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Biomedical subjects

H G Bohnet

Publications and source records attributed to H G Bohnet.

At least 73 records · Page 4Linked to original sources
PubMed1978

In vivo effects of antisera to prolactin receptors in female rats.

Antisera generated in guinea pigs against partially purified PRL receptors derived from rabbit mammary glands were tested for their effect on PRL binding and the biological effects of PRL in vitro and in vivo. Several dilutions of either normal guinea pig serum or anti-PRL receptor serum were incubated in vitro with homogenates of rat ovaries. Although specific binding of PRL was inhibited as much as 90% by the anti-serum, normal guinea pig serum had little effect. There was no inhibition of binding of LH and FSH to ovaries by these antisera. When these antisera were administered to normal cycling rats, the most pronounced effect was an increase in the number of corpora lutea, presumably due to the prevention of the luteolytic effect of PRL. When one of these antisera was given to adult rats immediately after parturition, weight gain of their pups decreased significantly, possibly reflecting a decrease of milk yield. Thus, passive immunization of animals with anti-PRL receptor sera modifies the actions of PRL on some of its target tissues.

Animals↗
PubMed1978

Effects of cimetidine on prolactin, LH, and sex steroid secretion in male and female volunteers.

The histamine H2-receptor antagonist cimetidine, which has recently been introduced for the treatment of gastric and duodenal ulcers and haemorrhage, respectively, stimulates prolactin (PRL) secretion. The release of PRL after a bolus injection of the compound is significantly higher in female than in male volunteers, and is more pronounced during the luteal than during the follicular phase of the menstrual cycle. Oral administration of the drug stimulates PRL to a similar extent as parenteral administration. Treatment of male and female volunteers with cimetidine for 20 days (1 g/day orally) resulted in elevated serum PRL concentrations in both sexes. Basal LH levels as well as the response to 25 microgram LH-RH were not significantly changed after treatment. Testosterone levels in males and oestradiol levels in females were not altered. Luteal progesterone, however, was significantly diminished in the menstrual cycles when cimetidine was given. The mechanism underlying the stimulatory effect of cimetidine on PRL secretion is not clear, but it does not seem that this ability is exerted via an inhibition of pituitary dopamine receptors. The dopaminergic effect of lisuride, an ergot alkaloid, could not be reversed by cimetidine.

Adult↗
PubMed1978

Gonadotrophin release during chronic administration of D-ser (TBU)6 LH-RH-EA in functional amenorrhoea.

Six women with long-standing functional amenorrhoea were treated with 5 microgram of D-Ser (TBU)6 LH-RH-EA twice daily for 14 days. The functional states of the gonadostats, as assessed by a 25 microgram LH-RH test dose, varied widely before the treatment was started whereas at the end of it they were uniformly low. In all patients D-Ser (TBU)6 LH-RH-EA induced gonadotrophin release, the peak values occuring between day 1 and 3 of therapy. Despite further injections mean gonadotrophin levels declined rapidly therafter and remained in the basal range for the rest of the study. Release of oestradiol was very uncharacteristic. No consistent ovarian response pattern was observed during the analogue administration. It is obvious that chronic stimulation with D-Ser (TBU)6 LH-RH-EA leads to a decreased responsiveness of the pituitary gland.

Adult↗
PubMed1977

Prolactin oversuppression.

Patients with primary infertility due to hyperprolactinemic corpus luteum insufficiency and oligomenorrhea were treated with Bromocriptin. Suppression of serum prolactin for up to four menstrual cycles resulted in a normalisation of the length of the cycle(32 vs 28 days) as well as of luteal progesterone secretion. In addition, ovulation occurred earlier after than before treatment (on day 14 vs day 18). When, however, prolactin concentrations reached levels of less than 120 muU/ml (3 ng/ml), which were observed during the 5th and 6th treatment course, reappearance of shortened luteal phase occurred probably due to oversuppression of prolactin. Premenstrual spottings were observed too. The data presented indicate that minimal prolactin is required for normal follicular maturation and luteal development. On the other hand, the gonadostat may be susceptable to the dopaminergic stimulus of Bromocriptin to a different extent as oversuppression of prolactin is not observed in hyperprolactinemic anovulatory syndromes. Thus, treatment with Bromocriptin requires a continuous monitoring of serum prolactin as well as individual treatment regimens.

Bromocriptine↗
PubMed1977

Localization of prolactin binding in prostate and testis: The role of serum prolactin concentration on the testicular LH receptor.

Specific binding sites for prolactin (PRL) and gonadotrophins on ventral and dorsolateral prostate as well as on Leydig cells and tubules of testes of rats at different ages were examined. The binding sites for PRL were found in greatest number in ventral prostate and in Leydig cells. LH binding sites were also more numerous than FSH binding sites in the latter. FSH sites were greater than LH sites in tubular preparations obtained from the testis. Specific binding (SB) of PRL in the Leydig cells reached a maximum at 45 days (4%) and in the case of LH a maximum of 12% was obtained at 70 days. In both preparations SB of FSH exhibited a plateau between 20 and 40 days (11%) followed by a gradual decline to 6% at 100 days. Following 20 dyas of treatment with Bromocriptin beginning at 20 days serum PRL was suppressed and SB of LH to the Leydig cells was significantly decreased, whereas SB of PRL and FSH was unaffected. These studies suggest that despite decreases in serum PRL, the number of PRL and FSH receptors remain unaltered. On the contrary, LH receptors in the rat testis are modulated by changes in serum PRL.

