Nitric oxide as neuromodulator of sympathetic transmission in rat vas deferens

Postorino, A.; Vetri, T.; Leggio, Loredana; Serio, Rosa; Bonvissuto, F.

doi:10.1046/j.1365-2680.1998.1810021.x

Cited by 16 publications

(17 citation statements)

References 22 publications

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“…1A). Although the nitrergic route did not seem to possess any physiological role, it has been demonstrated that exogenous NO could inhibit neurotransmission in rat vas deferens (Cederqvist and Gustafsson, 1994), although opposite effects, e.g., an enhancement of neurotransmission, have also been observed (Postorino et al, 1998;Ventura et al, 1998). In our experiments, NO released from SNAP clearly inhibited sympathetic neurotransmission (Fig.…”

Section: Discussioncontrasting

confidence: 44%

“…Although some reports have been published on the attenuation of neurotransmission by using NOS-inhibitors such as L-NAME or L-NNA (Vladimirova et al, 1994;Postorino et al, 1998), most researchers have observed no effect with these inhibitors (Allawi et al, 1994;Ventura and Burnstock, 1997;Ventura et al, 1998). These observations cast doubts on the participation of endogenous NO on neurotransmission in rat vas deferens.…”

Section: Discussionmentioning

confidence: 97%

“…Thus, considering that agmatine and NO share the same biosynthetic metabolic route and also that the stimulation of α 2 -adrenoceptors is able to cause nitric oxide-mediated vascular relaxation (Bockman et al, 1996), we reasoned that nitric oxide could play a role in the action of agmatine in the epididymal end of rat vas deferens. On the other hand, a role for NO in neurotransmission in the rat vas deferens remained controversial (Vladimirova et al, 1994;Ventura and Burnstock, 1997;Postorino et al, 1998). Therefore, in this work, we investigated the participation of a NO-pathway on the effects of agmatine in the vas deferens preparation.…”

Section: Introductionmentioning

confidence: 96%

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l-NAME pre-treatment partially inhibits the agmatine-evoked depression of the electrically induced twitch contraction of isolated rat vas deferens

Garcez-do-Carmo¹,

Santos²

2006

Life Sciences

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Section: Discussioncontrasting

confidence: 44%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 96%

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l-NAME pre-treatment partially inhibits the agmatine-evoked depression of the electrically induced twitch contraction of isolated rat vas deferens

Garcez-do-Carmo¹,

Santos²

2006

Life Sciences

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“…NOS is present not only in vascular endothelial cells (endothelial NOS) but also in perivascular nerves [neuronal NOS (nNOS)] (Moncada and Higgs, 1995;Sosunov et al, 1995). Inhibition of NOS by NOS inhibitors such as the nonselective NOS inhibitor N--nitro-L-arginine methyl ester (L-NAME) has been reported to augment the vasoconstrictor effect induced by PNS in various isolated blood vessels, whereas the enhanced PNS-induced responses to NOS inhibitors are reversed by L-arginine, a precursor for the synthesis of NO, and involve the endothelium-derived NO (Toda and Okamura, 1990;Postorino et al, 1998). On the other hand, several studies showed that NOS inhibitors have no effect on vasoconstriction in response to PNS in dog pulmonary arteries and human omental arteries without endothelium (Aldasoro et al, 1993;Segarra et al, 1999).…”

mentioning

confidence: 99%

Neuronal Nitric-Oxide Synthase Inhibition Facilitates Adrenergic Neurotransmission in Rat Mesenteric Resistance Arteries

