去甲肾上腺素刺激高原鼠兔CRF的分泌

用脑室注射神经递质去甲肾上腺素（ＮＥ）和ＲＩＡ法测定下丘脑正中隆起处促肾上腺皮质激素释放激素（ＣＲＦ）水平,研究ＮＥ对高原鼠兔下丘脑ＣＲＦ分泌的作用。脑室给予不同剂量ＮＥ３．７５,７．５,１５,３０μｇ／１００ｇＢＷ．正中隆起（ＭＥ）处ＣＲＦ含量分别增加到对照组的１０６．０５％,１３５．２８％（Ｐ＜０．０５）,１３８．９４％（Ｐ＜０．０１）,１０３．６５％,同时,血浆皮质酮浓度也分别增加到对照组的３２３．３５％（Ｐ＜０．０１）,３２３．３５％（Ｐ＜０．００１）,３４６．７１％,３６６．４７％。肾上腺切除后２天和６天时,下丘脑ＮＥ下降到对照的７６．３２％（Ｐ＜０．０５）,７６．２７％（Ｐ＜０．０１）,血浆皮质酮也下降到１６．５７％（Ｐ＜０．０１）,２．０５％（Ｐ＜０．００１）。上述结果表明,ＮＥ刺激高原鼠兔下丘脑ＣＲＦ的分泌并激活下丘脑垂体肾上腺皮质轴。肾上腺皮质激素对维持下丘脑ＮＥ水平和ＣＲＦ神经元活动有一定的紧张作用     

眼镜蛇毒细胞毒素的抗肿瘤作用

目的　研究眼镜蛇毒细胞毒素（ Ｃ Ｖ Ｃ Ｔ Ｘ）的体内抗肿瘤作用。方法　小鼠皮下、腹腔接种 Ｓ１８０ 、 Ｅ Ａ Ｃ后, 于接种部位注射不同剂量的 Ｃ Ｖ Ｃ Ｔ Ｘ, 每天 １ 次, 连续１０ 天, 观察瘤重抑制率和生命延长率。结果　适当剂量（０２～０８ｍ ｇ／ｋｇ） 的 Ｃ Ｖ Ｃ Ｔ Ｘ 能明显抑制肿瘤的生长 （ Ｐ＜ ００１）,小鼠的存活时间明显延长（ Ｐ ＜ ００１）。结论　 Ｃ Ｖ Ｃ Ｔ Ｘ 在小鼠体内对 Ｓ１８０ 、 Ｅ Ａ Ｃ有明显地抗肿瘤作用。     

日粮添加塞曼特罗（CIM）对大鼠生长胴体组成及GH水平的影响

选用２４只２月龄ＳＤ处女鼠配对分组,实验组日粮添加１０μｇ／ｇ塞曼特罗（ＣＩＭ）,试验期３０天。与对照组比较,ＣＩＭ显著提高大鼠生长速度（２７．３０％,Ｐ＜０．０１）和胴体比率,降低腰胁部脂肪重,提高腓肠肌、比目鱼肌和趾浅屈肌的鲜重和ＲＮＡ合量及ＰＮＡ／ＤＮＡ值,同时提高大鼠垂体和血清ＧＨ水平分别达３６．７０％（Ｐ＜０．０１）和２３．７７％（Ｐ＜０．０５）,降低血清脲氮含量。表明ＣＩＭ可显著促进大鼠生长,降低体脂含量,促进肌肉肥大,促进蛋白沉积。其作用机理可能还与其促进ＧＨ的合成和分泌有关。     

