Palytoxin-induced Contraction and Release of Endogenous Noradrenaline in Rat Tail Artery

Overview

Journal Br J Pharmacol

Publisher Wiley

Specialty Pharmacology

Date 1988 Sep 1

PMID 2905903

Citations 1

Authors

H Karaki

H Nagase

Y Ohizumi

N Satake

S Shibata

Affiliations

Soon will be listed here.

Abstract

1. The mechanism of the contractile effect of a potent marine toxin, palytoxin (PTX) on the rat isolated tail artery was examined. 2. PTX (10(-7) M) induced a contraction in the tail artery which was dependent on external Ca2+. This contraction was inhibited (by 75% or more) by 10(-6) M prazosin, 2.4 x 10(-5) M bretylium and 10(-4) M 6-hydroxydopamine (6-OHDA), and partially (by 40%) by 10(-5) M indomethacin. However, this contraction was not affected by 10(-6) M tetrodotoxin (TTX), 10(-6) M nifedipine or reserpine treatment. The PTX-induced contraction in reserpine-treated artery was partially inhibited by nifedipine and indomethacin but not by prazosin. 3. Transmural electrical stimulation induced a transient contraction which was dependent on external Ca2+. The contraction induced by electrical stimulation was inhibited by TTX, prazosin, bretylium, reserpine treatment and 6-OHDA but not by nifedipine or indomethacin. 4. PTX increased the release of noradrenaline from this artery. However PTX did not release noradrenaline from reserpine-treated arteries. PTX-induced noradrenaline release was only partially inhibited by TTX or by Ca2+-free solution. 5. These results suggest that PTX has pre- and postsynaptic effects in the rat tail artery. PTX may stimulate adrenergic nerves and release noradrenaline mainly by a TTX-insensitive and Ca2+-independent mechanism and partially by a TTX-sensitive and Ca2+-dependent mechanism. Further, PTX may also release prostaglandins and depolarize smooth muscle cell membrane to induce a contraction.

Citing Articles

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PMID: 7689407 PMC: 2175611. DOI: 10.1111/j.1476-5381.1993.tb13654.x.

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