Neurotransmitters adenosine triphosphate and noradrenaline induce nitric oxide release in rat vas deferens

Vetri, T.; Maio, Roberto Di; Bonafede, G.; Passafiume, L.; Postorino, A.

doi:10.1046/j.1365-2680.2000.00170.x

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…A previous study reported that sildenafil antagonizes the ATP response noncompetitively in VD, similar to PPADS [24]. On the other hand, an increased release of NO has been shown experimentally by exogenously administering ATP [25].…”

Section: αβ-Meatp-induced Contractile Responses Of Vdmentioning

confidence: 83%

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil

Gür¹,

Sikka²,

Knight³

et al. 2010

Asian J Androl

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Hypertension (HTN) is a risk factor for erectile dysfunction, but its effect on vas deferens (VD) contractility and the ejaculatory response has not been delineated. NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, was used for induction of nitric oxide (NO)-deficient HTN. Our aim was to evaluate the effects of L-NAME-induced HTN on rat VD contractility and to determine whether sildenafil affects VD contractility. A total of 36 male rats were divided into (1) control, (2) L-NAME-HTN, (3) sildenafil treated L-NAME-HTN groups. Group 2 was treated with L-NAME (40 mg kg -1 per day) in drinking water for 4 weeks. Group 3 received sildenafil (1.5 mg kg -1 per day, by oral gavage) concomitantly with L-NAME. The prostatic portion of the VD was subjected to electrical field stimulation (EFS, 1-20 Hz), and the P2X 1 agonist α,β-methylene ATP (α,β-meATP, 100 μmol L -1 -1 μmol L -1 ) and the α1-adrenoceptor agonist phenylephrine (Phe, 100 μmol L -1 -1 mmol L -1 ) were used to construct concentration-response curves. These experiments were repeated in the presence of P2X receptor antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 30 μmol L -1 ). VD contractions in response to EFS, α,β-meATP and Phe were significantly enhanced by L-NAME. Sildenafil treatment in the L-NAME group improved the contractile response of VD to EFS (20 Hz). In the presence of PPADS, the enhanced contractile response of VD to EFS and α,β-meATP in hypertensive rats was reversed. In the rat model of chronic NO depletion, the purinergic and adrenergic components and EFS affect VD contractility. The VD contractile response may be mediated more by the purinergic system than the adrenergic system, and sildenafil may alter the ejaculatory response in men with PE.

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Section: αβ-Meatp-induced Contractile Responses Of Vdmentioning

confidence: 83%

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil

Gür¹,

Sikka²,

Knight³

et al. 2010

Asian J Androl

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“…Sildenafil has an antagonism over ATP responses by purinergic receptor blockade or/and over NO. An increased release of NO has been shown experimentally by exogenous administered ATP 15 . NO increases intracellular cGMP level.…”

Section: Discussionmentioning

confidence: 93%

“…In the considerations of these, we suggest that sildenafil may inhibit EFS‐induced contractions over NO. EFS of vas deferens increases the release of NO by its frequency‐dependent effect 15 . Sildenafil antagonized the ATP and EFS‐induced contractions in vas deferens.…”

Section: Discussionmentioning

confidence: 99%

“…EFS (40 V, 20 Hz, 0.5 ms) of vas deferens induced biphasic responses in both segments. It has been demonstrated that EFS of vas deferens caused the release of ATP and NA and these could produce contractions by acting on postjunctional receptors 15,18 . ATP causes rapid and transient contractions by acting over purinergic P 2 receptors and occurs the 1st phase of biphasic response.…”

Section: Discussionmentioning

confidence: 99%

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Possible role of sildenafil in inhibiting rat vas deferens contractions by influencing the purinergic system

et al. 2005

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Aim : To evaluate the effect of sildenafil, a selective inhibitor of cyclic guanosine monophosphate (cGMP)-selective type 5 phosphodiesterase, on isolated rat vas deferens and its connections with the purinergic system. Methods : Epididymal and prostatic portions of isolated vas deferens were placed in organ baths containing Krebs' solution. Contractions were induced by noradrenaline (NA), adenosine triphosphate (ATP), α , β -methylene ATP and electrical field stimulation (EFS). The effect of sildenafil on the contractions was compared with suramin and Evans blue (EB).Results : NA, ATP, α , β -methylene ATP and EFS caused contractions in both portions of vas deferens. NA-induced contractions were unaffected by sildenafil and suramin but potentiated by EB. ATPinduced contractions were non-competitively inhibited in both portions by sildenafil and suramin but potentiated by EB. α , β -methylene ATP-induced contractions were unaffected by sildenafil but were inhibited in both portions by suramin and EB. EFS-induced contractions were inhibited by sildenafil and suramin while potentiated by EB. Conclusion : Sildenafil inhibited the contractions in both portions of vas deferens, as did suramin. We have suggested that purinergic system has a role in this antagonism and it seems to be mediated by an ATP-dependent mechanism instead of a receptor interaction.

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Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway

et al. 2022

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Neurotransmitters adenosine triphosphate and noradrenaline induce nitric oxide release in rat vas deferens

Cited by 4 publications

References 14 publications

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil

Possible role of sildenafil in inhibiting rat vas deferens contractions by influencing the purinergic system

Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway

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