Circulation and hemodynamics: Edited by Roland C. Blantz and Matthew R. WeirInteraction of intrarenal adenosine and angiotensin II in kidney vascular resistanceFranco, Marthaa; Pérez-Mendéz, Oscara; Martínez, Flaviob Author Information aDepartment of Nephrology, Instituto Nacional de Cardiología ‘Ignacio Chávez’, México City, Distrito Fedral, Mexico bDepartment of Pharmacology, Facultad de Medicina UASLP, San Luis Potosí, Mexico Correspondence to Martha Franco, MD, PhD, Department of Nephrology, Instituto Nacional de Cardiología ‘Ignacio Chávez’, Juan Badiano No.1, Mexico City, 14080 D.F., Mexico Tel: +5255 573 6902; fax: +5255 573 7716; e-mail: [email protected] Current Opinion in Nephrology and Hypertension: January 2009 - Volume 18 - Issue 1 - p 63-67 doi: 10.1097/MNH.0b013e32831cf5d3 Buy Metrics Abstract Purpose of the review The adenosine–angiotensin II (ADO-AngII) interaction plays an important role in the regulation of glomerular filtration rate, vascular resistance and tubuloglomerular feedback. Although the interaction was described more than 30 years ago, the intrinsic mechanisms of the synergism between both autacoids remains incompletely understood. Recent findings Current evidence suggests that ADO-metabolizing enzymes such as ecto-5′-nucleotidase or ADO deaminase, as well as enzymes that degrade ATP to adenosine, play an important role in the vasoconstrictor signals sent from the macula densa to the afferent arterioles when tubuloglomerular feedback is activated; increased ADO concentration induced by temporal infusion of AngII results in downregulation of A2 ADO receptors, leading to a predominant effect of A1 receptors; the alteration in the ADO receptors balance further contributes to the synergic interaction between ADO and AngII. Summary The ADO-metabolizing enzymes have become important regulators of the effects of ADO on the tone of the afferent and efferent arterioles. As AngII is able to increase de-novo renal ADO content through decrease of ADO-metabolizing enzymes, accumulation of ADO induces downregulation of ADO A2 receptor population without modifying ADO A1 receptor, thereby enhancing the constrictive effects of AngII in the renal vasculature. © 2009 Lippincott Williams & Wilkins, Inc.