Age Factors↗
PubMed1976

Prolactin binding sites in the male rat liver following castration.

Specific binding sites for prolactin (PRL) have been detected in membrane preparations from the liver of the male rat following castration. The magnitude of the increased binding following castration varied with the age of the animals and with the time after castration. The effect of castration did not appear to be PRL mediated, since increases or decreases of serum PRL levels after pharmacological agents had no effect on PRL binding. The pituitary, however, seems to have a critical role in mediating the increase in PRL binding. Adrenalectomy did not influence the extent of binding of PRL after castration. Testosterone administration, however, completely prevented the increased PRL binding which followed castration. These studies suggest that testosterone has a modulating effect on hepatic PRL binding sites. The maintenance of such binding activity requires not only PRL, but also a functioning pituitary.

Adrenal Glands↗
PubMed1976

Hyperprolactinemic anovulatory syndrome.

The functional status of the hypothalamo-pituitary-gonadal axis was investigated in 127 women with anovulatory disease. Radioimmunoassayable circulating LH, FSH, and prolactin concentrations were measured. An attempt was made to localize the functional lesion by utilizing the following criteria: 1. Hypothalamic function: a) clomiphene test based upon hormonal parameters; b) recording of the pulsatile LH fluctuation (spiking) and of basal FSH. 2. Pituitary function: determination of the gonadotropin reserve by means of a standardized LRH test. 3. Ovarian function: a) measurement of plasma E2 and progesterone levels by RIA; b) gestagen bleeding test. All patients had amenorrhea of up to 14 years duration. A total of 17 hyperprolactinemic patients (13.4%) was found. Eight of these patients never experienced galatorrhea, in 7 only transient galactorrhea was reported, and in 2 cases galactorrhea persisted. All hyperprolactinemic patients were found to be clomiphene non-responders as well as nonspikers. The pituitary LH reserve varied from practically none to normal. Baseline LH was low whereas that of FSH was normal. In accordance with this observation E2 levels, with two exceptions, were found to be in the lower range of normal female concentrations. Thus, all but two patients exhibited gestagen withdrawal bleeding. In conclusion, the hyperprolactinemic anvoluatory syndrome is not necessarily associated with galactorrhea. In all cases of amenorrhea syndromes with or without galactorrhea, hyperprolactinemia should be excluded as it is very often associated with anovulation. The hyperprolactinemic anovulatory syndrome includes the following features: 1. gestagen withdrawal bleeding. 2. subnormal to normal E2 levels. 3. clomiphene nonresponsiveness. 4. LH-hypogonadotropism. 5. lack of LH secretory episodes. 6. FSH-normogonadotropism.

Adult↗
PubMed1976

Effect of prolactin and growth hormone on prolactin and LH receptors in the dwarf mouse.

Dwarf mice (DW/J;dw/dw) which exhibit a deficiency of prolactin and GH secretion were treated for 8 days with ovine prolactin and/or human GH (10 or 20 mug/day) and the effect on hepatic and testicular prolactin receptors was investigated. In both sexes there was a significant increase in body weight after all hormone treatments, but an increment in testicular weight was observed only after prolactin administration. Prolactin treatment increased the specific binding % of prolactin in liver membranes in females but not males, and in testicular homogenates (together with an increase in LH receptors). The results suggest that lack of prolactin but not of GH retards sexual development in these mice. Treatment with prolactin partly counteracts this deficiency, and the effect may be mediated by the induction of hepatic and testicular prolactin and LH receptors.

Animals↗
PubMed1976

Induction of lactogenic receptors. I. In the liver of hypophysectomized female rats.

To identify the hormones which affect lactogenic receptors in the liver of chronically hypophysectomized female rats, hormones were injected s.c. for 7 days. Specific binding (%, SB) of labelled ovine prolactin (PRL) in liver membrane preparations (1000,000 X g pellet) of controls was 1%. Estradiol (E2), cortisone (Con), ACTH or bovine growth hormone (bGH) treatment did not induce hepatic binding sites for PRL. Human GH and a single dose of 2mg PRL (but not lower doses) increased SB of PRL. Treatment with oPRL plus ACTH was less effective than hGH plus ACTH (13 vs 28%); combinations of oPRL plus Con as well as administration of oPRL plus ACTH to hypophysectomized and adrenalectomized female rats did not induce SB for PRL. Therapy with oPRL plus hGH (26%) was more potent than oPRL plus bGH (2%). These studies suggest that PRL, GH, and ACTH induce and in concert with sex steroids, modulate the lactogenic receptors in the female rat liver. The effect of ACTH is not due to increased adrenal corticoid secretion.

Adrenalectomy↗
PubMed1976

Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor.

The role of growth hormone (GH), as well as prolactin and ACTH, in the induction of the PRL receptor was investigated both in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of s.c. injections, specific binding (% SB) of PRL in controls and rats treated with oPRL, hGH, ACTH, hCG, estradiol (E2), or testosterone (T) was approximately 1%. Treatment with oPRL plus ACTH increased SB to 4%; adding E2 to this combination produced a further increase to 8%, whereas the addition of T decreased hepatic binding to 1%. Combination of hGH with ACTH was most effective, giving a SB of 33%, which is similar to that observed in the liver of rats bearing a GH secreting tumor (36%). These studies suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.

Adrenocorticotropic Hormone↗