中枢注射U－50，488H对肾水钠钾的排出及PVH内TH－IR神经元活性的影啊

本工作用１２％乙醇麻醉的大鼠,观察了下丘脑室旁核（ＰＶＨ）微量注射Ｋ型阿片受体激动剂Ｕ－５０,４８８Ｈ对大鼠肾水钠钾排出的影响,以及第三脑室注射Ｕ－５０,４８８Ｈ对ＰＶＨ中多巴胺神经元活性的影响。结果如下：（１）ＰＶＨ微量注射Ｕ－５０,４８８Ｈ（５μｎ／ｕｌ）后２０ｍｉｎ内大鼠尿量开始增加（Ｐ＜０．０１）,持续约１００ｍｉｎ,４１—６０ｍｉｎ尿量增加达峰值（Ｐ＜０．００１）。（２）ＰＶＨ预先（１０ｍｉｎ）注射Ｋ型阿片受体阻断剂ＮＢＴ（Ｎｏｒ－ＢｉｎａｌｔｏｒｐｈｉｍｉｎｅＴｅｔｒａｈｙｄｒａｔｅ）（５μｇ／ｐｌ）可以阻断Ｕ－５０,４８８Ｈ所产生的利尿效应（Ｐ＜０．０１）。（３）第三脑室注射Ｕ－５０,４８８Ｈ（１０μｇ／１０ｕｌ）２０ｍｉｎ后,ＰＶＨ中酪氨酸羟化酶免疫反应阳性（Ｔｙｒｏｓｉｎｅｈｙｄｒｏｘｙｌａｓｅ－ｉｍｍｕｎｏｒｅａｃｔｉｖｉｔｙ,ＴＨ－ＩＲ）神经元数量减少,染色强度减弱,于注药后５０ｍｉｎ变化最为显著,１００ｍｉｎ时已恢复正常。上述结果表明：ＰＶＨ微量注射Ｕ－５０,４８８Ｈ可作用于Ｋ型阿片受体引起利尿效应;第三脑室微量注射Ｕ－５０,４８８Ｈ可抑制ＰＶＨ中ＴＨ－ＩＲ神经元的免疫活性。     

母兔配种后10小时血清中若干生理指标与子代性比的相关

测定日本大耳白兔母兔配种后１０小时血清中的１０项生理指标,并与母兔所产每窝仔兔的性比（雄性个体所占比率）进行对应分析（窝仔数＜６的数据未参与此项分析）。结果表明：母兔血清中ＦＳＨ、Ｔ（睾酮）、 Ｎａ＋和Ｍ２＋的浓度在高、低两个性比组间有显著差异, Ｔ３（三碘甲状腺原氨酸）的差异接近显著水平（Ｐ＜０．１）;并且,ＦＳＨ和Ｔ３与子代性比里显著负相关（ｒ分别为－０．５０和－０．４６）,Ｍｇ２＋与子代性比里显著正相关（ｒ＝０．３９）;同时,Ｍｇ２＋／Ｃａ２＋、Ｍｇ２＋×Ｎａ＋、Ｍｇ２＋×Ｋ＋和Ｔ３×ＦＳＨ与子代性比的相关分别为０．４０、０．４３、０．３９和－０．５３（Ｐ＜０．０５）。     

血管紧张素Ⅱ对大鼠心肌肌浆网Ca~(2+),Mg~(2+)-ATPase基因转录调节的影响

观察血管紧张素Ⅱ（ＡｎｇⅡ）对心肌肌浆网Ｃａ２＋,Ｍｇ２＋－ＡＴＰａｓｅ基因（ＳＥＲＣＡ２ａ）转录调节的影响,评价ＤＭＰ８１１对此效应的干预作用．６周龄雄性ＳＤ大鼠随机分为３组,每组６只．组１：生理盐水输注;组２：ＡｎｇⅡ输注＋ＤＭＰ８１１管饲（３ｍｇ·ｄ－１·ｋｇ－１）;组３：ＡｎｇⅡ输注（２００ｎｇ·ｍｉｎ－１·ｋｇ－１．１周后称其体重,取心脏并称重,提取心脏总ＲＮＡ后采用Ｎｏｒｔｈｅｒｎｂｌｏｔ的方法检测ＳＥＲ－ＣＡ２ａ的转录水平,采用ＲＴ－ＰＣＲ检测ＡｎｇⅡ１型受体（ＡＴ１）ｍＲＮＡ水平．实验后,组３心重（ＣＷ）、心重／体重（Ｃ／Ｂ）、ＡＴ１受体转录水平均高于组１（分别增加４．７±０．４％,４．９±０．９％和２４．７±３．５％;Ｐ＜０．０１）,而ＳＥＲＣＡ２ａ基因转录水平显著低于组１（降低２０．１±３．０％,Ｐ＜０．０１）,并且ＳＥＲＣＡ２ａｍＲＮＡ水平与ＡＴ１受体ｍＲＮＡ水平呈负相关（ｒ＝－０．７４,Ｐ＜０．０１）．ＡｎｇⅡ导致的上述改变能被ＤＭＰ８１１完全阻断．ＡｎｇⅡ通过其Ⅰ型受体的介导,诱导了ＳＥＲＣＡ２ａ的转录下调     

