The damaging effect of shock waves on intracellular calcium homeostasi
s in renal tubular cells has not been investigated previously. We have
examined the effects of shock waves on Madin Darby canine kidney (MDC
K) cells by determining the release of two cellular enzymes: glutamate
oxalactate transferase (GOT) and lactate dehydrogenase (LDH); and bot
h 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 membra
ne 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) tr
ansients 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+ pum
p on the endoplasmic reticulum membrane, and the effector molecules in
volved in regulating the [Ca2+](i) transients were slightly affected.
Shock waves appeared to cause a mild impairment in the mechanisms resp
onsible for the decay of the evoked [Ca2+](i) rises.