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)

Reserpine treatment in rats induces morphological and functional disturbances in exocrine glands which resemble those produced by cystic fibrosis. The general feature is a decrease in fluid secretion with a rise in mucous concentration and altered electrolyte composition. Chronically reserpinized rats have therefore been used as an animal model for the disease. It is known that cystic fibrosis men are infertile due to obstruction of the epididymal duct with inspissated material, a phenomenon that may be secondary to abnormal electrolyte and water transport in the epididymis. Male rats were treated with reserpine (0.5 mg/kg/day) for 12 to 14 days. At the end of the treatment, epididymal fluids were flushed out from the cauda epididymidis for measurement of spermatocrit, viscosity, total protein concentration, sperm concentration and motility. It was found that reserpine treatment caused a rise in viscosity (by 40%), spermatocrit, sperm concentration, and protein concentration. These changes were observed in the epididymis of rats that had been efferent duct-ligated before reserpine treatment. Despite a rise in viscosity of the fluid bathing the spermatozoa, the viability of the stored spermatozoa was apparently normal. Spermatozoa were able to initiate forward motility when suspended in a sodium-containing medium. Testis fluid secretion measured by weight gain after efferent duct ligation for 16 h was not affected by reserpine treatment. The change in viscosity probably was due to a decrease in fluidity in the epididymis. It is concluded that reserpine treatment in rats produced changes in the exocrine functions of the epididymis similar to those seen in other exocrine glands.
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PMID:Reserpine treatment increases viscosity of fluid in the epididymis of rats. 297 Feb 71

The concentrations of dopamine (DA), 5-hydroxytryptamine (5-HT) and noradrenaline (NA) in the rat vas deferens divided in eight or four sections were determined by high performance liquid chromatography with electrochemical detection. Dopamine and NA had the same regional distribution; their concentrations were maximal near the prostatic end and decreased towards the epididymis. The concentration of 5-HT also decreased from the prostatic to the epididymal end, but 5-HT did not follow the same regional distribution as DA and NA. Reserpine (0.02 or 0.2 mg/kg, i.p., 24 hr) and 6-hydroxydopamine (2 x 80 mg/kg, i.v., 6 days) decreased the contents of DA and NA; the concentrations of both amines were modified to a similar extent. Reserpine also diminished the content of 5-HT. Pargyline (200 mg/kg, i.p., 2 hr) increased the concentration of 5-HT while p-chlorophenylalanine (300 mg/kg, oral, 3 days) decreased the contents of the amine in some sections of the vas deferens. This study suggests that DA and NA co-exist in the same sympathetic neurons. Some of the 5-HT could be stored in mast cells as previously proposed, but the finding that tissue content of 5-HT changes after inhibiting the deamination or synthesis of the amine suggests that other source(s) of 5-HT distinct from mast cells exist in the rat vas deferens.
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PMID:Regional distribution of dopamine, 5-hydroxytryptamine, and noradrenaline in the rat vas deferens. 297 60

The effect of pretreatment with reserpine (1.0 mg/kg i.p. daily for 7 days) on beta-adrenoceptor-mediated responses has been measured in epididymal white and interscapular brown adipocytes, left atria and vas deferens of rats in order to investigate the classification of the receptors and whether they are innervated. Lipolysis was measured in adipocytes, and from the same rats, the beta 1-adrenoceptor-mediated positive inotropic responses of isolated paced left atria and beta 2-adrenoceptor-mediated inhibition of field stimulation-induced contraction of the vas deferens were examined. The agonists used were isoprenaline, oxyfedrine (atria only) and (except in brown adipocytes) ritodrine, which was a partial agonist in white adipocytes, atria and vas deferens. Atria and brown adipocytes exhibited beta-adrenoceptor supersensitivity after reserpine pretreatment, whereas vas deferens and white adipocytes did not. Reserpine-induced reductions in food intake and body weight did not appear to influence beta-adrenoceptor-mediated lipolysis, since restriction of the diet equivalent to that of reserpine-treated rats produced no change in white adipocyte sensitivity. Responses mediated via beta 1-, but not beta 2-adrenoceptors, display supersensitivity after chronic depletion of neuronal catecholamines with reserpine and this is evidence for innervation of this receptor subtype. Thus, atrial beta 1-adrenoceptors are assumed to be innervated, whereas vas deferens beta 2-adrenoceptors are not. The present results are consistent with histochemical evidence that brown, but not white, adipocyte beta-adrenoceptors are innervated. However, they are not compatible with conventional receptor classification studies, which suggest that rat brown and white beta-adrenoceptors are similar--either both beta 1 or both atypical.
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PMID:Beta-adrenoceptor sensitivity of brown and white adipocytes after chronic pretreatment of rats with reserpine. 302 2