MPS对白细胞减少小鼠白细胞数的影响

对分枝杆菌多糖（Ｍｙｃｏｂａｃｔｅｒｉａｌｐｏｌｙｓａｃｃｈａｒｉｄｅｓ,ＭＰＳ）的升高白细胞作用,用环磷酰胺（Ｃｙｃｌｏｐｈｏｓｐｈａｍｉｄｅ,ＣＰ）所致的白细胞减少小鼠动物模型进行了试验研究。受试药组分四个ＭＰＳ剂量组（ＣＰ＋不同剂量的ＭＰＳ）,并设阴性对照组（ＣＰ＋生理盐水）,阳性药对照组（ＣＰ＋惠尔血）和正常组（未用药）,隔日取血计数白细胞数。与阴性对照组比较,ＭＰＳ４０μｇ、２０μｇ和１０μｇ剂量组白细胞数下降少（第４天,Ｐ＜０．０５）;ＭＰＳ２０μｇ和１０μｇ剂量组回升迅速（第６天,Ｐ＜０．０５）。受试药组与阳性药对照组比较,无显著性差异。本试验结果表明ＭＰＳ与惠尔血在促进白细胞生成方面有相似的作用     

肾动脉内注射内皮素—1对麻醉大鼠肾神经传入放电的影响

本实验旨在观察肾动脉内注射ＥＴ－１对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）和肾神经传入放电（ＡＲＮＡ）的影响,以及ＥＴＡ受体阻断剂ＢＱ－１２３和硝苯吡啶（Ｎｉｆ）对ＥＴ生物学效应的拮抗作用。结果如下：（１）肾动脉注射ＥＴ－１（１μｇ／ｋｇ）后,平均动脉压（ＭＡＰ）先有短暂的降低（由１３．７７±０．１３ｋＰａ降至１０．２±１．１２ｋＰａ）,随后为较显著的持久增高,增值达３．４４±１．６０ｋＰａＰ＜０．００１）,ＨＲ无明显变化,ＡＲＮＡ增加１０８．３３±１６．６７％（Ｐ＜０．００１）。（２）肾动脉内注射ＥＴＡ受体选择性拮抗剂ＢＱ－１２３（１５０μｇ／ｋｇ）,ＥＴ－１的上述效应即被拮抗。与ＥＴ组相比差异非常显著（Ｐ＜０．００１）。（３）肾动脉内注射二氢吡啶敏感性Ｌ－型钙通道阻断剂Ｎｉｆ（０．１ｍｇ／ｋｇ）,也可明显抑制ＥＴ－１的上述效应,与ＥＴ组相比差异十分显著（Ｐ＜０．００１）。以上结果表明：肾动脉内注射ＥＴ－１引起的麻醉大鼠ＭＡＰ增高和ＡＲＮＡ积分增加的作用,可能是由ＥＴＡ受体介导的,其作用的细胞机制可能在于胞内钙超载     

中枢注射U—50,488H对肾水钠钾的排出及PVH内TH —IR神经元活性的影响

本工作１２％乙醇麻醉的大鼠,观察了下丘脑室旁核（ＰＶＨ）微量注射Ｋ型阿片受体激动剂Ｕ－５０,４８８Ｈ对大鼠肾水钠钾排出的影响,以及第三脑室注射Ｕ－５０,４８８Ｈ对ＰＶＨ中多马上胺神经元活性的影响。结果如下（１）ＰＶＨ微量注射Ｕ－５０,４８８Ｈ（５μｇ／ｌ）后２０ｍｉｎ内大量尿量开始增（Ｐ＜０．０１）,持续约１００ｍｉｎ,,４１－６０ｍｉｎ尿量增加达峰值（Ｐ＜０．００１）。（２）,ＰＶＨ预先（１０ｍ     

大豆黄酮对大鼠肌肉生长和几种内源激素水平的影响

给雄性、雌性和雄性去势大鼠皮下注射大豆黄酮［３ｍｇ／（１００ｇ体重·天）］１６天。结果：雄性大鼠日增重提高１４．７％（Ｐ＜０．０５）,耗料与增重比降低１２．０％,后腿肌重和后腿肌总ＲＮＡ含量显著增加,而总ＤＮＡ含量无显著变化;血清脲氮水平显著下降,血清睾酮、雌二醇、生长激素和β－内啡肽含量显著提高。雄性去势大鼠日增重、后腿肌重无显著变化,血清睾酮、生长激素和β－内啡肽水平虽显著高于对照组,但睾酮水平仅为同等条件下完整大鼠的８％左右。雌性大鼠日增重降低１９．０％（Ｐ＜０．０１）,耗料与增重比提高１７．８％,血清睾酮、雌二醇和生长激素水平显著降低。试验结果表明：大豆黄酮对大鼠肌肉生长和几种内源激素水平的影响呈现性别差异,对雄性大鼠肌肉生长的促进作用依赖于睾丸的内分泌机能。     

Urethral glands of the male mouse contain secretory component and immunoglobulin A plasma cells and are targets of testosterone.

