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Presence of neuropeptide Y in the rat seminal vesicle and its effects on noradrenaline- and nerve-induced contractions.

1. Immunohistochemical and functional studies have been performed to localize and determine the effects of neuropeptide Y (NPY) in the rat seminal vesicle. 2. An abundant presence of NPY-immunoreactive nerves, mainly concentrated in the smooth muscle layer of the seminal vesicle was found. Chronic 6-hydroxydopamine treatment (four doses of 50 mg kg-1 i.p. on days 1, 2, 4 and 6; rats killed one week after the last injection) led to a large reduction but not abolition of the NPY-immunoreactivity. 3. NPY (1-250 nM) did not affect the resting tone of the seminal vesicle. 4. The seminal vesicle was contracted by electrical field stimulation (EFS) and by exposure to 5 microM noradrenaline (NA). These contractions were abolished by phentolamine (1 microM). Tetrodotoxin (0.5 microM) abolished EFS-evoked contractions but did not affect NA-evoked contractions. 5. Seminal vesicles, from animals chronically-treated with reserpine (5 mg kg-1 i.p. on days 1 and 2; rats killed on day 3), were contracted by NA but not by EFS. 6. NPY (0.25-250 nM), concentration-dependently, inhibited EFS-evoked contractions by up to 70% maximum inhibition. Contractions evoked by EFS with short trains of pulses were inhibited by NPY to a greater degree than those with longer trains. 7. NPY had no significant effect on NA-evoked contractions. 8. These data provide strong evidence that the motor transmission in rat seminal vesicle is predominantly if not exclusively, adrenergic. It is further concluded that a rich NPY-containing innervation is present in the smooth muscle layer of rat seminal vesicle. The primary effect of NPY is modulation of adrenergic motor transmission by a prejunctional inhibition of NA release.

Animals↗

Induction of functional cytodifferentiation in the epithelium of tissue recombinants. II. Instructive induction of Wolffian duct epithelia by neonatal seminal vesicle mesenchyme.

When grown as renal grafts in adult male hosts, the upper (cranial), middle and lower (caudal) portions of fetal mouse and rat Wolffian ducts developed into epididymis, epididymis plus ductus deferens, and seminal vesicle, respectively. In heterotypic tissue recombinants, the epithelia from upper and middle Wolffian ducts were instructively induced to undergo seminal vesicle morphogenesis by neonatal seminal vesicle mesenchyme. Functional cytodifferentiation was examined in these recombinants using antibodies against major androgen-dependent, seminal vesicle-specific secretory proteins. The instructively induced Wolffian duct epithelia synthesized normal amounts of all of the secretory proteins characteristic of mature seminal vesicles, as judged by immunocytochemistry on tissue sections and gel electrophoresis plus immunoblotting of secretions extracted from the recombinants. In heterospecific recombinants composed of rat and mouse tissues, the seminal vesicle proteins induced were specific for the species that had provided the epithelium. This showed that the seminal vesicle epithelium in the recombinants was derived from instructively induced Wolffian duct epithelium and not from epithelial contamination of the mesenchymal inductor. Upper Wolffian duct epithelium, instructively induced to undergo seminal vesicle morphogenesis, did not express epididymis-specific secretory proteins, showing that its normal development had been simultaneously repressed.

Animals↗

Prevalence of epididymal, seminal vesicle, prostate, and testicular cysts in autosomal dominant polycystic kidney disease.

