The majority of beta(2)-adrenoceptor (beta(2)-AR) agonists is eliminated via the kidneys as an unchanged substance. It is likely that such agents will exert pharmacological effects during their passage through the nephron. However, these pharmacological effects have, to our knowledge, not been taken into consideration when using these compounds in clinical practice because the role of beta(2)-AR in the regulation of renal function remains unclear. Renal beta(2)-ARs are predominantly localized to the proximal tubular epithelia and the membranes of smooth muscle cells from renal arteries. From this morphologic evidence, it is proposed that beta(2)-AR activation may regulate glomerular function and thereby sodium and water balance in the nephron segments. Actually, beta(2)-AR agonists given acutely cause a marked decrease in glomerular filtration rate. On the other hand, beta(2)-AR agonists inhibit the renal production of inflammatory cytokines such as TNF-alpha. Furthermore, the administration of beta(2)-AR agonists is found to attenuate apoptosis associated with shigatoxin in the hemolytic uremic syndrome (HUS). Increased understanding of the pharmacological basis of beta(2)-AR function in the kidney provides important new information relevant to the clinical use of beta(2)-AR agonists in airway diseases and potential applications of these drugs in renal inflammation and injury associated with sepsis or HUS.