The occurrence and possible functions of mucosal immunity in the male urogenital tract have not been extensively investigated. In this study we used immunolabeling to localize secretory component (SC) and immunoglobulin (Ig) A in the urogenital tract of the male mouse. SC was located in the ventral prostate, while SC and IgA plasma cells were both detected in the urethral glands in the pelvic and bulbous portions of the urethra. SC and IgA were not observed elsewhere in the urogenital tract. We also examined the ventral prostate and urethral glands of sham-castrated, oil-treated castrated, and testosterone-treated castrated mice. There was a striking reduction in the size of the ventral prostate and urethral glands in oil-treated castrates compared to the other two groups, based on gross and histological morphology. Morphometric analysis showed that the cell and nuclear sizes of the urethral gland acinar cells were reduced after castration and restored to normal size by testosterone treatment. Androgen receptors (AR) were localized in the nuclei of urethral gland cells by immunocytochemistry using anti-AR antibodies. Labeling of SC and IgA plasma cells was similar in the urethral glands and ventral prostates of sham- and testosterone-treated castrates, but was reduced or absent at these sites in oil-treated castrates. These studies show that the ventral prostate and urethral glands may be sites for secretory immunity in the male murine urogenital tract, and that the urethral glands are targets for testosterone.     

Induction of metallothionein in the livers of female Sprague-Dawley rats treated with 2,3,7 ,8-tetrachlorodibenzo-p-dioxin

Metallothioneins (MTs) are cysteine-rich metal-binding proteins that exert cytoprotective effects against metal toxicity and external stimuli including ionizing or ultraviolet B irradiation. Since 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to cause an exaggerated oxidative stress response in animals and in different organs, we have studied possible involvement of MT in the oxidative responses induced by TCDD. Female Sprague-Dawley (SD) rats (6-week old) were administered a single oral dose of TCDD that varied from 1.0 to 4.0 microg/kg body weight. The serum and tissues were collected 7 days after dosing. Indicators of oxidative damage were assessed. Significant increases in serum 8-hydroxydeoxyguanosine (8-OHdG) levels were observed in the rats dosed with 2.0 and 4.0 microg TCDD/kg bw. Only 4.0 microg TCDD/kg bw produced a decrease in reduced glutathione concentration in the liver. Immunohistochemical staining revealed a TCDD-induced increase in heme oxygenase-1 (HO-1) expression in the hepatic macrophages (Kupffer cells). Under these conditions, MT protein as well as the mRNAs of MT-I and MT-II, were dose-dependently induced in the liver by TCDD doses from 1.0 microg/kg bw. TCDD-induced MT was found to localize in the parenchymal cells of the liver. Serum concentrations of cytokines (TNF-alpha, IL-1beta and IL-6) were not affected by TCDD. The hepatic concentrations of Cu, Zn and Fe were all increased significantly by TCDD administration. Our results suggest that MT levels are increased in the liver upon exposure to TCDD, perhaps by TCDD-generated reactive oxygen species, and that it may play a protective role in TCDD-induced oxidative stress responses as an antioxidant.     

Some histochemical studies on the prostate, urethral and bulbourethral glands of the one-humped camel (Camelus dromedarius)

Synopsis The histochemical localization of carbohydrates, ribonucleoproteins (RNA), lipids, some hydrolytic enzymes, succinate and lactate dehydrogenase and acetylcholinesterase were investigated in the prostate, urethral and bulbourethral glands of the camel. These glands probably secrete carbohydrate-protein complexes. In the bulbourethral glands, they are sulphated mucopolysaccharides. RNA was seen in the cytoplasm of the prostate and urethral glands. Neutral lipids were cytoplasmic and present in moderate amounts in the prostate and urethral glands and in traces, in the bulbourethral gland. Acid phosphatase-containing granules were abundant in the prostate, moderate in the urethral glands and in traces in the bulbourethral glands. Alkaline phosphatase was observed in the apical cytoplasm of the prostate and bulbourethral glands and in the ducts of the urethral glands. ATPase and adenosine 5-monophosphatase were seen in the basal laminae and interstitial tissue. In the urethral glands, adenosine 5-monophosphatase was distributed diffusely in the cytoplasm. Succinate dehydrogenase was seen in the urethral and bulbourethral glands. Varying degrees of lactate dehydrogenase activity was observed in all the glands. Acetylcholinesterase was confined to neural elements. The pars disseminata and the urethral glands were considered as two distinct glandular zones along the pelvic urethra. The significance of these histochemical results is discussed.     