OBJECTIVES: To assess the prevalence of cysts in the epididymis, seminal vesicles, prostate, and testes of patients with autosomal dominant polycystic kidney disease (ADPKD) and determine their clinical significance. Extrarenal cystic involvement is a well-known manifestation of ADPKD. Although a few reports exist about cysts in the epididymis, seminal vesicles, prostate, and testes, the true prevalence of cysts in these organs is not well known. METHODS: A prospective study, consisting of 104 male patients and 62 male controls, was designed at three medical centers to evaluate the prevalence of epididymal, seminal vesicle, prostatic, and testicular cysts in patients with ADPKD by abdominal, transrectal, and scrotal ultrasound examinations. RESULTS: Among the 104 patients, epididymal cysts were present in 19 (18%), seminal vesicle cysts were present in 41 (39%), and prostatic cysts were present in 7 patients (7%); the proportion in the control group was 24% (P >0.05), 2% (P <0.01), and 5% (P >0.05), respectively. Testicular cysts were detected in only 3 control patients. Of the 104 patients, 96 were married, and primary infertility was present in 5 patients (5%). CONCLUSIONS: We suggest that seminal vesicle cysts are frequent in ADPKD; epididymal cysts are not uncommon in ADPKD, but the frequency is not higher than in the control group; ADPKD should be looked for in patients with seminal vesicle cysts; and additional studies are necessary to evaluate the association between epididymal and seminal vesicle cysts and infertility in patients with ADPKD.

Adolescent↗

Amyloid deposition in seminal vesicles mimicking tumor invasion from bladder cancer: MR findings.

Amyloid deposition in the seminal vesicle is a not unusual finding at autopsy. A case of MR findings of amyloid deposition in the seminal vesicles with urinary bladder cancer is reported. Invasion of the seminal vesicle could not be excluded on T2-weighted imaging, but gadopentetate dimeglumine may be useful in its ability to differentiate amyloid deposition from seminal vesicle tumor invasion.

Aged↗

Congenital anomalies of the seminal vesicles: spectrum of computed tomographic findings.

Four cases of congenital seminal vesicle anomalies were evaluated using computed tomography. Abnormalities ranged from complete absence of the seminal vesicle to solid and cystic enlargement. Three cases had ipsilateral renal agenesis. Seminal vesicle lesions are uncommon, but may be detected more commonly in the future with increased use of computed tomography, and should be considered when evaluating males with pelvic masses.

Adolescent↗

[Seminal vesicle cyst and ipsilateral renal agenesis].

OBJECTIVES: To report one case of seminal vesicle cyst with renal agenesis. To describe its clinical, radiological and therapeutic characteristics. METHODS/RESULTS: 42-year-old male presenting with irritative voiding symptoms. Digital rectal examination revealed a soft irregular mass over the prostate. Diagnostic imaging tests showed an enlargement of the left seminal vesicle and ipsilateral renal agenesis. Surgery was carried out with excision of the seminal vesicle cyst by an extravesical and extraperitoneal approach. Two years later the patient remains asymptomatic. CONCLUSIONS: Cystic pathology of the seminal vesicle is rare. Diagnosis is based on clinical symptoms, digital rectal examination and imaging studies. Surgery is necessary for symptomatic cases.

Adult↗

Microvascular invasion of the seminal vesicles in adenocarcinoma of the prostate.

The objective of this article is to determine the relationship between microvascular invasion and seminal vesicle invasion in prostatic adenocarcinoma. Radical prostatectomies with seminal vesicle involvement were examined histologically and immunohistochemically with antibodies directed against S-100 protein and factor VIII. Microvascular invasion of the seminal vesicles showed a positive correlation with microvascular and capsular invasion of the prostate (P = 0.006 and 0.048, respectively) and lymph node metastases. Tumor progression was found in 8 of 14 (57%) patients with microvascular invasion of the seminal vesicles, compared with 3 of 22 (14%) without microvascular invasion (P = 0.001). Microvascular invasion of the seminal vesicles is predictive of tumor progression and lymph node metastases in prostatic adenocarcinoma.

Adenocarcinoma↗

Primary seminal vesicle carcinoma: an immunohistochemical analysis of four cases.

