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EFFECT OF METHOXAMINE ON NORADRENALINE RELEASE IN THE CAUDAL ARTERY OF HYPERTENSIVE RATS
Author(s) -
Shinozuka Kazumasa,
Kunitomo Masaru,
Bjur Richard A.,
Westfall David P.,
Hattori Keisuke
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.tb02982.x
Subject(s) - methoxamine , medicine , adenosine , endocrinology , endogeny , agonist , adenosine deaminase , chemistry , purinergic receptor , inhibitory postsynaptic potential , receptor
Summary 1. The effect of methoxamine, an α 1 ‐adrenoceptor agonist, on the overflow of endogenous noradrenaline (NA) was examined in the electrically field stimulated (EFS) caudal artery obtained from Wistar rats, Wistar‐Kyoto rats (WKY) and age‐matched spontaneously hypertensive rats (SHR). 2. Methoxamine inhibited the EFS‐evoked release of endogenous NA in the arteries from Wistar rats and WKY, but not in the arteries of SHR. 2‐chloroadenosine, a purinoceptor agonist, also inhibited the NA release in the arteries from normotensive rats but not in the arteries of SHR. 3. The inhibitory effect of methoxamine was blocked by adenosine deaminase and potentiated by adenosine uptake inhibitor, dipyridamole. 4. Methoxamine caused the release of adenine nucleotides and adenosine from the caudal arteries of WKY and SHR. 5. These suggest that the inhibitory effect of methoxamine on NA release is mediated by endogenous adenyl purines and that the failure of methoxamine to inhibit NA release in the caudal artery of SHR is due to a dysfunction of the pre‐junctional purinoceptors on sympathetic nerve terminals.