Ca2+ uptake by endoplasmic reticulum of renal cortex. II. Effects of uninephrectomy and parathyroidectomy

David W. Moskowitz, Keith A. Hruska

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Calcium uptake by the endoplasmic reticulum (ER) is important for cellular calcium homeostasis, yet its regulation in nonmuscle cells is poorly understood. We reported that Ca2+ uptake by a light fraction of canine renal cortical ER (LER) is stimulated by protein kinase C in vitro. Here we describe conditions in vivo that stimulated renal cortical LER Ca2+ uptake. Thirty minutes after contralateral nephrectomy in the dog, 45Ca2+ uptake into renal cortical LER was increased 42% above control LER. There was no difference in LER Ca2+ uptake 24 hours after uninephrectomy. Acute denervation did not reproduce the increase in LER 45Ca2+ uptake seen at 30 minutes after uninephrectomy, nor did prior thyroparathyroidectomy abolish it. Forty-eight hours after thyroparathyroidectomy, 45Ca2+ uptake activity into renal cortical LER was decreased ≈sevenfold. In a proximal tubular cell line (LLC-PK1), 30-minute incubation with 12-O-tetradecanoylphorbol-13-acetate doubled 45Ca2+ uptake into a nonmitochondrial pool. Pretreatment with epidermal growth factor halved ER Ca2+ uptake, whereas insulin-like growth factor and growth hormone, alone or in combination, had no effect. Our data suggest that Ca2+ uptake into renal cortical ER is stimulated acutely during compensatory renal growth, perhaps through protein kinase C, and is stimulated chronically by parathyroid hormone.

Original languageEnglish
Pages (from-to)42-47
Number of pages6
JournalCalcified Tissue International
Issue number1
StatePublished - Jul 1 1992


  • Calcium
  • Endoplasmic reticulum
  • In vivo
  • Kidney


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