Dual Inhibitory Action of ATP on Adrenergic Neuroeffector Transmission in Rabbit Pulmonary Artery

Husted, Steen; Nedergaard, Ove A.

doi:10.1111/bcpt.1985.57.3.204

Cited by 10 publications

(4 citation statements)

References 23 publications

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“…This result supports the data obtained from experiments conducted in the presence of suramin that neocuproine enhances purinergic mechanisms and when purinergic receptors are desensitized, the neocuproine facilitatory effect is failed [12,14,15,22,23] . Findings supporting our results have been obtained from our previous study on rat bladder [9] .…”

Section: Discussionsupporting

confidence: 89%

“…In this study, neocuproine enhanced the nonadrenergic-noncholinergic contractions of rat bladder detrusor smooth muscle to EFS and suramin or the prolonged exposure to ATP could prevent this facilitation effect. On the other hand, ATP application in different concentrations elicited a contraction on basal tone in a dose-dependent manner and the repeated application of this agent caused a desensitization on its contractile responses [22] . However, in the present study, neocuproine did not alter the basal tone.…”

Section: Discussionmentioning

confidence: 97%

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Neocuproine, a Copper (I) Chelator, Potentiates Purinergic Component of Vas Deferens Contractions Elicited by Electrical Field Stimulation

Göçmen¹,

Kumcu²,

Buyuknacar³

et al. 2005

Pharmacology

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Effects of the specific copper (I) chelator, neocuproine, on the purinergic and adrenergic components of nerve-evoked contractions were investigated in the prostatic rat vas deferens. Electrical field stimulation (EFS; 4 Hz) induced bimodal contractions of vas deferens tissue in the presence of α₁-adrenoceptor antagonist prazosin (to isolate the purinergic component) or purinoceptor antagonist suramin (to isolate the adrenergic component). Neocuproine significantly potentiated the purinergic component of the contractile responses to EFS. However, the same agent failed to elicit any significant effect on the adrenergic component of nerve-evoked contractions. The copper (II) chelator cuprizone could not affect the purinergic component of contractions. The potentiating effect of neocuproine which was reversible after washout of the drug, did not occur following the application of the pre-prepared neocuproine-copper (I) complex. A nitric oxide synthase inhibitor, L-nitroarginine; a cyclooxygenase inhibitor, indomethacin or an α₂-adrenoceptor antagonist, yohimbine, failed to alter the responses to neocuproine on the purinergic component of the contraction to EFS. Neocuproine did not elicit any significant effect on preparations in which the purinergic receptors were desensitized with α,β-methylene ATP. In conclusion, our results suggest that neocuproine potentiates the purinergic component of rat vas deferens contractions elicited by EFS, presumably by facilitating purinergic neurotransmission and that copper (I)-sensitive mechanisms can modulate purinergic transmission in this tissue.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 97%

Neocuproine, a Copper (I) Chelator, Potentiates Purinergic Component of Vas Deferens Contractions Elicited by Electrical Field Stimulation

Göçmen¹,

Kumcu²,

Buyuknacar³

et al. 2005

Pharmacology

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“…These data suggest that neocuproine enhances the postjunctional effect of ATP or enhances the release of ATP from nerves. The finding that the second application of neocuproine (20 or 200 M) did not cause an enhancement of the basal tone supports this speculation because repeated ATP applications elicited a desensitizing effect on the contractile responses (Husted and Nedergaard, 1985) and suppressed EFS-induced contractions (Sahin et al, 2000). Thus, repeated application of neocuproine can induce a desensitizing response similar to that induced by ATP (Namasivayam et al, 1999).…”

Section: Discussionmentioning

confidence: 63%

Effect of Neocuproine, a Copper(I) Chelator, on Rat Bladder Function

Göçmen

Giesselman²,

Groat³

2004

J Pharmacol Exp Ther

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The effects of a specific copper(I)-chelator, neocuproine (NC), and a selective copper(II)-chelator, cuprizone, on nonadrenergic-noncholinergic transmitter mechanisms in the rat urinary bladder were studied by measuring nerve-evoked contractions of bladder strips and voiding function under urethane anesthesia. After blocking cholinergic and adrenergic transmission with atropine and guanethidine, electrical field stimulation induced bimodal contractions of bladder strips. An initial, transient contraction that was blocked by the purinergic antagonist, suramin, was significantly enhanced by NC (20 and 200 M applied sequentially) but not affected by cuprizone. The facilitating effect, which was blocked by suramin and reversible after washout of the drug, did not occur following administration of neocuproine-copper(I) complex (NC-Cu). NC (20 M) significantly increased the second, more sustained contraction, whereas 200 M decreased this response. These effects of NC on the sustained contractions were not elicited by NC-Cu and not blocked by suramin. The nitric oxide synthase inhibitor, L-nitroarginine, did not alter the responses to NC. NC (20 M) elicited a marked increase in basal tone of the strips. This effect was less prominent after the second application of 200 M NC or with NC-Cu treatment or in the presence of suramin. In anesthetized rats, during continuous infusion cystometry, intravesical infusion of 50 M NC but not NC-Cu or cuprizone significantly decreased the intercontraction interval (ICI) without changing contraction amplitude. The ICI returned to normal after washout of NC. Suramin blocked this effect. These results indicate that NC enhances bladder activity by facilitating purinergic excitatory responses and that copper(I)-sensitive mechanisms tonically inhibit purinergic transmission in the bladder.

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“…An important advance was made when it was shown that excitatory junctional potentials recorded in the smooth muscle of rat intrapulmonary arteries in response to sympathetic nerve stimulation were mediated by ATP (Inoue and Kannan, 1988). Adenosine, acting prejunctionally, mediates release of transmitter from sympathetic nerves supplying the rabbit pulmonary artery (Husted and Nedergaard, 1985). Perivascular nerve stimulation of rabbit pulmonary artery elicits release of NA and ATP (Mohri et al, 1993).…”

Section: E Vasculaturementioning

confidence: 99%