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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneous contractility of rat epididymis was recorded in vivo and the effects of various autonomic drugs were studied. Norepinephrine, epinephrine, and orciprenaline produced a sudden increase in tonus and in the size and frequency of epididymal contractions. Phentolamine (an alpha-blocker agent) inhibited the effects of norepinephrine. On the other hand, alprenolol (a beta-blocker agent) inhibited the effects of orciprenaline but did not block the effects of norepinephrine. In addition, phentolamine and alprenolol decreased the spontaneous activity of the epididymis. Acetylcholine produced effects similar to those of norepinephrine. These effects were blocked by atropine. The results described would indicate the presence of the two receptors, alpha and beta, and that both are mediators of stimulatory effects.
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PMID:Effects of autonomic drugs on epididymal contractions. 0 41

[3-H]Epinephrine binding to isolated purified rat liver plasma membranes is a reversible process. An initial peak in binding occurs at about 15 min and a plateau occurs by 50 min. Optimal binding occurred at a membrane protein concentration of 125mug. Rat liver plasma membranes stored at-70 degrees C up to 4 weeks showed no difference in epinephrine binding capacity as compared to control fresh membranes. Epinephrine binding to liver plasma membranes was decreased by 79% by phospholipase A2 (phosphatide acylhydrolase EC 3.1.1.4), 81% by phospholipase C (phosphatidylcholine choline phosphohydrolase EC 3.1.4.3) and 59% by phospholipase D (phosphatidylcholine phosphatidohydrolase EC 3.1.4.4). Trypsin and pronase digestion of the membrane decreased epinephrine binding by 97 and 47% respectively. In the presence of 10-3M Mg-2+ ions, increasing concentrations of QTP decreased epinephrine binding to liver plasma membranes. A maximal effect was demonstrated with 10-5M GTP, representing an inhibition of 52% of the control. In a Mg-2+ -free system, epinephrine binding was unaffected by GTP. However, in a Mg-2+ -free system, increasing concentrations of ATP cause increasing inhibition of hormone binding. ATP at 10-3 M reduced epinephrine binding to 28% of the control. GRP (10-5 M) was shown to inhibit epinephrine uptake rather than epinephrine release from the membrane. [3-H]Epinephrine binding to isolated rat epididymal fat cells shows an initial peak within 5 min followed by a gradual rise which plateaus after 60 min. Epinephrine binding increased nearly linearly with increasing fat cell protein concentration (40-200 mug protein). GTP (10-5 M) and ATP (10-4 M) decreased epinephrine binding to rat epididymal fat cells by 41%. Nearly complete inhibition of binding was demonstrated with 10-2-10-3M ATP. Epinephrine analogs that contain two hydroxyl groups in the 3 and 4 position on the benzene ring act as inhibitors of [3-H]epinephrine binding to rat adipocytes. Alteration of the epinephrine side chain has relatively little influence on binding. Analogs in which one of the ring hydroxyl groups is missing or methylated are poor inhibitors of [3-H]epinephrine binding. Alpha-(phentolamine and phenoxybenzamine) and beta-(propranolol and dichorisoproterenol) adrenergic blocking agents were tested with respect to their ability to influence [3-H]epinephrine binding and their influence on epinephrine-stimulated lipolysis. Only dichloroisoproterenol significantly inhibited epinephrine binding (by 25%). The two beta-adrenergic blocking agents caused an inhibition of epinephrine-stimulated glycerol release, with propranolol being most effective. Phentolamine and phenoxybenzamine had no significant effect on the epinephrine stimulation of glycerol release by fat cells.
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PMID:Hormone action at the membrane level. IV. Epinephrine binding to rat liver plasma membranes and rat epididymal fat cells. 16 9

