Effect of potassium chloride on cytosolic calcium of brain synaptosomes of rats with chronic renal failure

Norepinephrine (NE) release from brain synaptosomes is dependent in major part on an adequate rise in cytosolic calcium ([Ca2+]i). A smaller or a greater calcium signal (delta [Ca2+]i) or delta[Ca2+]i/basal [Ca2+]i ratio in response to stimuli may interfere with NE release from brain synaptosomes. I...

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Bibliographic Details
Published inMineral and electrolyte metabolism Vol. 17; no. 3; p. 194
Main Authors Koureta, P, Smogorzewski, M, Massry, S G
Format Journal Article
LanguageEnglish
Published Switzerland 1991
Subjects
Animals
Brain - metabolism
Calcium - blood
Calcium - metabolism
Creatinine - blood
Cytosol - drug effects
Cytosol - metabolism
Kidney Failure, Chronic - metabolism
Male
Norepinephrine - metabolism
Parathyroidectomy
Phosphorus - blood
Potassium Chloride - pharmacology
Rats
Rats, Inbred Strains
Spectrophotometry, Atomic
Synaptosomes - drug effects
Synaptosomes - metabolism
Verapamil - pharmacology
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Summary:Norepinephrine (NE) release from brain synaptosomes is dependent in major part on an adequate rise in cytosolic calcium ([Ca2+]i). A smaller or a greater calcium signal (delta [Ca2+]i) or delta[Ca2+]i/basal [Ca2+]i ratio in response to stimuli may interfere with NE release from brain synaptosomes. In order to further evaluate the mechanism of reduced NE release from brain synaptosomes in chronic renal failure (CRF), we examined the changes in synaptosomal [Ca2+]i in response to KCl in normal, CRF, and normocalcemic, parathyroidectomized (PTX) CRF rats (CRF-PTX) and in CRF rats treated with verapamil (CRF-V). CRF rats displayed significantly (p less than 0.01) higher basal levels of [Ca2+]i and a higher delta[Ca2+]i and delta [Ca2+]i/basal [Ca2+]i ratio than in the other three groups of rats. These parameters were not different among normal, CRF-PTX and CRF-V rats. The data are consistent with the notion that the higher calcium signal and the higher ratio between signal and the basal [Ca2+]i in response to a stimulus in CRF are deleterious to synaptosomal function and are responsible, in part, for the reduced NE release by these structures in CRF.
ISSN:0378-0392