Nonadrenergic, noncholinergic responses of the rabbit detrusor
smooth muscle and the role of L-arginine/nitric oxide pathway in
these responses

As, Sahin; Ke, Atalik; Doğan, Necdet

doi:10.1358/mf.2000.22.1.795821

Cited by 6 publications

(9 citation statements)

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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%

“…Exposure time of ATP was 60 s for each application. In another series of experiments, neocuproine (200 mol/l) was applied to the tissue in the presence of an ATP analogue, ␣ , ␤ -methylene ATP (3 mol/l) to examine the effects of neocuproine on the EFS-evoked contractions on preparations in which the purinergic receptors were desensitized [12,14,15] .…”

Section: In Vitro Studiesmentioning

confidence: 99%

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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: In Vitro Studiesmentioning

confidence: 99%

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: 62%

“…This finding indicates that an NO pathway does not play a role in the facilitating effect of neocuproine. Previous studies indicated that NO was involved in the actions of other ions (nickel and manganese) on neurally evoked bladder contractions Lin-Shiau, 1997, 1998;Sahin et al, 2000). We considered the possibility that NO released in the bladder is not free NO but a sulfhydryl-containing compound, such as an S-nitrosothiol (Thornbury et al, 1992;Garcia-Pascual et al, 2000) and that neocuproine could affect the responses of S-nitrosothiols by its ability to chelate copper (De Man et al, 1999;Göcmen et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Exposure time of ATP was 60 s for each application. In some experiments, either ATP (10 or 100 M) or neocuproine (5 or 10 M) was applied to the bladder strips after prolonged (30-min) ATP treatment (10 or 100 M) to examine the effects on the EFS-evoked contractions or basal tone in preparations in which the purinergic receptors were desensitized (Driessen et al, 1993;Sahin et al, 2000).…”

Section: Methodsmentioning

confidence: 99%

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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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