The effects of norepinephrine, phentalamine, oxytocin, vasopressin, several prostaglandins, and indomethacin on the spontaneous motility of isolated guinea pig cauda epididymidis were explored. Phentolamine and indomethacin reduced the isometric peak tension of spontaneous epididymal contractions. Phentolamine also depressed the frequency. Both findings suggest that catecholamines and endogenous prostaglandins are in some way regulators of the spontaneous motility of the cauda epididymidis. Norepinephrine resulted in the development of a distinct, sustained, tonic contraction without phasic activity, whereas prostaglandins E1, E2, and F2 alpha elicited a tonic increase accompanied by frequent, superimposed, phasic contractions. Both oxytocin and vasopressin comparably enhanced epididymal motility, producing contractile responses similar to those observed with prostaglandins. Since the epididymal contractions can influence the time spent by spermatozoa in passing through the ductus epididymidis, the above-mentioned compounds could play an important role in spermatozoal transport via modulation of epididymal contractile activity. In addition, such naturally occurring substances might regulate the release of sperm from the last portion of the epididymis into the ductus deferens.
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PMID:Physiologic and pharmacologic studies on the motility of isolated guinea pig cauda epididymidis. 80 41

Electrical field stimulation of ring preparations of the epididymal (Ve) and prostatic (Vp) parts of the human isolated vas deferens produced contractions with similar frequency-dependence and appearance. The contractions of Ve, but not of Vp preparations were abolished by tetrodotoxin (10(-6)M). Noradrenaline (NA), phenylephrine, and methoxamine, but not clonidine induced repetitive, phasic contractions in both Ve and Vp preparations, and increased the amplitude of electrically induced responses. Clonidine concentration-dependently decreased electrically induced contractions in Ve preparations, but had no significant effects in Vp preparations. Phentolamine and prazosin abolished electrically induced contractions in Ve but not in Vp preparations. In Ve rings the contractions were increased by rauwolscine; no such effect was observed in Vp preparations. Isoprenaline, propranolol, acetylcholine and carbachol had no effects in the Ve or Vp preparations. Scopolamine and atropine reduced electrically induced responses. Clonidine decreased and rauwolscine increased the electrically induced release of 3H in both Ve and Vp preparations pre-loaded with 3H-NA. Phenylephrine, prazosin, isoprenaline, propranolol, carbachol and scopolamine had minor or no effects on the 3H release. Radioligand receptor binding experiments using 3H-prazosin and 3H-rauwolscine as ligands revealed similar densities of alpha 1- and alpha 2-adrenoreceptors in the human vas deferens. There seemed to be no differences in their distribution between the epididymal, middle and prostatic part of the organ. It is concluded that the neurotransmission in the human vas deferens is noradrenergic and mediated via alpha 1-adrenoreceptors. The prazosin and tetrodotoxin resistant part of the electrically induced contraction in Vp preparations may be caused by direct smooth muscle stimulation.
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PMID:Effect of drugs interacting with adrenoreceptors and muscarinic receptors in the epididymal and prostatic parts of the human isolated vas deferens. 299 31

1 The proposal that dopamine activates a different population of receptors from those activated by noradrenaline and phenylephrine to cause contraction of the rat vas deferens has been investigated using a preparation of the epididymal half of this tissue. 2 In preparations preincubated in cocaine, oestradiol and propranolol, to block sites of amine loss and beta-adrenoceptors, noradrenaline was the most, and dopamine the least, potent of the three agonists. Phentolamine competitively inhibited each of the agonists to a similar extent. Prazosin also inhibited the actions of the three agonists to a similar extent. These results indicate that the three agonists activate a single population of alpha 1-adrenoceptors to cause contraction in this preparation. 3 In experiments using the prostatic half of the rat vas deferens, in the presence of cocaine, oestradiol, propranolol and prazosin, noradrenaline was approximately 40 times more potent than dopamine in causing inhibition of twitches induced by electrical field stimulation. Yohimbine competitively antagonized the effects of the two agonists to a similar extent indicating that both act at the same population of alpha 2-adrenoceptors. 4 Taken together, these findings do not lend support to proposals that there are populations of specific dopamine receptors located pre- and postjunctionally in the rat vas deferens.
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PMID:Dopamine acts at the same receptors as noradrenaline in the rat isolated vas deferens. 629 87

