This article shows that ATP can be released through the basolateral membrane of the macula densa (MD) cells.

There is a maxi anion channel which is activated by sodium chloride (volume). ATP uses this channel to leave the MD cells into the extracellular mesangium.

ATP then can act in the extracellular mesangium cells and the afferent arteriole (contracting) using the P2Y receptors

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

13. Macula Densa Cell Depolarization Mediates Release of ATP When There is Increase in Sodium Chloride

14. The Extraglomerular Mesangial Cells Participate in the Signaling of the TGF