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

A study was carried out to investigate the role of the calcitonin gene-related peptide (CGRP) in the regulation of electrolyte transport in the rat and human epididymis. In monolayer cultures derived from the rat cauda epididymal cells, CGRP stimulated the short-circuit current (SCC) in a dose-dependent manner with the EC50 (concentration required to produce 50% of the response) at 15 nmol/l. This effect of CGRP was seen when the peptide was added to the basolateral aspect of the cells; apical addition having negligible effect. The CGRP-induced rise in the SCC was dependent on the presence of chloride in the bathing solution. Calcitonin had no effect on the SCC and did not affect the CGRP-induced rise in the SCC. The effect of CGRP on secretion was inhibited in a competitive fashion by the CGRP receptor antagonist CGRP(8-37). In contrast to bradykinin, angiotensin II and endothelin I, the effect of CGRP was independent of prostaglandin synthesis. Measurement of intracellular adenosine 3':5'-cyclic monophosphate showed a time- and dose-dependent increase upon stimulation with CGRP. CGRP also stimulated the SCC in monolayers grown from the human epididymis. The current could be inhibited by apical application of the chloride channel blocker, diphenylamine-2-carboxylate. Immunoreactive CGRP was found in the epithelia of rat and human cauda epididymidis. It is suggested that CGRP may regulate the electrolyte and fluid secretion in the epididymis, thereby providing an optimal microenvironment for the maturation and storage of spermatozoa.
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PMID:The role of calcitonin gene-related peptide in the regulation of anion secretion by the rat and human epididymis. 131 50

Confluent monolayers cultured from the rat cauda epididymidis have been shown to respond to angiotensin I (AI) and angiotensin II (AII) when studied under short-circuit conditions and bathed on both sides with Krebs-Henseleit solution. Both the decapeptide AI and the octapeptide AII elicited transient increases in short-circuit current (SCC) when added to the basolateral as well as to the apical surfaces, with the effect of basolateral application greater than that of apical application. The maximal responses produced by AI and AII were similar with median effective concentrations of 20 to 80 nmol/l. The increase in SCC by AII was dependent upon extracellular Cl- and was inhibited by addition of a Cl- channel blocker, diphenylamine 2-carboxylate, to the apical surface. These patterns of activity suggest that the SCC responses to angiotensins result from electrogenic chloride secretion. Pretreating the monolayers with captopril (100 nmol/l), an angiotensin-converting enzyme (ACE) inhibitor, reduced the response to basolateral application of AI, but completely abolished the response to AI added apically. These results suggest that the response to apical addition of AI was due to conversion of AI to AII which interacts with apical angiotensin receptors. This conversion was mediated by ACE which has been detected in epididymal monolayers. Of the endogenous ACE activity, 86% was found to be inhibited by captopril (100 nmol/l). Responses of the epididymal monolayers to angiotensins were mediated by specific angiotensin receptors. [Sar1,Ile8]-AII, a specific antagonist of the AII receptor, completely inhibited the responses to AI and AII but had no effect on the responses to bradykinin and endothelin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of angiotensins on electrogenic anion transport in monolayer cultures of rat epididymis. 216 24

To investigate the nature of the bradykinin-induced potentiation of electrically driven muscle twitches in the isolated vas deferens, bradykinin, noradrenaline and adenosine 5'-triphosphate (ATP) concentration-response curves were made with control, reserpinized and chemically sympathectomized rats. Bradykinin potentiated the ATP- but not the noradrenaline-induced contractions in the epididymal and prostatic segments of the ductus. The epididymal segment of the ductus did not respond to transmural electrical stimulation following reserpine treatment. Bradykinin potentiated the muscular contractions caused by exogenous ATP but not by noradrenaline. In contrast, the transmurally evoked twitches of the prostatic portion of the ductus remained almost unaltered; bradykinin increased the motor effect of ATP without modifying the potency of noradrenaline. All neuronally induced contractile activity was absent in sympathectomized rats; bradykinin potentiated the contractile effect of ATP without altering the noradrenaline-induced contractions. These results suggest that bradykinin potentiates the ATP-evoked contractions by acting postjunctionally.
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PMID:Involvement of postjunctional purinergic mechanisms in the facilitatory action of bradykinin in neurotransmission in the rat vas deferens. 254 29

