AJP - Renal Physiology, Vol 260, Issue 2 198-F203, Copyright © 1991 by American Physiological Society
Release of acetylcholine from isolated canine renal tissue
C. J. Pirola, A. L. Alvarez, S. Finkielman and V. E. Nahmod
Instituto de Investigaciones Medicas A. Lanari, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Slices of canine kidney were incubated with [3H]choline and Ringer-Krebs
solution for 30 min. Secretion of [3H]acetylcholine ([3H]ACh) was evoked by
either 1) an electrical field stimulation (0.5-1 Hz, 2 ms, 20 V) or 2)
high-potassium (57 mM) superfusion for 3 min to depolarize nerve terminals.
With these stimulatory schedules, the 3H release mainly consists of
[3H]-ACh. The ACh release is Ca2+ dependent and blocked in presence of a
Mg2(+)-rich medium. Thus suppression of ongoing neuronal activity by
tetrodotoxin and blockade of nicotinic receptors by hexamethonium reduced
the electrically evoked ACh release. With both stimulatory procedures, the
secretory response was modified by pilocarpine and atropine. In addition,
the release of [3H]ACh produced by electrical field stimulation was
inhibited by neostigmine, indicating the presence of functional presynaptic
receptors in cholinergic putative terminals. Activation of these receptors
depresses ACh secretion. The disruption of extrinsic renal nerves 7 days
before did not diminish [3H]ACh release caused by K+ stimulation and,
conversely, increased [3H]ACh released by electrical field stimulation.
These data support the presumed existence of cholinergic nerve terminals in
the canine kidney that can release ACh under suitable conditions of
stimulation.
