Juxtaglomerular Apparatus or Complex is a specialized region of a nephron where the afferent arteriole and Distal Convoluted Tubule (DCT) come in direct contact with each other. Juxtaglomeruar Apparatus (JGA) consists of:
1) Juxtaglomerular cells (modified smooth muscle cells) of afferent arteriole including renin containing (synthesizes and stores renin) and sympathetically innervated granulated cells which function as mechanoreceptors to sense blood pressure.
2) Macula densa cells (Na+ sensors) of Distal Convoluted Tubule (DCT) which function as chemoreceptors to sense changes in the solute concentration and flow rate of filtrate.
3) Juxtaglomerular/Extraglomerular mesangial cells (Lacis cells) forming connections via actin and microtubules which allow for selective vasoconstriction/vasodilation of the renal afferent and efferent arterioles with mesangial cell contraction.
Functions of Juxtaglomerlar Apparatus (JGA):
- Local transmission of Tubuloglomerular Feedback (TGF) at its own nephron via angiotensin II (AT II)
- Systemic production of Angiotensin II (AT II) as part of Renin-Angiotensin-Aldosterone System (RAAS)
Tubuloglomerular Feedback (TGF) Mechanism
The tubuloglomerular feedback mechanism has 2 components that act together to control GFR:
- Afferent arteriolar feedback mechanism
- Efferent arteriolar feedback mechanism
Increased renal arterial pressure leads to an increased delivery of fluid (increased osmolality or increased flow rate) to the macula densa. The macula densa senses the load and causes constriction of nearby afferent arteriole, increasing the resistance. This will return osmolality and filtrate flow rate to normal.
Decreased renal arterial pressure leads to a decreased delivery of fluid (decreased osmolality or decreased flow rate) to the macula densa. The macula densa senses this and causes:
- Vasodilation of afferent arteriole
- Constriction of efferent arteriole as a result of renin release by stimulated JG cells
Renin Angiotensin Aldosterone System (RAAS)
When systemic blood pressure decreases, there is decreased stretch of JG cells, which leads to their release of renin. Renin release causes the activation of renin-angiotensin mechanism, which ultimately leads to an increased blood pressure.