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.
Structure The juxtaglomerular apparatus consists of:
the juxtaglomerular cells, the macula densa, the Lacis cells or agranular cells.
Juxtaglomerular Cells Juxtaglomerular cells are specialized smooth
muscle cells of glomerular arterioles.
They produce and secrete renin.
Macula Densa Cells Macula densa cells are columnar epithelium
thickening of the distal tubule.
The macula densa senses any increase in the sodium chloride concentration in the distal
tubule of the kidney and secretes a locally active vasopressor, which acts on the adjacent
afferent arteriole to decrease glomerular filtration rate, 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 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 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 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.
Function
The juxtaglomerular cells secrete renin in response to:
Beta-1 adrenergic stimulation Decrease in renal perfusion pressure
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 Elevated renin due to renal artery stenosis
or a very rare renin-producing juxtaglomerular cell tumor of the kidney can produce secondary
hyperaldosteronism.
Hyperactivity of the renin-angiotensin-aldosterone system is manifested by hypertension with
hypervolemia, which is severe and not 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 Kidney
Renal corpuscle Juxtaglomerular cell tumor
Hyperaldosteronism References
External links Electron micrograph
Diagram