The Inhibition of Respiration and Phosphorylation in Kidney Mitochondria by Parathyroid Hormone Administered in Vivo

From the ¹ From the Veterans Administration Hospital and the University of Missouri at Kansas City School of Dentistry, Kansas City, Missouri 64106, and University of Kansas Medical School, Kansas City, Kansas 66103

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 hours after injection, were undiminished by 24 hours, and could be elicited with as little as 200 U.S.P. 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 no 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 calcium concentrations at twice normal level for 6 hours. 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.

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