Purpose of review: Intrarenal adenosine is present in the cytoplasm of renal epithelial cells and in the extracellular space. Adenosine is generated at high levels in response to imbalance between energy demand and supply (e.g. increased tubular sodium chloride transport or hypoxia) and activates cell membrane adenosine receptors to affect renal vascular and tubular functions. Adenosine regulates renal sodium and water excretion via a myriad of effects on renal hemodynamic, glomerular filtration rate, renin secretion and direct effects on the renal tubule epithelium. This review examines the direct effects of adenosine on renal tubular epithelial transport in light of the most recent evidence and discusses some physiologic and pathophysiologic implications.
Recent findings: Intrarenal adenosine affects proximal fluid and solute transport in a biphasic fashion. Under physiological conditions adenosine stimulates proximal tubular re-absorption, thus reducing the load delivered to the distal nephron. A supra-physiologic increase in adenosine such as in ischemia reduces reabsorption in the proximal tubule, thus reducing renal oxygen consumption.
Summary: Intrarenal adenosine and its receptors have important regulatory functions in the renal epithelium. A complete understanding of this autocrine/paracrine system holds great potential for novel therapeutic strategies, such as the use of nucleoside analogues for reno-protection in renal ischemia.