It is proposed that volatile anesthetics act through the modification of Ca
2+ homeostasis in excitable cells. To test this hypothesis, cardiac and ske
letal muscles were used as models to examine Ca2+ response, and Ca2+ regula
tory and delivery mechanisms. I found that halothane did not alter Ca2+ bin
ding to cardiac troponin C. However, halothane and isoflurane reversibly de
creased the Ca2+ affinity of calmodulin at low anesthetic concentration, an
d irreversibly increased the Ca2+ affinity of calmodulin at high anesthetic
concentration. The volatile anesthetics also increased the permeability of
light fraction of sarcoplasmic reticulum (SR) to Ca2+. I conclude that vol
atile anesthetics alter calcium homeostasis in cardiac and skeletal muscles
. This work was in part performed in collaboration with Giovanni Salviati a
nd the author benefited from Salviati's work in similar areas.