Primary adenocarcinoma of the seminal vesicles is an extremely rare neoplasm. Because prompt diagnosis and treatment are associated with improved long-term survival, accurate recognition of this neoplasm is important, particularly when evaluating limited biopsy material. Immunohistochemistry can be used to rule out neoplasms that commonly invade the seminal vesicles, such as prostatic adenocarcinoma. Previous reports have shown that seminal vesicle adenocarcinoma (SVCA) is negative for prostate-specific antigen (PSA) and prostate-specific acid phosphatase (PAP); however, little else is known of its immunophenotype. Consequently, we evaluated the utility of cancer antigen 125 (CA-125) and cytokeratin (CK) subsets 7 and 20 for distinguishing SVCA from other neoplasms that enter the differential diagnosis. Four cases of SVCA-three cases of bladder adenocarcinoma and a rare case of adenocarcinoma arising in a mullerian duct cyst-were immunostained for CA-125, CK7, and CK20. Three of four cases of SVCA were CA-125 positive and CK7 positive. All four cases were CK20 negative. All bladder adenocarcinomas and the mullerian duct cyst adenocarcinoma were CK7 positive and negative for CA-125 and CK20. In addition, CA-125 immunostaining was performed in neoplasms that commonly invade the seminal vesicles, including prostatic adenocarcinoma (n = 40), bladder transitional cell carcinoma (n = 32), and rectal adenocarcinoma (n = 10), and all were negative for this antigen. In conclusion, the present study has shown that the CK7-positive, CK20-negative, CA-125-positive, PSA/PAP-negative immunophenotype of papillary SVCA is unique and can be used in conjunction with histomorphology to distinguish it from other tumors that enter the differential diagnosis, including prostatic adenocarcinoma (CA-125 negative, PSA/PAP positive), bladder transitional cell carcinoma (CK20 positive, CA-125 negative), rectal adenocarcinoma (CA-125 negative, CK7 negative, CK20 positive), bladder adenocarcinoma (CA-125 negative), and adenocarcinoma arising in a mullerian duct cyst (CA-125 negative).

Adenocarcinoma↗

Differential distribution of pepsinogen II between the zones of the human prostate and the seminal vesicle.

Pepsinogen II (PG II) is a gastric proenzyme which has previously been found in both human seminal fluid and the prostate gland. However, no regional distribution of PG II has been noted within the prostate nor has it been found in the seminal vesicle. Bouins-fixed sections of central zone, peripheral zone and seminal vesicle, taken from 10 prostates removed at radical prostatectomy or cystectomy, were exposed to antibody against PG II and stained using the A-B-C immunoperoxidase technique. Formalin-fixed tissue from autopsy prostates of four men in the third decade, and six cases with BPH nodules, were also examined for PG II activity. In nine of 10 seminal vesicles, and seven of 10 central zone samples, more than 50 per cent of the cells stained positive for PG II. By contrast, in nine of 10 peripheral zone samples staining was present in five per cent or less of the epithelial cells. Similarly, PG II activity in the four autopsy prostates occurred almost entirely within the central zone and ended abruptly at the boundary between the peripheral and central zones. BPH nodules contained no PG II activity. These findings provide the first evidence that the central and peripheral zones may serve different biological functions. Embryologically it is currently thought that the prostate is of endodermal origin and the seminal vesicle of mesodermal origin. The presence of large amounts of PG II in both the seminal vesicle and central zone lends support to the hypothesis of a common mesodermal origin for these two structures.

Aged↗

[The morphological changes in the seminal vesicles in prostatic sclerosis].

A study is presented of morphological changes of the seminal vesicles removed during prostatectomy in 51 patients with sclerosis of the prostate and histological findings of the seminal vesicles were compared with roentgenological signs on the vesiculograms and clinical manifestations of the disease. Results indicate that the seminal vesicles undergo significant pathological changes in the development of sclerosis of the seminal vesicles requiring in some cases their surgical removal for restoration of the urodynamics in cystic-urethral segment.

Adult↗

Effect of LHRH analog on the seminal vesicles evaluated by transrectal sonography.

