Fluid imbibition as a factor in estrogen‐induced increase of prostatic weight in castrated rats

Corrales, J. J.; Kadohama, N.; Chai, Lee S.; Høisæter, Per Å.; Hampton, Michael; Murphy, Gerald P.; Sandberg, Avery A.

doi:10.1002/pros.2990020403

Cited by 6 publications

(4 citation statements)

References 19 publications

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“…In the present study, a fixative of high osmolality was used throughout and would presumably exert the same effects on all experiments. On the other hand, the apparent increase in the size of the lamina propria as observed in the seminal vesicle after oestradiol treatment may be attributed to water imbibi tion as reported by Corrales et al [21].…”

Section: Epitheliumsupporting

confidence: 57%

See 1 more Smart Citation

Ultrastructural Study of the Effects of 17β-Oestradiol on the Lateral Prostate and Seminal Vesicle of the Castrated Guinea Pig

Cc¹,

Wong²

1991

Cells Tissues Organs

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Administration of oestradiol to castrated animals induced hypertrophy of the secretory cells in the lateral prostate and seminal vesicle. In the lateral prostate, increases in the number of small highly electron-dense granules, multivesicular bodies and intercellular spaces were the prevailing effects 2 weeks after oestradiol treatment. There was also an apparent increase in the amount of cytokeratin intermediate filaments. Prolonged oestradiol administration for 4 weeks showed no appreciable changes in the glandular epithelium when compared with 2-week treatment. However, an increase in the thickness of the fibromuscular layer was observed. In the seminal vesicle, basal cell hyperplasia was associated with a concurrent increase in the size of intercellular spaces 2 weeks after oestradiol administration. There were also apparent increases in the volume of the lamina propria and in the number of stromal cells. An apparent increase in the density of collagen fibres in the stroma was observed 2 and 4 weeks after oestradiol administration. In conclusion the responses of the epithelium of the lateral prostate and seminal vesicle to a pharmacological dose of oestradiol are different. Prolonged oestradiol administration exerts a more prominent effect on the smooth muscle in the lateral prostate but not in the seminal vesicle. The effects of oestradiol may be mediated directly or indirectly through the other hormones.

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Section: Epitheliumsupporting

confidence: 57%

“…fluid accumulation as observed in the prostate gland of the Copenhagen rat after oestradiol treatment is partially suppressed after the administration of elymociavine. a prolactin-secretion-inhibiting agent [21]. Differ ences in blood prolactin between strains of rats may also influence the sensitivity of the prostate to oestrogen.…”

Section: Stromamentioning

confidence: 99%

Ultrastructural Study of the Effects of 17β-Oestradiol on the Lateral Prostate and Seminal Vesicle of the Castrated Guinea Pig

Cc¹,

Wong²

1991

Cells Tissues Organs

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“…It is possible that the depressed blood flow is an adjustment to decreased metabolic activity in the prostatic cells related to decreased production of vasodilating substances (eg, lactate and cyclic AMP). Estrogen treatment induces an increase in plasma prolactin [22]. Corrales et al [22] reported a concomitant prostatic oedema in Copenhagen rats which was antagonized by a prolactin secretion inhibiting agent.…”

Section: Discussionmentioning

confidence: 99%

Testosterone‐induced decrement of prostatic vascular resistance in rats is reversed by estrogens

et al. 1985

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The function and growth of the rat prostate are stimulated by androgens and inhibited by estrogens. To study the influence of these hormones on the prostatic blood flow, prostatic vascular resistance was measured in castrated adult rats, which were testosterone supplemented and treated with different estrogenic substances. Prostatic blood flow was measured using the microsphere technique. Testosterone supplementation for 8-9 days after castration resulted in decreased vascular resistance in both the ventral and dorsolateral prostates. In testosterone-supplemented rats, treatment for the same period of time with estradiol benzoate, ethinyl estradiol, and diethylstilbestrol induced increased vascular resistance in both the ventral and dorsolateral prostates. However, treatment with estromustine or estramustine did not change prostatic vascular resistance significantly. It was concluded that the testosterone-induced decrease of prostatic vascular resistance was reversed by estradiol, ethinyl estradiol, and diethylstilbestrol, possibly by a direct effect on the prostate.

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“…Additionally to androgens, both estrogens and proteohormones have been shown to modulate the regulation of rat prostatic function. (Corrales et al, 1981;Daehlin et al, 1985;Lohstroh, 1968;Negro-Vilar, 1980;Prieto and Carmena, 1983;Tisell, 1971;Tisell et al, 1976) (Figs. 5-8).…”

Section: Effects Of Experimentalmentioning

confidence: 99%

Effects of hormones on the prostate in adult and aging men and animals

Sinowatz

Amselgruber

Plendl

et al. 1995

Microscopy Res & Technique

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Literature on the effect of steroid hormones (androgens, estrogens, and other steroids), of peptide hormones (e.g., prolactin), and growth factors (e.g., EGF, FGF, TGF-beta), on the effect of castration and of experimental hormone application on the prostate is reviewed. Androgens have inductive, repressive, and interactive effects. They counterbalance an agonistic effect on proliferation and an antagonistic effect on cell death; they may influence DNA synthesis and induce the synthesis of substances with mitogenic effects on the prostate. Estrogens exert direct and indirect effects on the prostate. They suppress the secretion of gonatropins, thus repressing testicular androgen secretion. They stimulate the fibromuscular stroma and induce squamous metaplasia of the epithelium. Estrogens may also be involved in the onset of benign prostatic hyperplasia. Prolactin is preferentially bound in the diseased human prostate. An abundance of information has been gained on EGF, FGF, TGF-beta, and other growth factors. They may be involved in the development of prostatic hyperplasia. Castration leads to a striking reduction in prostatic size in a short period of time due to autophagic and heterophagic processes. In castrated individuals, the prostate is enriched in androgen-independent cells. Experimental hormone application involves the substitution of androgens as well as anti-androgens, long-term application of different hormones, and application of combinations of drugs. The results of several studies are described. Further directions in the field of prostate research should concentrate on the role of growth factors in prostate development and pathology and on the effect of certain lectins on prostate diseases. We think that the investigation of interactions between steroid hormones and growth factors in normal and pathological neovascularization of the prostate is important.

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Fluid imbibition as a factor in estrogen‐induced increase of prostatic weight in castrated rats

Cited by 6 publications

References 19 publications

Ultrastructural Study of the Effects of 17β-Oestradiol on the Lateral Prostate and Seminal Vesicle of the Castrated Guinea Pig

Ultrastructural Study of the Effects of 17β-Oestradiol on the Lateral Prostate and Seminal Vesicle of the Castrated Guinea Pig

Testosterone‐induced decrement of prostatic vascular resistance in rats is reversed by estrogens

Effects of hormones on the prostate in adult and aging men and animals

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