The damaging effect of shock waves on intracellular calcium homeostasis in renal tubular cells has not been investigated previously. We have examined the effects of shock waves on Madin Darby canine kidney (MDCK) cells by determining the release of two cellular enzymes: glutamate oxalactate transferase (GOT) and lactate dehydrogenase (LDH); and both the basal cytosolic calcium concentration ([Ca2+]i) and the [Ca2+]i rises evoked by Ca2+-mobilizing agonists after shock wave exposure (SWE). Immediately but transiently after SWE, the release of GOT and LDH increased by 15 % and 5-fold, respectively, implicating cell membrane damage; and within 1-7 h after SWE, basal [Ca2+]i was elevated by 15-141%. In SWE-treated cells, the peak amplitude of the [Ca2+]i transients evoked by ATP, bradykinin, thapsigargin and 2,5-Di-(t-butyl)-1,4-hydroquinone (BHQ) was slightly altered, and the plateau amplitude was markedly elevated. The ATP and bradykinin receptors, the Ca2+ pump on the endoplasmic reticulum membrane, and the effector molecules involved in regulating the [Ca2+]i transients were slightly affected. Shock waves appeared to cause a mild impairment in the mechanisms responsible for the decay of the evoked [Ca2+]i rises.