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Department of Pharmacology, University of Tübingen, D-72074 Tübingen, Germany
Freshly isolated rat juxtaglomerular cells (JGC) were superfused
to study renin secretion rate (RSR) at the cellular level. Effluates from the superfusion chamber collected in 20-min intervals showed a time-dependent decline in RSR from 85.5 ± 32 to
4.0 ± 2.4 ng ANG
I · ml
1 · h
1 · mg
protein
1 · min
1
within 100 min of collection (mean ± SE,
n = no. of JGC
preparations/superfusion chambers = 9/18). Addition of adenosine
deaminase type II (ADA II, 3 U/1.4 mg protein) to the superfusion
medium increased RSR more than fourfold to 402 ± 100 ng
in the first collection period, which dropped to 237.5 ± 67 ng ANG
I · ml
1 · h
1 · mg
protein
1 · min
1
(n = 9/18) within 100 min. This ADA II
effect was rapid in onset and fully reversible. When the purified ADA
type VII, with a 40-fold higher specific activity, was added to the
superfusate, RSR was increased only by 96 ± 17.8% compared with
controls. This ADA VII (5 U/30 µg) effect could be mimicked by the
selective adenosine A1-receptor
antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10
6 mol/l). Since albumin
stimulated RSR in a concentration-dependent fashion, to an extent
similar to that of ADA II, we assume that the ADA II effect was largely
unspecific in nature. We conclude that
1) superfusion of isolated JGC from
rats is suitable for investigations of renin secretion at the cellular
level, 2) the increase in RSR by ADA
II appears to be only in part due to deamination of endogenously
generated adenosine, and 3) albumin
in the superfusate induces a similar stimulatory effect as ADA II.
adenosine deaminase; adenosine A1 receptors; renin release; rat juxtaglomerular cells; 1,3-dipropyl-8-cyclopentylxanthine
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