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Decreased Angiotensin II -Stimulated Aldosterone Production, but Normal Inositol Phosphate Response in Adrenal Glomerulosa Cells from Streptozotocin-Induced Diabetic Rats: Role of lnsulin

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Authors
Kim, Seong Yeon; Sung, Yeon Ah; Cho, Bo Youn; Lee, Hong Kyu; Koh, Chang-Soon; Min, Hun Ki
Issue Date
1994-06
Publisher
Seoul National University College of Medicine
Citation
Seoul J Med, Vol.35 No.2, pp. 73-82
Keywords
AldosteroneAngiotensin IIInositol phosphateStreptozotocinDiabetic rats
Abstract
Streptozotocin(SlZ)-induced diabetic rats develop hyporeninemic
hypoaldosteronism during the progression of diabetes mellitus. However,the nature and
mechanism of aldosterone deficiency in diabetic rats still remain unclear and acute effects
of insulin on aldosterone production in-vitro are not known. We evaluated the
responses of aldosterone production to angiotensin 11 (AlI), potassium (K+), AClH and
insulin in adrenal glomerulosa cells prepared from SlZ-induced diabetic rats with and
without insulin treatment 2 weeks after diabetes induction. We also measured inositol
phosphateusing standardized anion exchange chromatography. Plasma renin activity and
aldosterone level were not different among control rats,untreated and insulin-treated
diabetic rats. Basal aldosterone production was similar in cells from the three groups.
Cells from untreated diabetic rats showed a significant decrease in the maximal All
(to-8M)-stimuiated aldosterone production and a tendency to be low in the maximal
K+(8.7 mM)-stimulated aldosterone production, compared with control rats (3.2±2.2
\IS 7.7±2.4, P (0.05 and 4.8±1.8 \IS 8.0±3.2 ng/105 cells/hr, 0.05 (P (0.1, respectively).
In contrast, there were no differences in All- and K+-stimulated aldosterone
production between control and insulin-treated diabetic rats. AClH (to-8M), however,
caused a similar effect on aldosterone production and insulin (I mU /ml for 1 hour) did
not alter either basal or agonists-stimulated aldosterone production in cells from the
three groups. All (to-8M)-induced IP formation among the three groups was similar
and did not change with the addition of insulin u mU / ml), These results indicate that
reduced response to All in the early phase of SlZ-induced diabetes in rats may be due
to the zona glomerulosa dysfunction secondary to chronic lack of insulin and the main
defect responsible for altered All effects may be located at some step(s) mediating All
action downstream from IP formation.
ISSN
0582-6802
Language
English
URI
http://hdl.handle.net/10371/7334
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)The Seoul Journal of MedicineThe Seoul Journal of Medicine Vol. 35 No.2 (1994)
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