The discovery of the ATP-driven calcium pump in the sarcoplasmic
reticulum membranes reaches back to the postwar (World War II)
years and would not be possible without the generous support
by the American scientific community. It was this community
that in pre- and postwar years gave shelter to many European
scientists, which in return stimulated scientific development
in the United States. These pre- and postwar relations helped
to establish the calcium pump as a physiologically relevant
mechanism in all kinds of cells. The pump and its counterpart,
the calcium release channel, proved to be controlled by various
intrinsic mechanisms. Rising hydrogen concentrations as occuring
in ischemic muscles switch off pump activity and counteract
allosterically caffeine-induced calcium release (CICR). Rising
phosphate or the presence of other calcium-precipitating anions,
on the other hand, prevents pump inhibition by intraluminal
calcium precipitation, which, simultaneously, can increase the
quantity of releasable calcium. The inactivation of CICR by
removing medium chloride must be considered as a hint of additional
mechanisms by which calcium-dependent activity regulation can
be modified.
