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Activation of the renal D1 R (dopamine D1 -like receptor) or AT2 R (angiotensin II type-2 receptor), individually or both, simultaneously, is necessary in the normal regulation of renal sodium (Na+ ) transport and blood pressure. However, little is known regarding the precise mechanism of this interaction. Pharmacological stimulation, membrane biotinylation, and cell surface immunofluorescence were used to study the effect of the D1 R/AT2 R interaction in human renal proximal tubule cells. D1 R activation of GαS stimulates AC (adenylyl cyclase) and induces apical plasma membrane recruitment of AT2 Rs. We now show for the first time the reciprocal reaction, AT2 R stimulation with Ang III (angiotensin III) leads to the apical plasma membrane recruitment of the D1 R. The cell-permeable second messenger analogs of cAMP (8-Br-cAMP) or cGMP (8-Br-cGMP) induce translocation of both D1 R and AT2 R to the plasma membrane. Inhibition of PKA (protein kinase A) with Rp-cAMPS and PKG (protein kinase G) with Rp-8-CPT-cGMPS blocks D1 R and AT2 R recruitment, respectively, indicating that both PKA and PKG are necessary for D1 R and AT2 R trafficking. Both 8-Br-cAMP and 8-Br-cGMP activate PP2A (protein phosphatase 2A), which is necessary for both plasma membrane recruitment of D1 R and AT2 R and the inhibition of sodium hydrogen exchanger 3-dependent Na+ transport. These studies provide insights into the D1 R/AT2 R transregulation mechanisms that play a crucial role in maintaining Na+ and ultimately blood pressure homeostasis.

hypertension

The Dopamine D <sub>1</sub> Receptor and Angiotensin II Type-2 Receptor are Required for Inhibition of Sodium Transport Through a Protein Phosphatase 2A Pathway

The Dopamine D 1 Receptor and Angiotensin II Type-2 Receptor are Required for Inhibition of Sodium Transport Through a Protein Phosphatase 2A Pathway

The Dopamine D ₁ Receptor and Angiotensin II Type-2 Receptor are Required for Inhibition of Sodium Transport Through a Protein Phosphatase 2A Pathway