The kidneys play a pivotal role in human physiology as they regulate heart and fluid homeostasis. They do so by regulating blood salt and mineral concentrations. This instrumental property of the kidneys is mediated by a small, yet very sophisticated functional unit, namely the nephron that filters unnecessary blood solutes into the urine while all necessary ions are carefully retained in the blood circulation. This "in and out" transition of ions across the vasculature is mediated by a battery of transmembrane protein-channels that facilitates the passage of solutes into and out of the blood circulation.

Purines are heterocyclic compounds with a broad range of physiologic effects. In the context of renal function, purines can trigger a variety of signaling pathways that control renal filtration rate. The vast majority of these signals are transmitted via distinct classes of transmembrane receptors that are generally divided into P1 and P2 super families. These receptors are further sub-grouped into A1, A2A, and A2B and A3 for the P1 class and respond to adenosine¹, while P2 receptors are divided into ionotropic P2X receptors and metabotropic P2Y receptors that respond to ligands such as ATP or ADP¹.

It is generally perceived that P1 receptors reduce renal filtration rate in response to adenosine by inducing vascular constriction², while members of the P2Y family counter this effect by releasing the vascular relaxation compound nitric oxide³.