The distal tubule courses back to the renal corpuscle from which it originated, and in doing so, it runs adjacent to the vascular pole of the corpuscle, near the extraglomerular mesangium, the afferent arteriole, and the efferent arteriole. The cells of the distal tubule wall at this point become very narrow, and their nuclei appear to be clumped closely together.
This micrograph shows a section of distal tubule as it undergoes this transition to clumped nuclei.
The closely-packed nuclei cause this region to stain densely, which gives it the name macula densa.
This micrograph shows an excellent macula densa.
This structure functions to alert the afferent arteriole of changes in urine osmolality.
The receptors in the arteriole, called the juxtaglomerular cells, the macula densa, the extraglomerular mesangium and perhaps the efferent arteriole comprise the juxtaglomerular apparatus.
The juxtaglomerular cells in the afferent arteriole consist of specialized renin-secreting smooth muscle cells that sit within the adventitia. These cells are in very close physical approximation with the macula densa.
The macula densa becomes stimulated under five circumstances:
- Low blood sodium
- Low blood volume or pressure
- Sympathetic stimulation of beta adrenergic receptor
- Increases in angiotensin levels
- Increased prostaglandin levels
When stimulated, the macula densa signals the juxtaglomerular cells to release renin into the circulation.
This micrograph shows renin, stained brown, localized to the modified smooth muscle cells around the afferent arteriole.
Renin converts angiotensin into angiotensin I which is further converted into angiotensin II. Angiotensin II increases blood pressure by constricting arerioles and by stimulating aldosterone secretion.
Aldosterone acts on distal tubule cells to increase sodium and chloride absorbtion.
Water follows those ions out of the distal tubule and blood volume increases, thereby maintaining the blood pressure.
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