The maximum horizontal area (MHA) of the seminal vesicles was measured in 20 prostatic cancer patients by means of transrectal sonography (TRS) after LHRH analog treatment. MHA of the seminal vesicles changed in parallel to the serum testosterone (T) level and decreased by 11-62%, compared with the baseline after LHRH analog treatment for 4 months. Two different patterns were observed for the change of MHA. In 9 cases, MHA of the seminal vesicles increased transiently and then decreased gradually, while in the other 11 cases, MHA decreased continuously from the beginning with no significant increase. Thus, the direct and dynamic response of the seminal vesicles to the change of serum T level was clarified.

Aged↗

The prevalence of seminal vesicle cysts in autosomal dominant polycystic kidney disease.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is a systemic hereditary disorder characterized by bilateral diffuse renal cysts. Extrarenal involvement is a well known manifestation of ADPKD. Data relating to the association between seminal vesicle cysts and ADPKD are limited. The aims of this study are to evaluate the frequency of seminal vesicle cysts in ADPKD and to assess the relationship between seminal vesicle cysts, with cysts in the liver and prostate, and creatininaemia. METHODS: Forty five male patients (mean age 40 years, range 13-67) were included in the study. Each subject underwent a formal interview, physical examination; and abdominal and transrectal ultrasonography. Three patients were infertile, but one of the patients also had varicocele. RESULTS: Seminal vesicle cysts were present in 27 (60%) patients. Liver and prostate cysts were present in 19 (42%) and five (11%) patients, respectively. There was a positive correlation between seminal vesicle cysts, cysts in the liver, and serum creatinine concentrations. CONCLUSION: Our conclusions are: (i) seminal vesicle cysts are not uncommon in ADPKD; (ii) ADPKD should be looked for in patients with seminal vesicle cysts, and (iii) the clinical significance of seminal vesicle cysts in ADPKD remains to be defined.

Adolescent↗

Molecular feminization of mouse seminal vesicle by prenatal exposure to diethylstilbestrol: altered expression of messenger RNA.

Exposure to estrogens during critical stages of development has been reported to cause irreversible changes in estrogen target tissues such as the reproductive tract. In fact, recent studies using mice describe prenatal estrogen exposure resulting in the expression of the major estrogen-inducible uterine secretory protein, lactoferrin (LF), by the seminal vesicles of the male offspring. Thus, we have studied the role of estrogens in abnormal and normal gene expression in the developing male reproductive tract using LF and seminal vesicle secretory protein IV (SVS IV), an androgen-regulated murine seminal vesicle secretory protein, as markers. Lactoferrin and SVS IV protein and mRNA expression were studied in histological samples by using the techniques of in situ hybridization (ISH) and immunohistochemistry (IHC). Seminal vesicle secretory protein IV was expressed in all (100%) epithelial cells of the control seminal vesicle, but this protein was decreased by castration. However, LF expression was undetectable by ISH or IHC in control seminal vesicle epithelium. Lactoferrin was inducible in 2% of the seminal vesicle epithelial cells from adult castrated mice treated with estradiol 17 beta (E2; 20 micrograms/kg/day for 3 days), indicating that a small percentage of the seminal vesicle cells could be induced to secrete LF after modification of the endocrine environment. Prenatal DES treatment (100 micrograms./kg. maternal body weight on days 9 through 16 of gestation) resulted in the male offspring exhibiting constitutive expression of LF in 5% of the seminal vesicle epithelial cells, while expression of the androgen-regulated protein SVS IV was slightly decreased. The maximal contrast between LF and SVS IV expression was observed in prenatally DES-treated mice that were subsequently castrated as adults and further treated with E2; LF was detected in 40% of the epithelial cells in these mice. Double immunostaining techniques revealed that epithelial cells which were making LF had ceased production of SVS IV. Since a large percentage of the epithelial cells in the intact prenatal DES exposed male was capable of expressing the normal gene product, SVS IV, it was concluded that DES treatment during prenatal development appears to imprint or induce estrogenic sensitivity in the adult seminal vesicle, causing increased production of LF. The results suggest that this altered protein response may be an example of atypical gene expression in male reproductive tract tissues following hormonal manipulation early in development.

