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

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.