Evidence for α1-adrenoceptor subtype predominance in the rat seminal vesicle

Adenekan, O. O.

doi:10.1111/j.2042-7158.1989.tb06453.x

Cited by 9 publications

(5 citation statements)

References 11 publications

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“…Such a mechanism was suggested by Sharif et a1 (1990) who performed a detailed study of clonidine on noradrenaline and phenylephrine responses in rat seminal vesicle, concluding that clonidine acted as a competitive antagonist at aI -adrenoceptors. Inhibition of noradrenaline by yohimbine is suggested to be due to antagonism of postjunctional al -adrenoceptors (Adenekan 1989;Sharif et al 1990), since the selectivity of yohimbine between a I -and HASSAN.SADRAE1 ET AL a,-adrenoceptors is in the order of tenfold (Kobinger & Pichler 1980;McGrath 1982). The reported absence of a,-binding sites in this tissue (Shima 1993) is entirely compatible with the effects of clonidine and yohimbine reported above.…”

Section: Discussionsupporting

confidence: 79%

“…However, there is little information about the functional significance of these peptides, although some authors point to the possibility of co-transmission between noradrenaline and neuropeptide Y , or ATP (Nakanishi & Takeda 1973;Meldrum & Burnstock 1985;Stjernquist et a1 1987;Wali & Greenidge 1989). Of the post-synaptic receptors in rat vesicular smooth muscle, adrenoceptors are mainly of the @,-subtype (Gokhale & Sharif 1983;Adenekan 1989;Sharif et a1 1990), and the cholinoceptors are muscarinic. The nature of any pre-synaptic receptors is unknown.…”

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confidence: 99%

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Mechanisms Involved in Electrically-induced Responses of Rat Seminal Vesicles

Sadraei

Large

Hughes

1995

Journal of Pharmacy and Pharmacology

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Contractile responses of rat isolated seminal vesicle were elicited by electrical field stimulation (EFS, 10 Hz, 1 ms, 40 V for 5 s), noradrenaline (1 x 10(-5) M) and carbachol (1 x 10(-5) M). Guanethidine (2 x 10(-5)-5 x 10(-4) M) progressively reduced the contraction induced by EFS and carbachol to 24 +/- 2 and 10 +/- 2%, respectively, at the highest concentration (n = 6), while potentiating noradrenaline contraction to a maximum of 154 +/- 14% at 2 x 10(-5) M (n = 6). Prazosin (1 x 10(-6) M) and atropine (2.5 x 10(-7) M) completely abolished the response to the corresponding agonist and each reduced the response to EFS to 64 +/- 8 and 61 +/- 3%, respectively (n = 6). In the presence of both atropine and prazosin a small contraction to EFS remained (14 +/- 4%, n = 6), which is unlikely to be due to ATP, since exogenous ATP did not induce a contractile response and had an inhibitory effect on EFS-induced responses. Clonidine (1.25 x 10(-5) M) completely blocked responses to noradrenaline and reduced the responses to EFS to 68 +/- 7% (n = 6). However, when both the adrenergic and cholinergic components of EFS were blocked by prazosin and atropine, clonidine potentiated the remaining response to EFS (323 +/- 82%, n = 4). Yohimbine (1 x 10(-5) M) blocked the response to noradrenaline and reduced the response to EFS to 37 +/- 5% (n = 6) while the carbachol response was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 79%

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confidence: 99%

Mechanisms Involved in Electrically-induced Responses of Rat Seminal Vesicles

Sadraei

Large

Hughes

1995

Journal of Pharmacy and Pharmacology

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“…17 The greater effects of these agents in the seminal vesicle than in the vasa deferentia may be related to the predominance of a1-adrenoceptors in the rat seminal vesicle. 18 These results are consistent with those of Hsieh et al, 19 who reported that sympatholytic drugs effectively attenuated contractile responses in the seminal vesicle induced by electrical nerve stimulation of lesser splanchnic nerve in rats. Although the a-blockers included in this study served as a positive, internal control to confirm the viability of this modified rat model, Cavallini demonstrated the therapeutic efficacy of a1-adrenergic blockers (alphuzosin and terazosin) for premature ejaculation in a double-blind, placebo-controlled, crossover clinical trial.…”

