links[edit]