Hatanaka

Hobara

Jin

et al. 2005

J Pharmacol Exp Ther

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The effects of nonselective nitric-oxide synthase (NOS) inhibitors [N--nitro-L-arginine methyl ester (L-NAME) and N--nitro-L-arginine (L-NNA)] and specific neuronal NOS (nNOSon adrenergic nerve-mediated vasoconstriction were studied in rat perfused mesenteric vascular beds without endothelium. Perfusion of L-NAME, L-NNA, or L-VNIO markedly augmented vasoconstrictor responses to periarterial nerve stimulation (PNS; 2-8 Hz) without affecting vasoconstriction induced by exogenously injected norepinephrine (NE). Addition of L-arginine, a precursor for the synthesis of nitric oxide (NO), reversed the augmentation of the PNS response by L-NAME. The PNS (8 Hz)-evoked NE release in the perfusate was increased by L-NAME perfusion. In preparations treated with capsaicin [a depleter of calcitonin gene-related peptide (CGRP)-containing nerves], L-NAME did not augment vasoconstrictor responses to PNS or NE injection. Combined perfusion of CGRP(8-37) (a CGRP receptor antagonist) and L-NAME induced additive augmentation of the vasoconstrictor response to PNS but did not affect the response to NE injection. In preparations with active tone produced by methoxamine and in the presence of guanethidine, L-NAME perfusion did not affect the vasodilator response induced by PNS. Immunostaining of the mesenteric artery showed the presence of nNOS-like immunopositive nerve fibers, which were absent in arteries pretreated with capsaicin. These findings suggest that NO, which is released from perivascular capsaicin-sensitive nerves, presynaptically inhibits neurogenic NE release to modulate adrenergic neurotransmission.

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“…In contrast, (Postorino et al. 1998; Nakanishi et al. 2006) reported that NO facilitates sympathetic neurotransmission in rat and guinea-pig vas deferens rather than inhibiting it.…”

Section: Discussionmentioning

confidence: 99%

Regulation of nerve-evoked contractions of rabbit vas deferens by acetylcholine

et al. 2015

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Stimulation of intramural nerves in the vas deferens of many species yields a classical biphasic contraction comprised of an initial fast component, mediated by P2X receptors and a second slower component, mediated by α1-adrenoceptors. It is also recognized that sympathetic nerve-mediated contractions of the vas deferens can be modulated by acetylcholine (Ach), however there is considerable disagreement in the literature regarding the precise contribution of cholinergic nerves to contraction of the vas deferens. In this study we examined the effect of cholinergic modulators on electric field stimulation (EFS)-evoked contractions of rabbit vas deferens and on cytosolic Ca2+ levels in isolated vas deferens smooth muscle cells (VDSMC). The sustained component of EFS-evoked contractions was inhibited by atropine and by the selective M3R antagonist, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP). EFS-evoked contractions were potentiated by Ach, carbachol (Cch), and neostigmine. The sustained phase of the EFS-evoked contraction was inhibited by prazosin, an α1-adrenoceptor antagonist and guanethidine, an inhibitor of noradrenaline release, even in the continued presence of Ach, Cch or neostigmine. The soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one enhanced the amplitude of EFS-evoked contractions and reduced the inhibitory effects of 4-DAMP. Isolated VDSMC displayed spontaneous Ca2+ oscillations, but did not respond to Cch. However, the α1-adrenoceptor agonist, phenylephrine, evoked a Ca2+ transient and contracted the cells. These data suggest that EFS-evoked contractions of the rabbit vas deferens are potentiated by activation of M3 receptors and reduced by activation of a sGC-dependent inhibitory pathway.

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Nitric oxide as neuromodulator of sympathetic transmission in rat vas deferens

Cited by 16 publications

References 22 publications

l-NAME pre-treatment partially inhibits the agmatine-evoked depression of the electrically induced twitch contraction of isolated rat vas deferens

l-NAME pre-treatment partially inhibits the agmatine-evoked depression of the electrically induced twitch contraction of isolated rat vas deferens

Neuronal Nitric-Oxide Synthase Inhibition Facilitates Adrenergic Neurotransmission in Rat Mesenteric Resistance Arteries

Regulation of nerve-evoked contractions of rabbit vas deferens by acetylcholine

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