
the inhibition of respiration and phosphorylation in kidney
mitochondria by parathyroid hormone administered in vivo.
   parathyroid hormone administered
in vivo to rabbits
produced a metabolic alteration
in kidney cortex
mitochondria, evidenced by
diminished respiratory rate,
respiratory control, and p:o
ratio with a series of substrates
including pyruvate plus
fumarate, succinate,
ketoglutarate, malate, citrate,
and isocitrate.  the adenosine
triphosphate-inorganic
phosphate exchange reaction
rate was decreased and
adenosine triphosphatase
activity was increased compared
to control mitochondria.
these changes did not become
apparent until about 12 hr.
after injection, were undiminished
by 24 hr., and could
be elicited with as little as 200
usp units of hormone.
under identical conditions liver
mitochondria were unaffected.
diphospho- and triphosphopyridine nucleotides
in combination frequently elevated
the respiration in
parathyroid-treated mitochondria
close to or above control
levels with citrate and isocitrate
but not with the
remaining substrates and had
no effect on respiratory
control with any of the substrates.
the effects of the
hormone could not be duplicated
by elevating and maintaining
in otherwise normal rabbits
serum ca concentrations
at twice normal level
for 6 hr. it is concluded
that the effects produced by
parathyroid hormone on kidney
are multiple in nature and
related to the ca++
raising potency of the preparations.
