Stroke, Vol 15, 475-480, Copyright © 1984 by American Heart Association
N Toda
In helically-cut strips of cerebral arteries isolated from dogs and
monkeys, the addition of 1 mM iodoacetic acid (IAA) produced contractions
during an early period (5 to 10 min) and also a prolonged exposure (50 to
70 min). The early contraction was abolished by exposure to Ca++-free media
containing EGTA, and significantly attenuated by treatment with procaine or
dantrolene. Verapamil, lidocaine, ATP and pyruvate did not inhibit the
contraction. On the other hand, the late contraction was not prevented by
exposure to Ca++- free, EGTA-containing media and by treatment with
procaine, dantrolene, lidocaine, ATP or pyruvate. Nitroglycerin and
papaverine did not relax the IAA-contracted arteries. In dog and monkey
mesenteric arteries and dog coronary, renal and femoral arteries, IAA
elicited contractions after a prolonged exposure, which were not inhibited
by soaking the preparations in Ca++-free, EGTA-containing media. Passive
tensions developed by rapid stretch in Ca++-free media did not differ in
IAA- treated and control arteries. During an early period of IAA actions,
Ca++ appears to be released from intracellularly stored sites in the amount
sufficient to produce significant contractions in cerebral, but not in
peripheral arteries. It is concluded that the involvement of Ca++ in the
late contraction induced by IAA is if any minimal, and such a contraction
may be associated with functional alterations induced by the metabolic
inhibitor in arterial tissues other than smooth muscle.
ARTICLES
Calcium independent contraction induced by iodoacetic acid in isolated cerebral arteries
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