Juxtaglomerular apparatus

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Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus
Renal corpuscle:The structure on the left in blue and pink is the renal corpuscle. The structure on the right is the renal tubule. The blue structure (A) is the Bowman's capsule (2 and 3). The pink structure is the glomerulus with its capillaries. At the left, blood flows from the afferent areteriole (9), through the capillaries (10), and out the efferent arteriole (11). The mesangium is the pink structure inside the glomerulus between the capillaries (5a) and extending outside the glomerulus (5b). Juxtaglomerular apparatus is "D".

The juxtaglomerular apparatus is a microscopic structure in the kidney that regulates the function of each nephron. The juxtaglomerular apparatus is named for its proximity to the glomerulus: It is found between the vascular pole of the renal corpuscle and the returning distal convoluted tubule of the same nephron. This location is critical to its function in regulating renal blood flow and glomerular filtration rate. The three cellular components of the apparatus are the macula densa of the distal convoluted tubule, smooth muscle cells of the afferent arteriole known as juxtaglomerular cells, and extraglomerular mesangial cells(Lacis cells[1]).


The juxtaglomerular apparatus consists of: (1) the juxtaglomerular cells, (2) the macula densa, (3) the Lacis cells or agranular cells.[2]

Juxtaglomerular Cells (Granular Cells)[edit]

The renin in kidney extracts and the blood stream are produced by Juxtaglomerular cells(JG cells). These epitheliod cells are located in the media of the afferent arterioles as they enter the glomeruli. [3]

Lacis cells[edit]

Renin is also found in lacis cells that are located in the junction between the afferent and efferent arterioles, but their significance in this location is unknown


Macula Densa Cells[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] The macula densa senses any increase in the sodium chloride concentration in the distal tubule of the kidney and secretes a locally active (paracrine) vasopressor, which acts on the adjacent afferent arteriole to decrease glomerular filtration rate (GFR), as part of the tubuloglomerular feedback loop.

To be specific, excessive filtration at the glomerulus or inadequate sodium uptake in the proximal tubule/thick ascending loop of Henle brings to the distal convoluted tubule fluid that has an abnormally high concentration of sodium. Apical Na-K-2Cl cotransporters move sodium into the cells of the macula densa. The macula densa cells do not have enough basolateral Na/K ATPases to excrete this added sodium, so the cell's osmolarity increases. Water flows into the cell along the osmotic gradient, causing the cell to swell. 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. Adenosine vasoconstricts the afferent arteriole via A1 receptors and vasodilates (to a lesser degree) efferent arterioles via A2 receptors, which decreases GFR. Also, adenosine inhibits renin release in JG 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.

A decrease in GFR means less solute in the tubular lumen. As the filtrate reaches the macula densa, less NaCl is reabsorbed. The macula densa cells detect lower concentrations of Na and Cl and upregulate nitric oxide synthetase (NOS). NOS creates NO, which 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.


The juxtaglomerular cells secrete renin in response to:

  • Beta-1 adrenergic stimulation
  • Decrease in renal perfusion pressure (detected directly by the granular cells)
  • Decrease in NaCl concentration at the macula densa, often due to a decrease in glomerular filtration rate, resulting in slower filtrate movement through the proximal tubule and, thus, more time for reabsorption.

Clinical significance[edit]

Elevated renin due to renal artery stenosis or a very rare renin-producing juxtaglomerular cell tumor of the kidney can produce secondary hyperaldosteronism (as opposed to primary hyperaldosteronism aka Conn syndrome, usually due to a functional adrenal adenoma).

Hyperactivity of the renin-angiotensin-aldosterone system is manifested by hypertension with hypervolemia, which is severe and not responsive (or minimally responsive) to medications/lifestyle modifications that would usually control essential hypertension. In addition, patients with hyperaldosteronism will have hypernatremia, hypokalemia, and metabolic alkalosis.

See also[edit]


  1. ^ Ganong. Ganong's Review of Medical Physiology. TATA McGRAW HILL. pp. 705,674. ISBN 978-1-25-902753-6. 
  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. 

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