Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The mechanical response of the longitudinal smooth muscle of the rat vas deferens to stimulation of its motor nerves by a single pulse has been examined. The motor nerves were stimulated in vivo via the spinal outflows in the pithed rat or in vitro by field stimulation. 2. The contraction in the whole vas consisted of two components, an initial, rapid, brief contraction reaching a maximum at 300 msec and a second, slower and more prolonged contraction reaching its maximum at 600 msec. When the isolated vas was divided into prostatic and epididymal halves the contribution of these two components varied. The initial rapid component was more prominent in the prostatic half and the slower, second component more prominent in the epididymal half. Lowering the bath temperature caused, in both halves, these two components to merge into a single, slow, prolonged response. Both components were more rapid and briefer than the equivalent response of rat anococcygeus. 3. The second, slow component was abolished by alpha-adrenoceptor antagonist drugs, potentiated and prolonged by drugs which inhibit the neuronal uptake of noradrenaline and absent from tissues taken from rats pre-treated with reserpine, suggesting that the neurotransmitter for this component is noradrenaline. 4. These experiments were extended to the mouse or guinea-pig vas deferens. Both showed the same two component mechanical response as the rat vas and in both the second, slow component was preferentially inhibited by alpha-adrenoceptor antagonists and potentiated by drugs blocking noradrenaline uptake. 5. Drugs known to reduce the response to repetitive nerve stimulation of the vas were examined for their effect on the response to a single stimulus. Lysergic acid diethylamide preferentially inhibited the second, slow phase of contraction whereas apomorphine preferentially inhibited the first rapid phase. Guanethidine inhibited responses but any differential effects could not be analysed due to its stimulant properties. 6. These results show that there are two components even to the response to a single stimulus. The second of these appears to be adrenergic while the transmitter responsible for the first remains to be determined.
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PMID:Adrenergic and 'non-adrenergic' components in the contractile response of the vas deferens to a single indirect stimulus. 3 66

1. Guanethidine at 5 x 10(-6) M strongly inhibited rat prostatic but not epididymal vas deferens, reflecting differences in innervation and the neurogenic field stimulation responses of these tissues. 2. Adenosine and ATP inhibited the field stimulation responses of rat prostatic vas deferens by 56 and 50% respectively. A 10-min pretreatment with 10(-4) M caffeine partly reversed this inhibition, by 55% in the case of adenosine and 60% for ATP. 3. Pretreatment for 10 min with 5 microM quinidine failed to significantly alter the extent of either adenosine or ATP inhibition of the field stimulation responses of rat prostatic vas deferens. 4. 8-Phenyltheophylline, the selective blocker of the A1 subtype of the P1 receptor, partly reversed adenosine-induced inhibition of the vas deferens FS responses. NECA, the selective agonist of the A2 subtype of the P1 receptor, very strongly inhibited vas deferens FS responses. 5. Field stimulation responses of human vas deferens were also inhibited by both adenosine and ATP but to a lesser extent and more variably than in rat tissue. 6. Adenosine and ATP inhibition was reversed by caffeine pretreatment, but far more variably than in rat tissue, and quinidine was without significant effect on inhibition of the responses. 7. It is concluded that in these tissues adenosine and ATP may operate via a P1 type receptor of both A1 and A2 subtypes and that a P2 type receptor may be lacking.
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PMID:Purinergic modulation of field stimulation responses of rat and human vas deferens smooth muscle. 176 Nov 93

Guanethidine, a chemical that selectively abolishes peripheral noradrenergic nerves, was used to investigate the role of sympathetic innervation in the maintenance of epididymal sperm quantity and quality. Four groups of 10 adult male rats each were treated daily for 21 days, by i.p. injections, with either 0 (saline vehicle), 6.25, 12.5, or 25 mg/kg guanethidine. Norepinephrine content was reduced to undetectable levels in the cauda epididymidis in all guanethidine groups after 3 wk of treatment and was reduced to 7.4% of the control values after 1 wk of 6.25 mg/kg treatment. While body weight gain was significantly decreased at 12.5 and 25 mg/kg compared to that in controls, there was a significant increase in the weights of the seminal vesicles/coagulating glands in all treated groups. The number of homogenization-resistant spermatids per testis and the daily sperm production per testis remained unchanged. The weight of the epididymis was significantly increased at 6.25 and 12.5 mg/kg. Moreover, the number of cauda epididymal sperm and the transit time were increased significantly at 6.25 mg/kg (10.2 days) compared to values in the control cauda (6.3 days). Neither serum testosterone levels nor LH was affected in a dosage-related manner. There were no effects of guanethidine treatment on cauda epididymal sperm motility or morphology. A quantitative analysis of detergent-extracted cauda epididymal sperm proteins by SDS-PAGE revealed no differences, but there were diminutions in seven proteins in homogenates of caput/corpus tissue. Histologic analysis of testis and epididymis sections revealed no differences between control and denervated animals. In a subsequent experiment the lowest effective dosage (6.25 mg/kg) was given to rats for 1 wk, and an increased number of cauda epididymal sperm and a delay in sperm transit were observed. Our results indicate that low-dosage guanethidine exposure denervates the epididymis within 1 wk, thereby delaying epididymal transit; however, neither 1- nor 3-wk exposure produces qualitative changes in the sperm.
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PMID:Rat epididymal sperm quantity, quality, and transit time after guanethidine-induced sympathectomy. 974 40

