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

✍ Scribed by David W. Moskowitz; Keith A. Hruska

• Publisher: Springer
• Year: 1992
• Tongue: English
• Weight: 614 KB
• Volume: 51
• Category: Article
• ISSN: 1432-0827
• DOI: 10.1007/bf00296216

✦ Synopsis

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 stimulate 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 approximately 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.