Central and peripheral action of testosterone propionate on scent gland morphology and marking behaviour in the Mongolian gerbil

Scent gland size and activity and frequency of marking under standard conditions were compared in five groups of male and female gerbils: (1) intact, sham-operated controls, (2) intact with scent glands excised, (3) gonadectomized, (4) gonadectomized injected with 1000 μg testosterone propionate (TP) on alternate days, and (5) gonadectomized with a low dose (25 μg) TP applied topically to the ventral scent gland on alternate days. The animals were housed in individual cages and tested for marking in an open field arena with plastic pegs.The scent gland is not required in either sex for the behavioural act of marking. Topical application of a dose of TP too low to exert a systematic effect restored the scent gland but not marking. Injection of sufficient TP to restore seminal vesicle weight restored marking, as well as the scent glands.It was concluded that in the male, both marking behaviour and scent gland size are controlled by the testes. The effect of androgens on marking is mediated directly through the central nervous system, and not through peripheral stimulation of the glands.Females have smaller glands and mark less than males. The ovaries appear to have little control over marking frequency, and some control over scent gland size. It is possible to stimulate marking behaviour to supernormal levels by TP injection, but not by topical application.     

Nuclear zinc in the three lobes of the rat prostate gland

The prostate gland concentrates Zn more than any organ in the body and Zn is increased and decreased in benign prostatic hyperplastic and adenocarcinoma of the prostate, respectively. Zn is a key structure in zinc finger proteins and hence is involved in cell proliferation and differentiation. The role of Zn may be attributed to a zinc binding protein, metallothionein (MT), which can be induced by certain metals, e.g. Cd. Induced MT may be involved in Zn metabolism and transport in the prostate gland. X-ray microanalysis was used to detect quantitatively the Zn in the nuclei of the glandular epithelium of the gland. It was found that Zn concentration was elevated and reduced in the lateral and dorsal lobes, respectively, after Zn treatment, but the Zn concentration was elevated in the lateral lobe after cadmium treatment. The ventral lobe did not show any substantial change in Zn concentration after either treatment. These results suggest that the three lobes of the gland respond differently to treatment. The variations in the response may reflect different mechanisms of Zn transport and metabolism in the three lobes of the rat prostate. Binding Zn to MT may indicate the involvement of MT in the metabolism and transport of zinc, an effect which may be modified by treatment.     

Arguments against the prostatic origin of the R-3327 Dunning H tumor

The Dunning tumor, originally described as a carcinoma of the rat dorsal prostate, has for long been used as an experimental model of prostatic cancer. We have recently presented a number of morphological findings that are incompatible with the prostatic origin of the H-subline of the Dunning tumor. In this paper, biochemical and immunohistochemical markers of rat prostate and mammary gland are studied in the R-3327 Dunning H tumor. Pieces of the H tumor were inoculated in male or lactating female rats. The electrophoretic protein pattern of Dunning tumor extracts was more similar to that of the mammary gland than the dorsolateral prostate. Proteins selectively appearing after metabolic labeling in Dunning tumors grown in lactating rats corresponded to labeled proteins in mammary glands from the same animals. Secretory proteins typical of the lateral prostate (SVS II) and dorsal prostate (transglutaminase) could not be detected immunohistochemically in the Dunning tumor. Western blot studies of tumor extracts and slot blot analysis of RNA preparations from the tumor confirmed the absence of SVS II and prostate specific transglutaminase from the Dunning tumor. On the other hand, the presence of mammary gland proteins such as milk fat globule membrane proteins, lactoperoxidase and lactalbumin were detected in the Dunning tumor by immunohistochemistry and Western blotting, but were absent from the dorsolateral prostate. Transferrin-mRNA, expressed in the male urogenital tract and also in the liver and other tissues, was detected in the mammary gland and Dunning tumor, but not in the dorsolateral prostate. The absence of mammary gland secretory beta-casein in the Dunning tumor was related to the elevated Ha-ras oncogene expression in the tumor, previously reported to suppress casein expression. The findings clearly demonstrate that the prostate cannot be the origin of the Dunning tumor, presently being used in prostatic cancer research. The designation prostatic adenocarcinoma for this tumor is therefore invalid. Furthermore, the data support our view that mammary gland might be the origin of the Dunning tumor, although the derivation from the bulbourethral or the parotid glands cannot strictly be excluded.     

