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KMID : 0368119920220030431
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Korean Circulation Journal
1992 Volume.22 No. 3 p.431 ~ p.444
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Effect of Tetramethylammonium on the Release of Endothelium Derived Relaxing Factor in Rabbit Thoracic Aorta
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Abstract
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Tetramethylammonium (TMA) is one of the synthetic compounds of nicotine that act at ganglionic site. The major action of TMA consis5ts of initial stimulation followed by a more persistent depression of all autonomic ganglia by binding to a
cholinergic
receptor.
It is well believed that the level of membrane potential in arterial smooth muslcle is an important regulator of tension development. Depolarization and hyperpolarization by only fe millivolts results in significant changes in tension. In
general,
the
agents which induce membrane depolarization leads to vasoconstriction whereas hyperpolarizing agents of vascular smooth muscle induce vascular relaxation.
The present study was undertaken to elucidate the effect of TMA on vascular contractility in the isolated rabbit thorcic aorta with or without endothelial cell. and the mechanisms involved in the change of vascular contractiolity by TMA.
@ES The results obtained are summarized as follows:
@EN 1) In the presence of endothelial cells. tMA induced a relaxation of the aorta precontracted with norepinephrine but induced a contraction in the aorta without endothelial cells, indicating that in the rabbit aorta. relaxations produced by
TMA
were
the endothelium-dependent.
2) The addition of inhibitor such as methylene blue. hemoglobin, hydroquinone and p-bromophenacyl bromide during the TMA-induced relaxation reversed the contractile tension to a level similar to or higher than that before the addition of TMA in
rabbit
thoracic aorta. This relaxant effect of TMA suggests that the TMA-induced relaxation in rabbit aorta is due to the release of endothelium derived relaxing factor (EDRF).
3) Relaxation induced by TMA was antagonized by atropine and thus the TMA does seem to act on the muscarinic receptors.
4) TMA reduced the norepinephrine-induced Ca++ influx into rabbit smooth muscle membrane.
From the above results. it may be concluded that TMA-induced vascular relaxation in rabbit aorta is due to the release of EDRF. Mechanism involved in the relaxation induced by TMA may be the stimulation of soluble guanylate cyclase and increased
tissue
cGMP concentratiopns.
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