This is a region where, in each nephron, the distal convoluted tubule touches the afferent arteriole. The juxtaglomerular cells are part of the afferent arteriole and the macula densa is part of the distal tubule. Renin is secreted from the JG cells and is important in regulating systemic blood pressure. This region also regulates local blood pressure to control the rate of filtrate formation in its glomerulus-- a mechanism called 'tubuloglomerular feedback'.
Renin (R) is secreted (solid-headed dashed arrow) into the blood by the juxtaglomerular cells (JGC). The end effect is to lower blood pressure. This enzyme catalyzes the first step in the formation of angiotensin II as described in the Angiotensin II section of the previous mini-tutorial. There are several mechanisms that control renin secretion.
There is an inverse relationship (dashed arrow) between sodium (Na+) concentration and the secretion (solid head on arrow) of renin. An increase in sodium causes a decrease in renin. One result of decreased renin is decreased sodium reabsorption due to decreased aldosterone levels.
For an excellent discussion of hyper- and hyponetremia click here.
The relationship with renal blood pressure (BP) is also inverse (dashed arrow). An increase in renal blood pressure caused a decrease in renin.
An increase in systemic blood pressure (BP) activates (solid arrow) pressure receptors (PR) in the large arteries near the heart. These send stimulatory signals (blunt-headed solid line) to the vasodilator center (VD) (VD circle). The VD center sends inhibitory signals (blunt-headed dashed line) to the vasoconstrictor center (VC) (VC circle).
Without input from the VD center the fibers from the VC center send a constant stream of stimulatory signals (solid arrow) to the juxtaglomerular cells (JGC) and the vascular smooth muscle (VCN) of the afferent arteriole. This causes a base line secretion (solid-headed dashed arrow) of renin (R) and a basal state of constriction in these these arterioles. With input from the VD center the activity of the VC center decreases (blunt-headed dashed line) to reduce renin secretion and vasoconstriction in the afferent arteriole.
High glomerular blood pressure cause a high rate of filtration (F). The greater the volume of filtrate formed the more rapidly it passes through the nephron. This rapid flow allows some solutes to pass through the proximal tubule and Henle's loop without being reabsorbed. The result is increased rate of flow and increased osmotic pressure (OP) in the distal convoluted tubule of this nephron.
The macula densa (MD) on the tubule side of the juxtaglomerular apparatus is sensitive to the osmotic pressure (OP) and/or the rate of flow of the filtrate. These cells seem to produce a yet unknown compound that inhibits dashed arrows the JGC from producing renin in this nephron.
It is also speculated that increased osmotic pressure (OP) stimulates the production of some compound that directly affects (solid arrow) the vascular smooth muscle (VCN) of the adjacent afferent arteriole. The result is decreased (dashed arrow) glomerular blood pressure leading to a decreased rate of filtrate (F) production in this nephron.
Last Updated: 7/19/2005