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EFFECTS OF CAPTOPRIL ON [ 3 H]‐NOREPINEPHRINE RELEASE IN RAT CENTRAL NERVOUS SYSTEM
Author(s) -
Tsuda Kazushi,
Tsuda Seiko,
Nishio Ichiro,
† Yoshiaki Masuyama,
Goldstein Menek
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02074.x
Subject(s) - captopril , medulla oblongata , norepinephrine , endocrinology , medicine , stimulation , hypothalamus , chemistry , central nervous system , adrenal medulla , catecholamine , biology , dopamine , blood pressure
SUMMARY 1. The present study was performed to investigate the effects of captopril (an angiotensin converting enzyme inhibitor, ACE‐I) on noradrenergic transmission in the rat central nervous system. 2. Slices of rat hypothalamus and medulla oblongata were prepared and prelabelled with [ 3 H]‐norepinephrine. Slices were continuously superfused with Krebs‐Ringer solution, and electrical stimulation (1 Hz) was performed. 3. Captopril significantly inhibited the stimulation‐evoked [ 3 H]‐norepinephrine release from rat hypothalamic slices in a dose‐dependent manner (S2/S1 ratio: control 0.904 ± 0.025, n = 6, captopril l × 10 ‐5 mol/L 0.617 ± 0.043, n = 6, P <0.05, captopril 5 ×10 ‐5 mol/L 0.547±0.037, n = 6, P <0.05). However, the basal release of [ 3 H]‐norepinephrine was not affected by captopril. 4. Captopril also reduced the stimulation‐evoked [ 3 H]‐nor‐epinephrine release in the medulla oblongata (S2/S1 ratio: control 0.878 ± 0.018, n = 6, captopril 3.3 × 10 ‐5 mol/L 0.624 ± 0.046, n = 6, P <0.05). 5. These results show that captopril might inhibit the stimulation‐evoked norepinephrine release in rat hypothalamus and medulla oblongata. Although the precise mechanisms underlying the neurosuppressive effect of captopril are still uncertain, the finding suggests that the inhibition of noradrenergic transmission might be related to the central action of the ACE‐I.