Adrenergic and purinergic compounds contract the longitudinal muscles of the rat vas deferens. Whereas ATP and related purinergic analogs produced contractions of greater magnitude in the prostatic half as compared to that of the epididymal end, the magnitude of the alpha 1-adrenoceptor-induced responses was larger in the epididymal than in the prostatic half of the rat ductus. Chemical sympathectomy following a 48 hr 6-hydroxydopamine-treatment (6-OHDA) caused a leftward displacement of the concentration-response curves for adrenergic and purinergic drugs, this effect being more evident in the prostatic segment. Sympathectomy caused a significant increase in the maximal response induced by ATP and adrenergic compounds which was more evident in the prostatic half of the rat ductus. The denervation-induced supersensitivity was stimulus-specific since angiotensin II and acetylcholine showed no significant change in potency. In the case of bradykinin, there was a manifest increase in the maximal response of the prostatic segment of the ductus of the chemically denervated tissues. In addition, denervation also caused an increase in the potency of prazosin and phentolamine as alpha 1-adrenoceptor blocking agents; denervation did not change the potency of yohimbine as an alpha 2-adrenoceptor blocker.
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PMID:Purinergic supersensitivity following sympathectomy adds further support to co-transmission in the rat vas deferens. 285 33

The application of bradykinin to the isolated, transmurally stimulated rat vas deferens caused two effects: increase of the basal tension of the tissue and potentiation of the magnitude of electrically driven twitches. These bradykinin responses were not evenly distributed along the ductus. The direct contractile action of bradykinin was found to be stronger in the epididymal half of the tissue while the potentiation of the muscle twitches was more pronounced in the prostatic half of the rat ductus. Bradykinin is more potent to potentiate the electrically driven twitches than to act as a postjunctional agonist. Tyr-bradykinin, [Tyr5]bradykinin and [Tyr8]bradykinin exhibited significant differences in the potency ratio to produce each of these responses. [Thi5,8,D-Phe7]bradykinin is a weak postjunctional agonist but was a full agonist to potentiate the electrically induced twitches. Furthermore, this compound antagonized the bradykinin-induced contractions. [Hyp3,Thi5,8,D-Phe7]bradykinin was devoid of agonist activity at either pre- or postjunctional sites; it behaved as a pure antagonist and was more than potent its non-hydroxylated analog. The addition of a D-Arg residue at the amino terminal increased the antagonist potency significantly. The pA2 of D-Arg-[Hyp3,Thi5,8,D-Phe7]bradykinin to antagonize the postjunctional effect of bradykinin was 6.35, a value that differed significantly from the value of 6.93 required to block the prejunctional effect of the peptide. The bradykinin receptor antagonists did not modify significantly the magnitude of the contractile responses caused by angiotensin II, norepinephrine or 5-hydroxy-tryptamine.
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PMID:Bradykinin receptor antagonists used to characterize the heterogeneity of bradykinin-induced responses in rat vas deferens. 289 46

In order to investigate the role of pericytes (PCs) at microvascular level, a PC line from rat epididymal fat pads was isolated and its prostanoid production in culture was further examined. PC cultures were characterized morphologically by phase contrast and electron microscopy. PC prostanoid production was compared with that of a smooth muscle cell (SMC) line isolated from bovine aorta. The same PGI2 production magnitude was assayed in PC and SMC cultures, but TXA2 and PGF2 alpha synthesis was 8-10 times higher in the PC line. At 4-day postconfluence, when PC layers started retraction, prostanoid synthesis was significantly lower than at confluence. Histamine and bradykinin (both 100 nM) acted similarly, increasing the PGI2 basal production of PC cultures. The results argue for a possible contractile role of PCs at microvascular level.
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PMID:Culture of pericytes isolated from rat adipose microvasculature and characterization of their prostanoid production. 306 95

1. Exogenous adenosine triphosphate (ATP) stimulated the short circuit current (SCC) in primary monolayer cultures of rat epididymal cells when added to the apical but not to the basolateral side of the monolayers. Half-maximal stimulation was achieved at 5 x 10(-8) M ATP. 2. The increase in SCC induced by ATP was dependent on the presence of extracellular Cl in the bathing solutions. 3. The effects of other adenosine derivatives, and purine and pyrimidine nucleotides were studied. Their orders of potency in stimulating SCC were: ATP greater than adenosine diphosphate much greater than adenosine monophosphate, adenosine, and ATP greater than inosine triphosphate greater than guanosine triphosphate greater than cytidine triphosphate. These results indicate that ATP interacts with a P2-purinoceptor at the apical membrane of the epididymal cells. 4. The SCC response to ATP was not blocked by 8-phenyltheophylline, a P1-purinoceptor antagonist or by propranolol. Although pretreatment of the cultures with piroxicam abolished the SCC response to bradykinin, it did not affect the response to ATP. This indicates that the SCC response to ATP was not mediated by an increase in the synthesis of prostaglandins. 5. Serosal to mucosal Cl flux (Js-m Cl) and net water flux were measured in the luminally perfused rat epididymis in vivo. ATP (1 microM) added to the luminal perfusion solution caused an increase in Js-m Cl and net water secretion by the epididymal duct. 6. Since spermatozoa contain a high concentration of ATP, it is proposed that ATP released from spermatozoa may affect anion and fluid secretion by the epididymis. The control of secretion via the apical purinoceptors offers a means by which spermatozoa regulate the fluidity of their own environment.
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PMID:Control of anion and fluid secretion by apical P2-purinoceptors in the rat epididymis. 321 90