1. KCl produced a biphasic contraction in the intact rat vas deferens. Both components were larger and the initial rapid phasic component was faster in the prostatic portion than the epididymal portion. In some experiments the epididymal phasic response was a single slow contraction, while in others it had a mixture of fast and slow responses. 2. Phentolamine reduced the phasic response but not the tonic response of the intact vas deferens. This effect was not observed after denervation produced by chronic guanethidine treatment. 3. Both phases of the response to KCl 160 mmol/l were substantially reduced by phentolamine in the epididymal portion. In the prostatic portion phentolamine produced only slight inhibition of the phasic component and had no effect on the tonic component. 4. Isoprenaline had no effect on the response to KCl 160 mmol/l but reduced both phases of the response to KCl 50 mmol/l. This effect was antagonized by propranolol. 5. It is concluded that part of the phasic component of the response to KCl in the rat vas deferens is due to the release of noradrenaline from intramural nerves.
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PMID:KCl contractions in the rat intact and bisected vas deferens: contribution of endogenous noradrenaline release. 683 53

1 5-Hydroxytryptamine (5-HT) (5.16-1291 microM) produced a phasic contraction followed later by rhythmic contractions in the rat vas deferens, primarily in the epididymal half. 5-HT (129 microM) produced no response in Ca2+-free solution. Nifedipine (0.29 microM) or verapamil (2.04 microM) inhibited the initial phasic response to 5-HT, but inhibition of the rhythmic contractions required concentrations 5 fold (nifedipine) or 30 fold (verapamil) higher. 2 Methysergide (2.13 microM) abolished the phasic and reduced the frequency of the rhythmic contractions. Phentolamine (2.65 microM) did not affect the phasic response but reduced the amplitude of the rhythmic contractions. The combination of phentolamine (2.65 microM) and methysergide (2.13 microM) completely abolished the response to 5-HT (129 microM). 3 Desipramine (1.32 microM) had no effect on the phasic response to 5-HT (129 microM), but the rhythmic contractions were reduced in amplitude with no effect on their frequency. 4 In vasa deferentia removed from reserpine-treated or from guanethidine-denervated rats, both phasic and rhythmic components of the 5-HT (129 microM) contraction were augmented due to supersensitivity. 5 It is concluded that the phasic component of the 5-HT contraction is mediated by post-junctional 5-HT receptors, while the rhythmic component is mediated by the combination of post-junctional 5-HT receptors and noradrenaline released from neuronal stores. Assuming that nifedipine and verapamil are acting solely by inhibition of calcium channels, the phasic and rhythmic components of the 5-HT response may be mediated through separate Ca2+ channels. If this is correct, one channel might be a voltage-dependent channel and the other could be similar to, but distinct from the channel mediating the response to methoxamine.
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PMID:The contractile effects of 5-hydroxytryptamine on the rat isolated vas deferens. 715 Aug 68

1. Age-related changes in the reactivity of postsynaptic alpha-adrenoceptors of isolated portions (epididymal and prostatic) and in whole vas deferens have been studied using 4, 12 and 20 month-old rats. 2. The pD2 values for adrenaline-induced contractions were reduced in the epididymal portion and whole vas deferens of middle-aged and old animals, but not in the prostatic portion. No age related change to phenylephrine or clonidine sensitivity was observed. 3. pA2 values of prazosin and yohimbine were not changed by aging in any preparation. Phentolamine pA2 values were reduced in the epididymal portion and in the whole vas deferens when adrenaline, but not when phenylephrine concentration-response curves were displaced by the antagonist. The mean pA2 value of yohimbine (6.78) indicates that this antagonist blocks alpha(1)-adrenoceptors in the rat vas deferens. 4. The data presented here suggest that age-related decreases in the sensitivity to adrenaline and phentolamine (when measured by displacing adrenaline concentration-effect curves) in the whole vas deferens are probably due to a variation in the proportion of alpha(1)-adrenoceptor subtypes in the epididymal portion of the rat vas deferens.
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PMID:Age-related changes in the reactivity of postsynaptic adrenoceptors in the rat vas deferens: differences between the epididymal and prostatic portion. 927 74