This article shows that the sequence for the release of ATP from the macula densa (MD) cells is probably as follow:

• Increased GFR causes an increase in the sodium chloride concentration reaching the macula densa.
• Sodium chloride is transported to the intracellular space of the MD cell.
• Chloride leaves the MD cell by a chloride channel, causing membrane depolarization of the MD cell.
• Calcium enters the MD cell via a calcium channel across the basolateral membrane of the MD cell.
• The calcium entry leads to ATP release into the extraglomerular mesangium

Credits

Renal Corpuscle Image. 2019. Downloaded under a Creative Commons Attribution-Share Alike 4.0 International License from Wikimedia Commons. Author: Shypoetess. No changes were made.

Posts in this series

1. Overview

2. Overview (cont)

3. The Macula Densa Cells May Sense Tubular Salt Content Using a NHE2 Exchanger

4. The Macula Densa Cells Also Can Sense Sodium and Chloride Concentrations Using the NKCC2 Transporter

5. PGE2 Inhibits nNOS in the Macula Densa Cells

6. MAP Kinases are Activated by Low Tubular NaCl and Stimulate COX-2 Expression

7. Inhibition of nNOS in the Macula Densa leads to an Exaggerated TGF Response

8. The EP4 Receptor in the Juxtaglomerular Granular Cells Seems to be the Most Important for the Action of PGE2

9. The Juxtaglomerular Granular Cells are More Numerous in the Afferent Arteriole

10. Angiotensin II Acts on the Afferent and Efferent Arterioles, But Increases More Resistance in the Efferent Arteriole

11. Angiotensin II, Mediated by AT1 Receptors, Stimulates Nitric Oxide Release in Afferent Arterioles

12. Angiotensin II Effects are Different in the Afferent and Efferent Arterioles