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J Am Soc Nephrol 10:84-92, 1999
© 1999 American Society of Nephrology

REGULAR ARTICLES

Elevated Myocardial Cytosolic Calcium Impairs Insulin-Like Growth Factor-1-Stimulated Protein Synthesis in Chronic Renal Failure

DAVID PEIYUAN QING*, HU DING*, JAY VADGAMA{dagger}, YAN YUAN WU{dagger} and JOEL D. KOPPLE*

* Division of Nephrology and Hypertension and Department of Medicine, Harbor-UCLA Medical Center, Torrance, California, and UCLA Schools of Medicine and Public Health.
{dagger} Charles R. Drew University of Medicine and Science, Department of Medicine, Los Angeles, California.

Correspondence to Dr. Joel D. Kopple, Professor of Medicine and Public Health, Harbor-UCLA Medical Center, 1000 West Carson Street, Box 406, Torrance, CA 90509. Phone: 310-222-3891; Fax: 310-782-1837; E-mail: Kopple{at}HUMC.EDU

Abstract. Rats and humans with chronic renal failure (CRF) are reported to have resistance to recombinant human insulin-like growth factor-1 (rhIGF-1). Because basal cytosolic calcium ([Ca2+]i), a second messenger, may be increased in CRF, this study was conducted to examine whether elevated basal [Ca2+]i may cause resistance to IGF-1. Cardiomyocytes from four groups of rats were studied: untreated CRF, CRF with parathyroidectomy (PTX), CRF with the calcium channel blocker felodipine (F), and sham operation of the kidney (SO). CRF was created by ligation of two-thirds of the left renal artery and contralateral nephrectomy. Rats from each group were pair-fed the same diet for 20 to 22 d. Basal [Ca2+]i in cardiomyocytes (nM) in the CRF rats (102.0 ± 2.8; SEM), was significantly higher than in each of the CRF-PTX, CRF-F, and SO groups (65.2 ± 1.9, 63.8 ± 2.6, and 63.5 ± 2.0, respectively; P < 0.01). rhIGF-1 increased cardiomyocyte [Ca2+]i in all four groups of rats. The rise in [Ca2+]i was significantly diminished in the CRF rats (P < 0.05) and did not differ among the CRF-PTX, CRF-F, and SO rats. Protein synthesis after incubation with 0, 50, 100, 200, or 400 ng/ml rhIGF-1 was lower in cardiomyocytes from CRF rats than in each of the other three groups (P < 0.05) and was significantly less in the CRF-F rats compared with SO animals. IGF-1 receptor mRNA and IGF-1 receptor number and affinity were not different among the four groups. These findings suggest that cardiomyocytes from CRF rats display elevated basal [Ca2+]i and attenuated rhIGF-1-induced increase in [Ca2+]i; basal protein synthesis is decreased, and IGF-1-stimulated protein synthesis is impaired; elevated basal [Ca2+]i seems to contribute to this diminished response to rhIGF-1.




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