W-7 at calmodulin-antagonistic concentrations facilitates noradrenaline release from rat brain cortex slices

Reimann, Wolfgang; Köllhofer, Ursula; Wagner, Bernd

doi:10.1016/0014-2999(88)90186-0

Cited by 7 publications

(2 citation statements)

References 10 publications

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“…This is in marked contrast to the release-inhibiting effects of these agents (W7 and trifluoperazine) in brain synaptosomes (DeLorenzo, 1985), which has been interpreted as evidence for a role for calmodulin in the process of neurotransmitter release (DeLorenzo, 1981;; see also Llinas et al, 1985). How-ever, other studies have also failed to observe inhibition of neurotransmitter release in various systems (Publicover, 1985;Jinnai et al, 1986;Reimann et al, 1988) using W7, trifluoperazine and calmidazolium. Thus, there may not be a universal role for calcium-calmodulin kinases in neurotransmitter release processes.…”

Section: Discussionmentioning

confidence: 83%

Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Costa

Barrington

Majewski

1993

British J Pharmacology

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1 The Ml selective muscarinic agonist, McNeil A 343, enhanced the electrically evoked release of noradrenaline from postganglionic sympathetic nerves in mouse atria. This has been found previously to be due to activation of muscarinic receptors of the Ml subtype, probably located on sympathetic nerve terminals. The present study investigated the signal transduction mechanisms involved in the releaseenhancing effects of McNeil A 343. The release of noradrenaline from mouse atria was assessed by measuring the electrically-induced (3 Hz, 60 s) outflow of radioactivity from atria which had been pre-incubated with [3H]-noradrenaline.

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Section: Discussionmentioning

confidence: 83%

Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Costa

Barrington

Majewski

1993

British J Pharmacology

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“…It was assumed that this contraction was caused by a release of endogenous noradrenaline from sympathetic nerve terminals [Hidaka et al, 1981;Asano and Hidaka, 1985]. This hypothesis was sup ported by investigations of Reimann et al [1988], who reported an enhancement of stimulation-evoked NA release in rat brain cortical slices. However, this hypothesis could not explain the contraction induced in rat aorta, because of the lack of innervation of this organ.…”

Section: Discussionmentioning

confidence: 73%

Effect of Calmodulin Antagonists on Contraction and <sup>45</sup>Ca Movements in Rat Aorta

Wermelskirchen

Koch²,

Wilhelm³

et al. 1989

Pharmacology

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To study the selectivity of calmodulin antagonists it was assumed that they should inhibit noradrenaline (NA)- and K⁺-induced contractions similarly without an accompanying inhibition of ⁴⁵Ca uptake. Therefore, in isolated rat aorta the effects of W-7, calmidazolium and trifluoperazine on contraction and ⁴⁵Ca uptake elicited by K⁺ and NA were investigated. Calmidazolium (10^–5–10^–4 mol/l) elicited an incomplete inhibition of K⁺-and NA-induced contraction and ⁴⁵Ca uptake. Trifluoperazine inhibited the NA-induced contractions at lower concentrations (10^–8–10^–6 mol/l) than the K⁺-induced contraction (10^–6–10^–4 mol/l). The K⁺- and NA-induced ⁴⁵Ca uptake was blocked by trifluoperazine (10^–5 mol/l). W-7 (10^–5–10^–4 mol/l) inhibited the K⁺- and NA-induced contraction, however, in the same concentration range W-7 diminished the K⁺- and NA-induced 45Ca uptake. In conclusion, the results indicate that calmidazolium and trifluoperazine are hardly useful as calmodulin antagonists because of their additional properties, whereas W-7 seems to be the least unspecific of the calmodulin antagonists studies.

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Effects of drugs on calmodulin-mediated enzymatic actions

Ovádi

1989

Progress in Drug Research

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W-7 at calmodulin-antagonistic concentrations facilitates noradrenaline release from rat brain cortex slices

Cited by 7 publications

References 10 publications

Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Effect of Calmodulin Antagonists on Contraction and <sup>45</sup>Ca Movements in Rat Aorta

Effects of drugs on calmodulin-mediated enzymatic actions

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W-7 at calmodulin-antagonistic concentrations facilitates noradrenaline release from rat brain cortex slices

Cited by 7 publications

References 10 publications

Evidence that M1 muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Evidence that M1 muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Effect of Calmodulin Antagonists on Contraction and <sup>45</sup>Ca Movements in Rat Aorta

Effects of drugs on calmodulin-mediated enzymatic actions

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Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C

Evidence that M₁ muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C