1. The effects of sodium nitroprusside, acetylcholine and bradykinin on cardiac output and its distribution were studied in the anaesthetized, vagotomised rat preparation by use of 113Sn-labelled microspheres. 2. All three vasodilators lowered peripheral arterial blood pressure, but only bradykinin significantly reduced total peripheral resistance without reducing cardiac output. Bradykinin caused tachycardia, but this was offset by a reduction in stroke volume. These effects of bradykinin were not altered by indomethacin (4 mg kg-1). Acetylcholine and sodium nitroprusside both caused significant (P less than 0.05) reductions in stroke volume and cardiac output. 3. Bradykinin reduced vascular resistance in the liver, stomach, small intestine, large intestine, pancreas/mesentery, epididimides, skeletal muscle and fat. These responses were not affected by indomethacin, whereas, the reduction in vascular resistance in the brain induced by bradykinin was abolished by indomethacin. 4. Acetylcholine caused a reduction in renal vascular resistance, where bradykinin had no effect. However, acetylcholine did not cause any haemodynamic changes in the bradykinin-sensitive intestinal vasculature. 5. Acetylcholine caused vasoconstriction in the coronary and epididymal vasculature. Bradykinin in the presence of indomethacin induced vasoconstriction in the skin. 6. In conclusion, the data show that, with the possible exception of the brain and the skin, the vasodilator actions of bradykinin can adequately be transduced (presumably by endothelium-derived relaxing factor, EDRF) in the absence of prostacyclin synthesis. Additionally, these results indicate that the vasculature of the stomach, pancreas/mesentery, epididimides and skeletal muscle are equally sensitive to both acetylcholine and bradykinin, whereas the kidneys showed selectivity towards acetylcholine and the intestines towards bradykinin. These results may indicate differential receptor populations.
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PMID:The effects of endothelium-dependent vasodilators on cardiac output and their distribution in the anaesthetized rat: a comparison with sodium nitroprusside. 326 37

The application of bradykinin to isolated segments of the epididymal or prostatic portion of the rat vas deferens increased the basal muscular tension mainly of the epididymal portion of the organ. Upon low frequency transmural electrical stimulation, the epididymal and the prostatic end of the organ both reacted to the application of bradykinin with an increase of twitch height. The increase in muscular tension observed in the epididymal portion of the ductus was resistant to tetrodotoxin but obliterated by 1 microM verapamil or nifedipine. The augmentation of the magnitude of the electrically driven muscle twitches was blocked by tetrodotoxin but not affected by 1 microM verapamil or nifedipine. Preincubation of the segments of the ductus with 10 microM indomethacin significantly reduced the increase in basal muscular tension caused by low concentrations of bradykinin but did not affect the electrically driven muscle twitches. Results suggest the existence of bradykinin receptors in the nerve endings of the adrenergic terminals of the organ and in the smooth muscle membrane. Whereas the neurogenic response found in both segments of the organ was of equal magnitude, the musculotropic response was predominantly found in the epididymal half of the organ.
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PMID:Pre- and postsynaptic bradykinin responses in the rat vas deferens: asymmetric distribution of the postsynaptic effect. 369 98

The different segments of the guinea pig vas deferens circular muscle exhibit differential response patterns upon pharmacological stimulation. Namely, apart from barium chloride, the affinity and intrinsic activity of certain agonists and the strength of maximum contractions they induce appear to decrease along the path from the epididymis toward the prostate. If one subdivides the vas deferens into 3 parts of equal length such as epididymal, medial and prostatic portions, then adrenaline, acetylcholine, acetyl-beta-methylcholine, dopamine, histamine and bradykinin induce contractions on each of the 3 parts; whereas tyramine, ephedrine elicit responses in the epididymal and medial portions; amphetamine, DMPP, serotonin and PGF2 alpha in turn provoking contractions exclusively on the epididymal portion. The effects of adrenaline and noradrenaline are blocked by phentolamine and tolazoline; the responses to acetylcholine, acetyl-beta-methylcholine and carbamyl-beta-methylcholine are antagonized by atropine over a specific concentration range. The effects of tyramine, ephedrine and amphetamine are inhibited by phentolamine in an remarkably low dose range (pA2 = 13.51 +/- 0.09; 14.54 +/- 0.31; 14.35 +/- 0.12). The situation was the same when tyramine-dibenamine and tyramine-phenoxybenzamine combinations were tested (pD'2 = 14.03 +/- 0.37; 13.26 +/- 0.03). Based on these findings the presence of a peculiar alpha adrenergic receptor is suggested on the sympathetic postganglionic fibres. In addition to the already identified alpha adrenergic, muscarinic cholinergic and histamine H1 receptors, we could show the presence of dopaminergic receptors too in the vas deferens circular muscle.
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PMID:Pharmacological responses by different portions of guinea pig vas deferens circular muscle preparation. 612 18


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