Section: Discussionsupporting

confidence: 91%

In vivo rat model to measure hypogastric nerve stimulation-induced seminal vesicle and vasal pressure responses simultaneously

Paick

2004

Int J Impot Res

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This study presents a modified in vivo model in which the intraluminal pressures of the seminal vesicle and vas deferens can be measured simultaneously. Male Sprague-Dawley rats were grouped based on agent administered: serotonin, clomipramine, fluoxetine, sertraline, paroxetine, prazosin, terazosin, and tamsulosin. The control responses to hypogastric nerve stimulation (HNS) were recorded in each animal, and HNS was repeated after each drug administration. Serotonergic agents resulted in concentration-dependent inhibition of the HNS-induced seminal vesicle pressure increases (clomipramine4serotonin4fluoxetine4sertralineEparoxetine). On the other hand, only serotonin and clomipramine significantly inhibited vasal pressure responses. a-Adrenergic blockers inhibited both intraluminal pressure responses in a concentration-dependent manner. This model illustrates the importance of the hypogastric nerve for the stimulation of the seminal tract, with attention focused on the seminal vesicle. This model may be useful for the evaluation of drugs for the treatment of premature ejaculation.

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“…Sympathetic, noradrenergic fibers have been visualized within the smooth muscle layers of the seminal vesicles [6][7][8], in which the release of noradrenaline results in muscle contractions, mediated via otl-adrenoceptors [9,10]. Sympathetic innervation may also be visualized by immunolabeling neuropeptide Y (NPY), which is found in all noradrenergic terminals in the pelvic viscera of male rats [11].…”

Section: Introductionmentioning

confidence: 99%

Location, Immunohistochemical Features, and Spinal Connections of Autonomic Neurons Innervating the Rat Seminal Vesicles1

Kepper

Keast

1997

Biology of Reproduction

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With the use of retrograde tracing techniques, selective spinal nerve transections, and immunohistochemistry to label noradrenergic and peptidergic pathways, this study has for the first time defined in detail the autonomic innervation to the rat seminal vesicles. The majority of this innervation originates from the bilateral major pelvic ganglia, whereas very few neurons are located in the accessory, inferior mesenteric, or paravertebral chain ganglia. Neuropeptide Y was the most abundant marker, followed by tyrosine hydroxylase (an enzyme involved in noradrenaline synthesis), and then vasoactive intestinal peptide. Sympathetic axons with tyrosine hydroxylase and neuropeptide Y supplied vascular and nonvascular smooth muscle whereas parasympathetic, cholinergic neuropeptide Y terminals were associated with the glandular epithelium. In contrast, vasoactive intestinal peptide was found only in cholinergic neurons, which may have either parasympathetic or sympathetic spinal connections. The latter were far more prevalent, demonstrating a substantial sympathetic cholinergic innervation to the seminal vesicles. Vasoactive intestinal peptide axons were associated with the glandular epithelia, as well as vascular and nonvascular smooth muscle. Axons associated with the secretory epithelia may regulate secretion or perhaps provide trophic support. Finally, acute damage to preganglionic sacral and lumbar nerves caused a transient increase in glandular weight.

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Evidence for α1-adrenoceptor subtype predominance in the rat seminal vesicle

Cited by 9 publications

References 11 publications

Mechanisms Involved in Electrically-induced Responses of Rat Seminal Vesicles

Mechanisms Involved in Electrically-induced Responses of Rat Seminal Vesicles

In vivo rat model to measure hypogastric nerve stimulation-induced seminal vesicle and vasal pressure responses simultaneously

Location, Immunohistochemical Features, and Spinal Connections of Autonomic Neurons Innervating the Rat Seminal Vesicles1

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