Separation of adrenergic and non‐adrenergic contractions to field stimulation in the rat vas deferens

Brown, D. A.; Docherty, James R.; French, A M; Macdonald, Angus; McGrath, J.C.; Scott, N C

doi:10.1111/j.1476-5381.1983.tb11010.x

Cited by 126 publications

(88 citation statements)

References 20 publications

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“…Conotoxin inhibited contractions elicited by field stimulation of noradrenergic nerves in epididymal portions of the rat vas deferens, which are predominantly mediated by noradrenaline (McGrath, 1978;Brown et al, 1983 previously shown that conotoxin also inhibits responses to field stimulation in the prostatic portion of the rat vas deferens, where ATP is the predominant transmitter (Sneddon & Westfall, 1984 (Clasbrummel et al, 1989). Relaxations of smooth muscle elicited by noradrenergic nerve stimulation were inhibited by conotoxin in the rat and rabbit jejunum.…”

Section: Effects Ofconotoxin On Noradrenergic Transmissionmentioning

confidence: 98%

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

Luca

Rand

et al. 1990

British J Pharmacology

101

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1 The effects of co-conotoxin GVIA (conotoxin), a potent inhibitor of neuronal N-type Ca2+ channels, have been examined on responses to stimulation of noradrenergic, cholinergic and non-adrenergic, noncholinergic (NANC) nerves in a range of isolated tissues to investigate the role of conotoxin-sensitive Ca2 + channels in neurotransmission. 2 Contractions elicited by field stimulation of noradrenergic nerves in rat and mouse anococcygeus muscles, rabbit ear artery and rat vas deferens (epididymal portion) were inhibited by conotoxin. Responses to noradrenaline, and to adenosine triphosphate in the vas deferens, were not affected. 3 Positive chronotropic responses to field stimulation of noradrenergic nerves were inhibited by conotoxin in rat and mouse atria, but responses to noradrenaline and tyramine were not affected. 4 The stimulation-induced release of noradrenaline was inhibited by conotoxin in the rabbit ear artery and in rat and mouse atria. 5 Relaxations in response to stimulation of the noradrenergic perivascular mesenteric nerves were reduced or abolished by conotoxin in rat and rabbit jejunum. The response to noradrenaline in rat jejunum was not affected. 6 Contractions elicited by stimulation of cholinergic nerves were inhibited by conotoxin in rat jejunum and mouse ileum (perivascular mesenteric nerves), and in guinea-pig taenia caeci (field stimulation). Responses to acetylcholine in rat jejunum and mouse ileum were not affected. 7 Contractions elicted by stimulation of the cholinergic plus NANC pelvic nerves were inhibited by conotoxin in rabbit colon, and to a lesser extent in guinea-pig colon. The stimulation-induced contraction of the guinea-pig colon was inhibited by conotoxin by a greater proportion in the presence than in the absence of atropine. Responses to acetylcholine were not affected in the rabbit colon but were slightly reduced in the guinea-pig colon. 8 Relaxations in response to field stimulation of NANC nerves were inhibited by conotoxin in guineapig taenia caeci and rat gastric fundus strips, and in rat anococcygeus muscle when the tone was raised by guanethidine but not when it was raised by carbachol. The relaxations produced by sodium nitroprusside in the rat gastric fundus and anococcygeus were not affected. 9 Contractions of the rat bladder elicited by stimulation of the peri-urethral nerves, which are NANCand cholinergically mediated, were relatively insensitive to inhibition by conotoxin. The responses were almost completely abolished by tetrodotoxin. 10 The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin.11 The inhibitory effect of conotoxin was inversely proportional to the frequency of stimulation (in several preparations) and to the Ca2+ concentration in the bathing solution (in rat vas deferens). These observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation-secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated st...

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Section: Effects Ofconotoxin On Noradrenergic Transmissionmentioning

confidence: 98%

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

Luca

Rand

et al. 1990

British J Pharmacology

101

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“…Thus,`pure' presynaptic a 2 -adrenoceptor antagonistic actions of test compounds cannot be determined in this type of experimental condition. Brown et al (1983) have reported that the non-adrenergic component is dominant in the contraction induced by electrical stimuli in the prostatic portion of the vas deferens when stimulation was carried out at a lower frequency, viz., 0.1 Hz. Thus, the same stimulation frequency was used in the present study.…”

Section: Discussionmentioning

confidence: 99%

α₂‐adrenoceptor antagonist properties of OPC‐28326, a novel selective peripheral vasodilator

