@article{APS7727,
author = {Francis Ifejika ACHIKE and Chiu-Yin KWAN},
title = {Characterization of a novel tetrandrine-induced contraction in rat tail artery.},
journal = {Acta Pharmacologica Sinica},
volume = {23},
number = {8},
year = {2016},
keywords = {},
abstract = {AIM: In an attempt to pharmacologically characterize the Chinese antihypertensive
drug, tetrandrine, we observed in rat-tail arteries, an unusual contraction in
tissues that were stimulated with high [KCl] and not those stimulated with
phenylephrine. The characteristics of this contraction were studied.
METHODS: Segments of perfused ventral rat-tail arteries (RTA) were contracted
with a depolarizing concentration (120 mmol/L) of KCl or with phenylephrine (3.0
micromol/L). At peak contraction, they were exposed to tetrandrine (40
micromol/L), which caused marked relaxation in each case. Washing the RTA led to
an unusual, slowly-declining contraction, hereafter referred to as
tetrandrine-induced contraction (TIC) which was also observed when the tissues
were exposed to 80 micromol/L, but not 10 micromol/L or 20 micromol/L of
tetrandrine.
RESULTS: Pretreatment with phentolamine (non-selective alpha-adrenoceptor
antagonist), prazosin (selective alpha1-adrenoceptor antagonist) or
6-hydroxydopamine (for denervation), but not rauwolscine or atropine abolished
the TIC. Treatment with ouabain (Na+/K+-ATPase inhibitor) did not sustain the
contraction. Changing the depolarizing concentrations of KCl to 80 mmol/L or 100
mmol/L did not alter the TIC, but at 60 mmol/L, it was abolished.
CONCLUSION: The data show that tetrandrine induces a K+-dependent contraction of
the RTA through a neuronal mechanism involving alpha1-adrenoceptors. It is
speculated that this contraction may be a factor in the reported absence of
postural hypotension in the clinical use of tetrandrine.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/7727}
}