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The Ewha Medical Journal
Ewha Womans University School of Medicine

Ewha Med J 1997; 20(1):13-21

pISSN: 1598-7450

DOI: https://doi.org/10.12771/emj.1997.20.1.13

Original Article

The Angiotensin II-Stimulated Phospholipase Activity in Adrenal Glomerulose Cells of Diabetic Rats

Yeon-Ah Sung

Copyright ⓒ 1997. Ewha Womans University School of Medicine. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Published Online: Jul 24, 2015

Abstract

Objectives

Diabetic patients develop hypoaldosteronism which frequently caused hyperkalemia and metabolic acidosis and diabetic hypoaldosteronism is associated with selective unresponsiveness of aldosterone to angiotensin II(A II), but mechanism of defect in A II stimulated aldosterone response still remain unclear.

To elucidate the mechanism of defect in A II stimulated aldosterone response and whether the defect was corrected by insulin treatment. author evaluated the responses of aldosterone production to A II, K+ and ACTH. I also evaluated the products of phospholipase C(PLC) and phospholipase D(PLD) activation important for increase of intracellular calcium and protein kinase C activation after A II activation in adrenal glomerulosa cells prepared from streptozotocin induced diabetic rats.

Methods

Two weeks after induction of diabetes by streptozotocin, rats were sacrificed by decapitation. The aldosterone production to A II, K+ and ACTH was measured by RIA. Inositol triphosphate(IP3) and diacylglycerol(DAG) generated by activation of PLC and phosphatidic acid(PA), phosphatidylethanol(PEt) and DAG generated by activation of PLD were measured by anion exchange column and thin layer chromatography.

Results

1) Plasma renin activity and aldosterone level were not different among control rats, untreated and insulin treated diabetic rats.

2) basal, ACTH and K+-stimulated aldosterone production were similar in cells from the three groups(p>0.05), but A II stimulated aldosterone production was significantly decreased in cells from untreated diabetic rats compared with control and insulin treated diabetic rats(p<0.05).

3) A II-induced IP3, PA, PEt and DAG generation was similar among the three groups(p>0.05).

Conclusion

These results suggested that decreased A II-stimulated aldosterone response was present in glomerulosa cells from strepzptocin induced diabetic rats and reversed by insulin treatments. The main defect of altered A II response of zona glomerulosa might be located in the step distal to the activation of phospholipase.

Keywords: Hypoaldosteronism; Phospholipase; Angiotensin II