Adenosine and Kidney Function

Abstract

In this review we outline the unique effects of the autacoid adenosine in the kidney. Adenosine is present in the cytosol of renal cells and in the extracellular space of normoxic kidneys. Extracellular adenosine can derive from cellular adenosine release or extracellular breakdown of ATP, AMP, or cAMP. It is generated at enhanced rates when tubular NaCl reabsorption and thus transport work increase or when hypoxia is induced. Extracellular adenosine acts on adenosine receptor subtypes in the cell membranes to affect vascular and tubular functions. Adenosine lowers glomerular filtration rate (GFR) by constricting afferent arterioles, especially in superficial nephrons, and acts as a mediator of the tubuloglomerular feedback, i.e., a mechanism that coordinates GFR and tubular transport. In contrast, it leads to vasodilation in deep cortex and medulla. Moreover, adenosine tonically inhibits the renal release of renin and stimulates NaCl transport in the cortical proximal tubule but inhibits it in medullary segments including the medullary thick ascending limb. These differential effects of adenosine are subsequently analyzed in a more integrative way in the context of intrarenal metabolic regulation of kidney function, and potential pathophysiological consequences are outlined.

Purinergic signalling in the kidney in health and disease

“…Factors such as nitric oxide, arachidonic acid breakdown products or angiotensin (ANG) II modulate the described cascade. NOS I neuronal nitric oxide synthase, COX-2 cyclooxygenase-2 (reproduced from [384], with permission of the American Physiological Society) ATP increased medullary blood flow in a NO-dependent manner [71]. In salt-loaded rats, ATP caused vasoconstriction in the outer medulla without affecting inner medullary flow.…”

Adenosine mediates transforming growth factor‐beta 1 release in kidney glomeruli of diabetic rats

“…The nucleoside adenosine regulates essential renal functions by means of local modification of its extracellular bioavailability to activate members of the P 1 purinoceptor family enclosing A 1 , A 2A , A 2B and A 3 adenosine receptor (AR) subtypes [7]. All subtypes have been detected in the glomerulus, but their physiological roles have been scarcely studied [8][9][10].…”

Therapeutic dose of Ginkgo biloba extract 761 may alter the urine excretion of Wistar rats

“…More insights into the regulation of the kidney function can provide not only a better understanding of pathophysiological processes, but also eventually, the development of new therapeutic approaches (Vallon et al, 2006). On a recent search of the specific literature there were less than ten references which appeared upon a cross-search using "nephrotoxicity" and Ginkgo biloba as keywords.…”