Short-term effects of prolactin on prostatic function in rats with lisuride-induced hypoprolactinaemia

The effects of a single injection of ovine prolactin on prostatic function were monitored in intact, intact androgenized and castrated-androgenized rats rendered hypoprolactinaemic after 7 days of treatment with a potent dopamine agonist, lisuride. Hypoprolactinaemia was associated with reductions in ventral prostate weight, polyamine levels, lateral lobe zinc and the concentration of the ventral prostate protein prostatein, but an elevation in the level of cytosolic oestradiol binding. Whether these differences attained statistical significance depended on whether the animals were intact, intact-androgenized or castrated-androgenized. With the exception of ventral prostate weight and lateral lobe zinc concentrations, a single injection of prolactin restored or reversed these changes towards control levels within 12 h, which could not be explained by an indirect effect of the hormone on adrenal or testicular function. No effects of lisuride or prolactin were observed with regard to the content of fructose in the coagulating gland or in the degree of prolactin binding to prostatic membranes.     

The Impact of Exogenic Testosterone and Nortestosterone-Decanoate Toxicological Evaluation Using a Rat Model

The impact of exogenic testosterone (T): 1.5 and 3.0 mg/kg.bw) and 19-nortestosterone 17-decanoate (ND): 1.5 and 7.5 mg/kg.bw) in castrated male rats was evaluated based on: (a) weight increase of the androgen target tissues, respecting the Hershberger methodology; (b) the 17α and β-testosterone, 17 α and β-estradiol and 17 α and β-nortestosterone levels using the GC-MS/MS technique; and (c) observation of the serum free thyroxine levels (T₄). Results revealed that T and ND significantly increased the weight of androgen target tissues as follows: ND was more influential on seminal vesicles, levator ani-bulbocavernosus muscle (LABC) and Cowper''s glands and T (at a dose of 3.0 mg/kg.bw) influenced the weight of the ventral prostate and glans penis. Serum samples analyzed for steroid hormone levels showed the presence of 17β-testosterone, 17β-estradiol and 17β-nor-testosterone, in castrated male rats injected with testosterone and nortestosterone, but no significant differences were found between thyroid responses and thyroid hormone levels. The results of this research proved the disrupting activity of T and ND when administered in high doses and the useful application of the Hershberger bioassay in the case of ND.     

Sexual differences and effects of castration on secretory mode and intracellular calcium ion dynamics of golden hamster Harderian gland

The aim of the present work was to study the sexual differences in secretory mechanisms and intracellular calcium ion dynamics in the Harderian gland of the golden hamster. In both sexes the Harderian gland consisted of small and large lobes. In the intact control male glands the secretory portions of both lobes showed wide lumina that contained secretory material and cytoplasmic fragments, suggestive of the occurrence of exocytosis and apocrine secretion. After perfusion with HEPES-buffered Ringer's solution containing 10 microM carbamylcholine (CCh), the glandular cells showed features of enhanced secretion and a rise in intracellular calcium concentration ([Ca2+]i). In the intact control female gland the lumina of most secretory portions in the large lobe contained porphyrin accretions, and exocytosis was the sole secretory mechanism. Stimulation of the large lobe with 10 microM CCh did not raise [Ca2+]i or cause enhanced secretion. The small lobe in females resembled the male gland in secretory functions, and CCh administration caused enhanced secretion and a rise in [Ca2+]i. Castration in males abolished apocrine secretion; exocytosis became the sole secretory mechanism, and stimulation of the glandular cells with CCh did not cause enhanced secretion or induce a rise in [Ca2+]i. To the contrary, in females, castration restored apocrine secretion and CCh administration caused enhanced secretion and a rise in [Ca2+]i. Castration did not affect the secretory mechanisms and the effect of CCh on the glandular cells in the small lobes of both male and female glands. The present study points to the possibility that sex hormones may control the functioning or expression of muscarinic receptors in the Harderian gland of the golden hamster.