Guanethidine, a chemical that selectively blocks sympathetic noradrenergic neurons, was used to investigate the role of sympathetic innervation in the fertility of rat epididymal sperm, using both natural mating and in utero insemination protocols. This animal model correlates, at least in part, with spinal cord injury (SCI) in men. Adult male rats were treated daily by i.p. injections, for 21 or 42 days, with 0 or 6.25 mg/kg guanethidine. To compare the effects of guanethidine-induced sympathectomy with those following surgically induced sympathectomy, the inferior mesenteric ganglion and the proximal hypogastric nerves were removed in another group of rats. Both chemically and surgically induced sympathectomy increased the weight of the epididymis and seminal vesicles/coagulating glands as well as the number and the transit time of cauda epididymal sperm. Neither serum testosterone levels nor LH was affected by treatment with guanethidine. Using natural mating, no litters were produced by guanethidine-treated rats. Chemically denervated rats failed to produce copulatory plugs or ejaculate into the uterus. However, distal cauda epididymal sperm from chemically or surgically denervated rats displayed normal fertilization ability (80%) using in utero inseminations. In addition, the sperm of denervated rats did not show abnormal sperm chromatin structure using an assay that detects DNA damage. We conclude that sympathectomy delays the transit of sperm through the cauda epididymidis and produces ejaculatory dysfunction but does not compromise sperm quality in the distal cauda epididymidis. Moreover, these data provide compelling evidence that there is no association between the prolonged transit time of sperm within the epididymis, i.e., pre-ejaculatory sperm aging, and the fertility of those sperm, which has important implications for artificial insemination using sperm from men with SCI.
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PMID:Fertility of rat epididymal sperm after chemically and surgically induced sympathectomy. 974 41

A simple technique for local chemical sympathectomy of peripheral tissues is described using guanethidine. Multiple microinjections of guanethidine were made into inguinal or epididymal white adipose tissue (IWAT and EWAT) pads or spleens of hamsters. Guanethidine virtually abolished the sympathetic innervation of both EWAT and IWAT, as measured by the absence of significant norepinephrine (NE) tissue content two weeks later and as suggested by the two-fold increase in IWAT mass characteristic of surgically induced WAT denervation. These measures were not affected in the contralateral pads given equivolumetric injections of saline. Guanethidine injections into the spleen lead to a functional sympathectomy, as indicated by significant depletions of NE content. Because guanethidine treatment did not decrease body mass, induce ptosis, or spread to closely associated adjacent tissue (contralateral EWAT pad), no chemical-induced malaise or global sympathetic denervation was suggested. Guanethidine was more effective than two other local sympathectomy treatments, injections of the sympathetic neurotoxin anti-dopamine-beta-hydroxylase saporin or surgical denervation, in decreasing IWAT NE content and increasing IWAT pad mass. Collectively, these results suggest that locally applied, chemical sympathectomy with guanethidine provides an effective, restricted method for sympathectomizing WAT, spleen and likely other peripheral tissues.
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PMID:Novel method for localized, functional sympathetic nervous system denervation of peripheral tissue using guanethidine. 1164 Sep 54

The epididymal sperm transit time seems to have an important role in the process of sperm maturation, and it seems that alterations to the transit can harm the process. The aim of the present work was to evaluate the influence of altered sperm transit time through the epididymis on sperm parameters and fertility of rats, as well as the role of testosterone in the alterations. Sprague-Dawley adult male rats were randomly assigned to four different groups and were treated for 12 days: (i) 10 microg/rat/day DES, to accelerate the transit; (ii) 6.25 mg/kg/day guanethidine sulphate, to delay the transit; (iii) same treatment as group 1, plus androgen supplementation; (iv) control animals received the vehicles. Guanethidine treatment delayed the sperm transit time through the epididymal cauda, provoking increased sperm reserves in this region. Animals exposed to DES showed an acceleration of sperm transit time in the epididymis, and consequently decreased sperm density in both epididymal regions, the caput-corpus and cauda, and diminished sperm motility. In both cases sperm production was not altered. Testosterone supplementation was able to restore the transit time to values close to normality, as they were higher than in the control rats. The same occurred in relation to sperm motility. Rats exposed to DES presented lower fertility after in utero artificial insemination using sperm collected from the proximal cauda epididymis. Therefore, it was concluded that the acceleration of rat sperm transit time appeared to harm normal sperm maturation, thus decreasing sperm quality and fertility capacity, in an androgen-dependent way.
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PMID:Effects of altered epididymal sperm transit time on sperm quality. 1782 22