Orito

Kishi

Imaizumi

et al. 2001

British J Pharmacology

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1 Antagonistic properties of OPC-28326 ([4-(N-methyl-2-phenylethylamino)-1-(3,5-dimethyl-4-propionyl-aminobenzoyl)] piperidine hydrochloride monohydrate), a selective peripheral vasodilator, were investigated by analysing the data from functional studies in various tissues from the rat and binding studies of the drug to a 2 -adrenoceptor subtypes. 2 Using a human recombinant receptor and rat kidney cortex, we found that OPC-28326 displays a nities to a 2A -, a 2B -and a 2C -adrenoceptors with K i values of 2040, 285, and 55 nM, respectively. The K i values of yohimbine for a 2A -, a 2B -, and a 2C -adrenoceptors were 3.0, 2.0 and 11.0 nM, respectively. 3 B-HT 920, an a 2 -adrenoceptor agonist, produced a pressor response via peripheral postsynaptic a 2 -adrenoceptor stimulation (thought to be an a 2B -subtype) in a reserpine-pretreated pithed rat preparation. OPC-28326 (3 ± 30 mg kg 71 , i.v.) and yohimbine (0.3 ± 3 mg kg 71 , i.v.) caused dosedependent rightward shift in the pressor dose-response curve induced by B-HT 920. The apparent pA 2 values were 1.55 (0.87 ± 2.75, 95% con®dence interval) and 0.11 (0.06 ± 0.21) mg kg 71 , respectively. The potency of OPC-28326 was about 14 times less than that of yohimbine. 4 Clonidine inhibited the tension developed by electrical stimulation, of the rat vas deferens, by its peripheral presynaptic a 2A/D -adrenoceptor action. OPC-28326 (1 ± 100 mM) and yohimbine (10 ± 1000 nM) caused a rightward shift in the concentration-response curve of clonidine. The pA 2 values were 5.73 (5.54 ± 5.91) and 7.92 (7.84 ± 8.01), respectively, providing evidence for a potency of OPC-28326 of about 155 times less than that of yohimbine. 5 Mydriasis was induced by brimonidine via stimulation of central a 2A/D -adrenoceptors in anaesthetized rats. Intravenous OPC-28326 had no e ect on this action, even at a very high dose of 10 mg kg 71 i.v., while yohimbine (0.1 ± 0.3 mg kg 71 i.v.) inhibited mydriasis in a dose-dependent manner, indicating that OPC-28326 was at least 100 times less potent than yohimbine in regard to the anti-mydriatic e ect. 6 These data suggest that OPC-28326 preferentially exerts peripheral and postsynaptic antagonistic actions on the a 2B -and a 2C -adrenoceptor subtypes.

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“…It also binds to nicotinic receptors from adrenergic varicosities resulting in noradrenaline release (Carneiro;Markus, 1990). Noradrenaline appears to be the main transmitter in rat vas deferens and its effects are abolished by α-adrenergic but not by β-adrenergic antagonists (Brown et al, 1983). There are also strong evidences for the participation of a non-cholinergic and non-adrenergic neurotransmitter in rat vas deferens (Sneddon et al, 1982;Burnstock, 1984).…”

Section: Introductionmentioning

confidence: 93%

Relaxant effect of the aqueous extract of Erythrina vellutina leaves on rat vas deferens

Santos¹,

Alves²,

Antoniolli³

et al. 2007

Rev. bras. farmacogn.

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RESUMO: "Efeito relaxante do extrato aquoso das folhas de Erythrina vellutina em ducto deferente de rato". O objetivo deste trabalho foi avaliar o efeito do extrato aquoso das folhas de Erythrina vellutina (AE) sobre ducto deferente de rato. Nesta preparação, o AE inibiu as contrações induzidas por estímulo elétrico de campo de maneira dependente da concentração. Esta inibição não foi afetada após atropina (10 -5 M), propanolol (10 -5 M), prazosin (10 -5 M) ou yohimbina (10 -5 M), sugerindo uma ação indireta do AE sobre receptores colinérgicos ou adrenérgicos. A incubação da preparação com os antagonistas de canais de K + , tetraetilâmonio (10 -6 M) ou 4-aminopiridina (10 -6 M) não alterou o efeito inibitório induzido pelo AE. Entretanto, a glibenclamida (10 -6 M) atenuou signifi cantemente este efeito, sugerindo um possível envolvimento de canais de K + dependentes de ATP. Além disso, o AE (0.15 mg/mL) não alterou as contrações induzidas por noradrenalina (10 -5 M), ATP (10 -4 M) ou KCl (80 mM), descartando uma interação do AE com um sítio pós-sináptico. Em conclusão, estes resultados demonstram que o efeito inibitório do AE pode ser devido a uma interação pré-sináptica com canais de K + dependentes de ATP em neurônios simpáticos de ducto deferente de rato.Unitermos: Erythrina vellutina, ducto deferente de rato, canal de K + dependente de ATP. ABSTRACT:The effect of the Aqueous Extract from the leaves of Erythrina vellutina (AE) on rat vas deferens preparation was evaluated in this work. The AE inhibited the muscle contractions induced by electrical fi eld stimulation (EFS) in a concentration-dependent manner. This inhibition was not affected by atropine (10 -5 M), propanolol (10 -5 M), prazosin (10 -5 M) or yohimbine (10 -5 M), suggesting that there is no direct interaction of the AE with cholinergic nor adrenergic receptors. Incubation of vas deferens with the K + channel antagonists, tetraethylamonium (10 -6 M) or 4-aminopyridine (10 -6 M) had also no effect on the AE-induced inhibition. On the other hand, glibenclamide (10 -6 ) signifi cantly attenuated the effect of the AE, suggesting a possible involvement of ATP-dependent K + channels. The AE (0.15 mg/mL) did not alter the contractions induced by noradrenaline (10 -5 M), ATP (10 -4 M) nor KCl (80 mM), against an interaction of the extract with post-synaptic sites. The data presented suggests that the inhibition of the electrically driven muscle twitches by the AE could be due to a pre-synaptic interaction of the extract with ATP-dependent K + channels from vas deferens sympathetic neurons.

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Separation of adrenergic and non‐adrenergic contractions to field stimulation in the rat vas deferens

Cited by 126 publications

References 20 publications

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

α₂‐adrenoceptor antagonist properties of OPC‐28326, a novel selective peripheral vasodilator

Relaxant effect of the aqueous extract of Erythrina vellutina leaves on rat vas deferens

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Separation of adrenergic and non‐adrenergic contractions to field stimulation in the rat vas deferens

Cited by 126 publications

References 20 publications

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

α2‐adrenoceptor antagonist properties of OPC‐28326, a novel selective peripheral vasodilator

Relaxant effect of the aqueous extract of Erythrina vellutina leaves on rat vas deferens

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Product

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α₂‐adrenoceptor antagonist properties of OPC‐28326, a novel selective peripheral vasodilator