Abstract:
:Intracellular accumulation of Mn2+ augmented the contractions induced by norepinephrine and acetylcholine in the guinea pig isolated vas deferens. Contractions repeatedly induced by norepinephrine, acetylcholine, or a high concentration of K+ decreased depending on the incubation time in Ca(2+)-free medium. The rate of decrease of all contractions was delayed by intracellularly accumulated manganese. In the Mn(2+)-loaded preparations, the tonic components of the contractions induced by norepinephrine and acetylcholine, but not K+, were highly resistant to extracellular Ca2+ elimination. Ryanodine abolished the initial phasic component but did not affect the tonic component of norepinephrine- and acetylcholine-contractions in Mn(2+)-loaded preparations in Ca(2+)-free medium. In Ca(2+)-depleted preparations, the tonic contraction induced by norepinephrine was restored after the Mn(2+)-loading procedure, and the magnitude of this tonic contraction was comparable to the tonic component of the norepinephrine contraction in the normal medium before Mn2+ loading. The tonic contraction was reproducible in medium without either Mn2+ or Ca2+. These results suggested that intracellular Mn2+ can support norepinephrine-induced tonic contractions. In the Ca(2+)-depleted Mn(2+)-loaded preparations, K+ also induced a tonic contraction in the presence of extracellular Mn2+. However, this contraction was much smaller than that induced by norepinephrine. These results suggested that intracellular Mn2+ augmented contractions not only via an increase in intracellular Ca2+ availability but also via the direct action of Mn2+ on contractile mechanisms, and that this action is highly specific for developing and/or maintaining tonic contractions mediated by receptor activation in the guinea pig isolated vas deferens.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Tsunobuchi-Ushijima H,Gomi Ydoi
10.1016/0014-2999(95)00664-8subject
Has Abstractpub_date
1996-01-11 00:00:00pages
235-41issue
2-3eissn
0014-2999issn
1879-0712pii
0014-2999(95)00664-8journal_volume
295pub_type
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