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Angiology
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Renal Ca2+ + Mg2+ ATPase in Congestive Heart Failure Due to Diabetes

Animesh Sahai, M.D., F.A.C.A.

WINNEPEG, CANADA, Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

Steven J. Weiser, B.Sc.

Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

Pallab K. Ganguly, M.D., F.A.C.A.

Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

Pallab K. Ganguly, M. D. , F.A. C. A.

Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

The authors have previously shown that atrial natriuretic peptide (ANP) mediates its cellular effects in part by changes in Ca2+ homeostasis in kidney cortex and that Ca2+ + Mg2+ ATPase is linked to ANP receptors, being reciprocally modulated by the guanylate cyclase system. The present study was designed to examine the status of this coupling in diabetes-induced congestive heart failure and the effect of its alterations on the functional integrity of the renal cell. Ca2+ + Mg2+ ATPase and guanylate cyclase were tested in hypertensive-diabetic rats (D+H), which develop congestive heart failure (CHF) at ten weeks following streptozotocin (65 mg/kg) injection and abdominal aortic constriction. The ATPase activity was measured by the release of 32P from [{gamma}-32P]ATP in the medium. While the guanylate cyclase activity was decreased very rapidly in the hypertensive-diabetic group, the sensitivity of the Ca2+ pump to ANP was increased at an early stage (three weeks) and decreased at a late stage (ten weeks) of CHF.

The authors conclude that a defect in coupling between the Ca2+ pump and the ANP-receptor system as observed in the D + H group may contribute to the development of nephropathy and CHF.

Angiology, Vol. 44, No. 10, 769-775 (1993)
DOI: 10.1177/000331979304401002


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