Animals↗

[Atypical fibrous histiocytoma of the seminal vesicle].

OBJECTIVES: To describe a rare case of fibrous histiocytoma of the seminal vesicles. METHODS: A tumor occupying the entire hypogastrium, extending beyond the umbilical region were the only remarkable findings in our 47-year-old male patient that prompted us to perform complementary studies such as US, contrast-enhanced radiological evaluation (urography, cystography, colon enema and intestinal transit time) and laparoscopy that disclosed an extraperitoneal tumor with no precise location. A large tumor involving the seminal vesicles was found at surgery and resected. The histological analyses disclosed an atypical fibrous histiocytoma of the seminal vesicles. RESULTS: Patient outcome was satisfactory. CONCLUSIONS: Because tumors of the seminal vesicles are uncommon, it is practically impossible to diagnose this tumor type preoperatively.

Genital Neoplasms, Male↗

Localization and molecular heterogeneity of sulfated glycoprotein-2 (clusterin) among ventral prostate, seminal vesicle, testis, and epididymis of rats.

In the rat reproductive tract, sulfated glycoprotein 2 (SGP-2) is present in the ventral prostate, seminal vesicle, testis, and epididymis. In the ventral prostate, SGP-2 is associated with the process of programmed cell death, while in the testis and epididymis a role for SGP-2 in sperm maturation has been proposed. Available information suggests that there are both inter- and intra-organ variations in SGP-2 localization, molecular forms, and response to androgen ablation. In the present study, localization of SGP-2 within the ventral prostate, seminal vesicle, and epididymis was compared by immunohistochemistry. In the ventral prostate of intact rats, immunoreactive SGP-2 was confined to a discrete population of epithelial cells lining the proximal ducts. Epithelial cells in other regions of the ventral prostate did not stain for SGP-2. A similar staining pattern was observed for the seminal vesicle; a small population of SGP-2-expressing epithelial cells was found in epithelium that did not stain for SGP-2. The epididymis also demonstrated a non-uniform staining pattern. The caput displayed strong immunoperoxidase reaction over the apical membrane and stereocilia of all principal cells. Principal cells also showed variable degrees of cytoplasmic staining ranging from weak to strongly positive. The corpus and cauda showed a similar staining pattern. After castration, all epithelial cells in the ventral prostate and seminal vesicle became intensely positive for SGP-2 staining. In the caput and cauda epididymis there was an increase in the number of principal cells demonstrating strong intracellular staining for SGP-2. These results suggest that as observed previously in the regressing ventral prostate, increased intracellular SGP-2 staining may also be associated with the regressing epididymis and seminal vesicle. Differences in molecular forms of SGP-2 were investigated by two-dimensional Western and lectin blots. Molecular forms of SGP-2 differed between testis and epididymis but were similar between ventral prostate and seminal vesicle. Prostate and seminal vesicle forms of SGP-2 differed from those of both testis and epididymis. Analysis of terminal carbohydrate present on the various SGP-2 molecular forms also confirmed the existence of heterogeneity. These results demonstrate the presence of multiple molecular forms of SGP-2 in various organs of the male reproductive tract in rats and suggest a possible variation in functional activity and/or half-life of SGP-2 in these organs.

Animals↗

Effect of noradrenaline on rubidium (86Rb) efflux in the rat isolated seminal vesicle.

