The endothelin peptides comprise a family of potent and long-lasting vascoconstrictors, to which the renal microcirculation is particularly susceptible. Increased renal endothelin expression is observed after a variety of injurious stimuli, including ischemia, and persists for days after resolution of the initial injury. Autoinduction of its own production is likely to be a central mechanism underlying endothelin's prolonged effects. Furthermore, antagonizing endothelin reveals its role in maintaining the postischemic glomerular dysfunction that typifies ischemic acute renal failure.