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Verapamil Prevents the Metabolic and Functional Derangements in Pancreatic Islets of Chronic Renal Failure Rats^*

PRASERT THANAKITCHARU, GEORGE Z. FADDA, SUHA M. HAJJAR and SHAUL G. MASSRY

Division of Nephrology, the Department of Medicine, University of Southern California School of Medicine Los Angeles, California 90033

Address all correspondence and requests for reprints to: Shaul G. Massry, M.D., Department of Medicine, Division of Nephrology, University of Southern California School of Medicine, 2025 Zonal Avenue, Los Angeles, California 90033.

Abstract

Glucose-induced insulin secretion is impaired in rats with chronic renal failure (CRF), and this defect is due to PTH-induced derangement in the metabolism of pancreatic islets, including an elevated basal level of intracellular calcium, low basal ATP content, low glucose-stimulated ATP and ATP/ADP ratio, and decreased maximum velocity of Ca²⁺-ATPase. Chronic treatment of CRF rats with verapamil prevented the impairment of insulin secretion. The present study examined the mechanism through which verapamil exerts this action. CRF rats treated with verapamil had high levels of serum PTH, but normal baaal ATP content, a greater rise in ATP and ATP/ADP ratio after exposure to glucose, normal intracellular calcium and higher maximum velocity of Ca²⁺-ATPase. The results demonstrate that treatment of CRF rats with verapamil was associated with marked improvement or normalization of the CRF-induced metabolic derangements in pancreatic islets despite no effect on the serum level of PTH. The data are consistent with the notion that verapamil prevents the derangements in insulin secretion in CRF rats by blocking the action of PTH on the islets. (Endocrinology 129: 1749–1754,1991)

Footnotes

^* This work was supported by Grant DK-29955 from the NIDDK.

Fellow of the WHO.

Fellow of the National Kidney Foundation of Southern California.

Received April 30, 1991.

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