The effect of noradrenaline (NA) on the efflux of rubidium (86Rb) from the rat isolated seminal vesicle was studied in the absence and presence of phentolamine and papaverine. Strips of spirally cut seminal vesicles were incubated in radioactive 86Rb (10 microCi.ml-1) for 2 h. Radioactivity was measured using an autogamma spectrometer, and the flux data were expressed in terms of rate constants per minute, of the reactive isotope efflux. A concentration-effect curve for the effect of NA on rat seminal vesicles was constructed, alone and in the presence of phentolamine (1 mumol/l) or papaverine (5 mumol/l). The results showed that NA (10-1,000 mumol/l) produced concentration-dependent contractions in the rat seminal vesicle. These responses were greatly reduced by phentolamine but markedly enhanced by papaverine. NA significantly increased 86Rb efflux from rat seminal vesicles (control rate constant 0.0042 +/- 0.001; test 0.0064 +/- 0.002, means +/- SE; n = 8 rats; p less than 0.001). This increase (52%) occurred within an exposure of 7 +/- 1 min to NA. Phentolamine decreased the NA-induced increase in 86Rb efflux, by 75 +/- 2%, whereas papaverine enhanced it by 86 +/- 5% of the control value. The mechanism of NA-induced increase in 86Rb efflux was not further investigated but was interpreted in terms of an increase in intracellular K+ (here represented by 86Rb), which will leave the cell (efflux) after initial membrane depolarization.

Animals↗

Development of secretory protein synthesis in the seminal vesicles and ventral prostate of the male rat.

Functional development of the ventral prostate and seminal vesicles in the male rat has been examined by incubating tissue with [35S] methionine and using specific antisera to detect the synthesis of individual marker proteins. 4 major secretory proteins of the seminal vesicles were chosen along with 4 major prostatic secretory peptides, including 3 which form the prostatic steroid-binding protein. None of the seminal vesicle proteins was synthesised before 25-30 days but all were then induced in parallel to reach adult values by 45-50 days. The 3 peptides of the prostatic steroid-binding protein were synthesised at the earliest age studied (10 days) and were also induced in parallel to maximal levels by 25-30 days. In contrast, the 4th prostatic marker, a glycopeptide, was not synthesised until about 25 days. Treatment of male rats from 3 days of age with testosterone induced precocious development of the seminal vesicles, causing substantial synthesis of marker proteins well before their synthesis would normally have been expected, and also advanced the synthesis of the prostatic 22 K glycopeptide. The results confirm that functional development in the ventral prostate precedes that of the seminal vesicles but that within the ventral prostate there is a considerable difference in the developmental profiles of its secretory proteins.

Animals↗

[Diagnosis and treatment of seminal vesicle cyst].

OBJECTIVES: To deepen the understanding of patients with seminal vesicle cyst for correct diagnosis and treatment. METHODS: Sixteen patients with seminal vesicle cysts were treated in the period of January 1980-May 2002. Their symptoms, diagnostic results, treatment and outcomes were analyzed retrospectively. The mean age of these patients at diagnosis was 31 years (range 19 - 43). Two patients were associated with ipsilateral renal agenesis. Symptoms included hematospermia in 12 (75%) patients, urinary frequency in 8 (50%), hematuria after ejaculation in 6 (27.5%), perineal malaise in 6 (27.5%), infertility in 3 (13.7%), pain after ejaculation in 3 (13.7%), scrotal pain in 2 (12.5%) and dysuria in 1 (6.3%). Cyst was palpable in 81.3% patients on digital rectal examination. All patients underwent intravenous urography and cystoscopy. Others received ultrasonography, CT scanning, MRI, and vasovesiculography. The size of masses ranged from 3.8 cm x 3.0 cm x 2.6 cm to 9.6 cm x 5.2 cm x 5.0 cm. Final open surgery consisted of vesiculectomy (4 patients) and partial vesiculectomy (12). RESULTS: Postoperative course was uneventful except in 1 patient with epididymitis. All patients were free of symptoms after open surgery. CONCLUSIONS: Seminal vesicle cysts are rare but should be considered in men with hematospermia and otherwise inexplicable bladder irritation symptoms, perineal discomfort or other genitourinary complaints of unknown etiology. Diagnosis consists of digital rectal examination, transrectal and abdominal ultrasonography, CT scan or MRI. Vesiculectomy and partial vesiculectomy give excellent results.

Adult↗