Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Lloyd, Helen; Meares, J. D.; Jacobi, Joan

doi:10.1002/ijc.2910110110

Cited by 26 publications

(11 citation statements)

References 12 publications

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“…The results presented here are compatible with the gener ally accepted concept that E: stimulates prolactin synthesis [4,5,8,10,12,16] and thereby facilitates increased basal PRL secretion [11,18,20,26]. Details of the mechanisms, whereby 2-OH-estrone suppresses PRL secretion [22] are unknown.…”

Section: Discussionsupporting

confidence: 79%

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Wollesen¹,

Knigge²,

Larsen³

1982

Neuroendocrinology

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This study was undertaken to test whether ratios between plasma concentrations of different estrogens would be more determinant of prolactin (PRL) secretion than plasma concentrations of estrogens per se have been found to be. Oral administration of micronized 17β-estradiol in a dose of 2 mg b.i.d. for 1 month to 7 postmenopausal women raised plasma estrone (E₁) from a median of 29 to 683 pg/ml and plasma 17β-estradiol (E2) from a median of 5.7 to 131 pg/ml. The E₁/E₂ ratios rose from a median of 4.01 to 4.92 (P_Wilcoxon (P_w) > 0.025). Basal serum PRL increased from a median of 79.2 to 100 μlU/ml (P_w) > 0.025). However, the area under the curve of the PRL response to TRH increased from a median of 2,553 mm² before to 3,919 mm² after treatment (P_w <0.025). Highly significant correlations existed between the E1/E2 ratios and the PRL responses to TRHboth before (r_Spearman (r_s) = 0.964) (P_Spearman (P_s) <0.005) and after (r_s = 1.000) (P_s < 0.00025) estradiol treatment, whereas no correlations (P_s <0.679) existed between plasma concentrations of Ei or E2 per se and either basal serum PRL or PRL response to TRH. The regression curves of best fit between the E1/E2 ratios and the PRL responses to TRH were hyperbolic both before (r = 0.884) and after (r = 0.996) treatment. These results, showing that the E1/E2 ratio rather than the plasma Ei or E2 concentrations per se are correlated to the PRL responses to TRH, imply that the metabolic conversion rate of estrogens modulates PRL secretion.

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Section: Discussionsupporting

confidence: 79%

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Wollesen¹,

Knigge²,

Larsen³

1982

Neuroendocrinology

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“…A number of studies have reported that oestrogen treatment of intact or castrated male rats causes an enhancement of blood prolactin concentration (van der Gugten et al 1970;Kwa et al 1972a;Lloyd et al 1973;Kalra et al 1973;Mallampati 8c Johnson 1973). The present results, however, show that in blood samples of oestrone treated castrated males taken without stress the prolactin concentration was only slightly higher than in intact males.…”

Section: Figmentioning

confidence: 97%

Plasma Prolactin in Undisturbed Cannulated Male Rats; Effects of Perphenazine, Frequent Sampling, Stress and Castration Plus Oestrone Treatment

Mattheij

Pijkeren

1977

Acta Endocrinologica

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Blood was collected from undisturbed male rats by means of chronically indwelling intrajugular cannulae and the plasma prolactin (PRL) concentration was determined by a radioimmunoassay. The effect of perphenazine, frequent bleeding, handling and brief ether stress in normal males and of stress in castrated oestrone treated males was determined. The plasma PRL concentration in undisturbed intact males was low. Castration plus oestrone treatment for 3 or 7 weeks had little or no effect on the PRL concentration. Neither frequent blood sampling nor removal of 3 ml blood over a period of 5 h affected plasma PRL concentration. Intravenous administration of perphenazine caused a striking and prolonged increase in plasma PRL in intact males. Brief handling or mild ether stress caused a significant rise in PRL within 2 min in intact males; 15\p=n-\20 min later PRL had returned to the undisturbed level. Brief ether stress in oestrone treated castrates induced a comparable pattern of prolactin release, although of greater magnitude. In these animals a second stress one hour later induced a similar response. It is concluded that chronic cannulation neither affects the unstressed prolactin level nor interferes with the ability of the adenohypophysis to release PRL. The results also indicate that when rats are handled a truly stress free sample can only be obtained when the blood is drawn within one minute after the initial disturbance of the animal. The evidence presented indicates that oestrone treatment increases the responsiveness of male rats to stress-induced PRL release.

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“…The significance of weight loss and of the psychiatric features of anorexia nervosa in patients with amenorrhoea has been emphasised, [6][7][8][9][10][11][12][13][14][15][16][17][18] and these factors accounted for many of our patients. The recent suggestion that low body weight renders patients more susceptible to impairment by the OC of subsequent reproductive performance'9 seems improbable: patients with loss of weight occurred with equal frequency in both groups, and probably the cause of the reproductive disturbance was not the previous OC treatment but the psychiatric components of anorexia nervosa and the metabolic effects of self-starvation.20-2 Similarly, a significant number of patients in both groups had other obvious psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

Post-“Pill” Amenorrhoea—cause or Coincidence?

Jacobs

Knuth

Hull

et al. 1978

Obstetrical & Gynecological Survey

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Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Cited by 26 publications

References 12 publications

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Plasma Prolactin in Undisturbed Cannulated Male Rats; Effects of Perphenazine, Frequent Sampling, Stress and Castration Plus Oestrone Treatment

Post-“Pill” Amenorrhoea—cause or Coincidence?

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