Search PubMed⌕ Search

Biomedical subjects

P Eneroth

Publications and source records attributed to P Eneroth.

At least 235 records · Page 13Linked to original sources
PubMed1983

Effect of the peptide PHI-27 on prolactin release in vitro.

The present study demonstrates that PHI, a peptide belonging to the glucagon-secretin group and thus structurally similar to VIP, can release prolactin from dispersed rat anterior pituitary cells and also causes release of prolactin from hemipituitaries. PHI-like immunoreactivity has previously been demonstrated in a hypothalamic system with nerve endings in the median eminence, and, taken together, these findings suggest that PHI may represent a physiologic prolactin-releasing factor.

Animals↗
PubMed1983

An evaluation of early pregnancy HCG determination as a prognostic tool for fetal outcome.

In a retrospective study of 150 pregnant women with high or low serum HCG levels at the time they sought acute advice at the ward, two categories of women were found: a majority (n = 111) who had abdominal pain and/or vaginal bleeding, and a minor group (n = 39) who worried about their condition but were otherwise symptom free. The underlying reason for the difference in clinical outcome amongst 'bleeding' and 'concern' women with both high and low HCG serum values are discussed. It is concluded that women with abnormal HCG levels in early pregnancy deserved close attention in the 3rd trimester.

Abortion, Spontaneous↗
PubMed1983

Possible role of somatostatin in the regulation of the sexually differentiated steroid metabolism and prolactin receptor in rat liver.

The regulation of the sexually differentiated metabolism of 4-[4-14C]androstene-3,17-dione and the presence of PRL receptors in rat liver were studied. Electrolytic lesions in male rats placed in a restricted area in the anterior hypothalamic periventricular area caused a feminization of hepatic steroid metabolism (i.e. increased the 5 alpha-reductase and decreased the 6 beta- and 16 alpha-hydroxylase activities) and of the levels of PRL receptors (increased binding of [125I]-labeled human PRL). After periventricular lesions, histochemical analysis revealed a decrease in somatostatin-like immunoreactive cell bodies in the periventricular area. Also the number of immunoreactive somatostatin fibers in the median eminence was dramatically reduced. Somatostatin levels in the median eminence, as measured by RIA, were reduced to approximately 2-10% of control values after periventricular lesions. Large lesions in the amygdaloid complex in male rats caused a partial feminization of hepatic steroid metabolism and PRL receptors. Passive immunization during 4 days by multiple injections of an antiserum generated against somatostatin resulted in a partial feminization of the male rat liver. When somatostatin was injected into female rats, the PRL receptors were reduced to approximately 60% of the control female receptor levels. The present study indicates that the anterior periventricular hypothalamic area is important in the control of the sexually differentiated steroid metabolism and PRL receptors in the liver and that the amygdaloid complex also may have regulatory influences on this system. A possible central neuro-endocrine mediator of these sex differences in the liver could be somatostatin or a related compound.

Androstenedione↗
PubMed1983

Pulse administration of estradiol-17 beta cancels sex difference in behavioral estrogen sensitivity.

No sex differences were found in the capability of estradiol-17 beta (E2) to induce female sexual behaviors in adult gonadectomized rats when it was administered by a pulsatile schedule and followed by progesterone. Administration of E2 in constant-release implants resulted in a clear behavioral sex difference, with females showing higher levels than males. The ovaries of proestrous females were shown to secrete E2 in a pulsatile manner and the schedule of E2 administration which cancelled the behavioral sex difference produced pulses of serum E2 of an amplitude which was within the physiological range. Thus, the sex difference in behavioral E2 sensitivity is dependent upon the manner of E2 administration and if a physiological schedule of E2 administration is employed the sex difference is cancelled.

Animals↗
PubMed1983

Purification of liver feminizing factor from rat pituitaries and demonstration of its identity with growth hormone.

The identity of the pituitary factor responsible for the maintenance of a female pattern of hepatic steroid metabolism and a female level of PRL receptors has been established. Fractionation of pituitary extracts revealed that only the GH fraction had the capacity to feminize liver metabolism of androstenedione (i.e. increase 5 alpha-reductase activity and decrease 16 alpha-hydroxylase activity) and to induce PRL receptors to a female level in hypophysectomized animals. The purification of pituitary GH was performed by chromatofocusing followed by gel filtration on Sephadex G-75. GH obtained from male or female pituitary glands showed an identical chromatographic behavior and both preparations had a mol wt of 22,000 and an isoelectric point of 6.1 when analyzed by analytical sodium dodecyl sulfate-gel electrophoresis and isoelectric focusing, respectively. The degree of homogeneity of GH varied between 93% and 97% as judged from sodium dodecyl sulfate-gel electrophoresis. Purified male and female GH were equally efficient in feminizing the liver metabolism. Since degradation of the native mol wt 22,000 form reduced the feminizing capacity, we believe that the intact hormone is needed for the feminization.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1983

Effects of hysterectomy and uterine extracts on growth hormone, somatomedin, prolactin, thyrotrophin and thyroid hormones in adult rats.

Plasma concentrations and anterior pituitary content of growth hormone (rGH), thyroid stimulating hormone (rTSH), and rat prolactin (rPrl) as well as the plasma concentrations of triiodothyronine (T3), thyroxine (T4) and somatomedin A (SM-A) have been determined in intact, castrated or hysterectomized adult rats with and without treatment with steroid-free, crude uterine extracts. Hysterectomy caused a significant increase in the plasma GH but decrease in the plasma TSH concentrations. Injection of crude, steroid-free uterine extracts for 14 days had the following effects: decreased plasma GH concentration of intact rat and anterior pituitary GH content of both intact and castrated animals; increased plasma TSH and T3 concentrations above the ovariectomized control; decreased pituitary content of prolactin in castrated rats. The plasma levels of immunoreactive somatomedins A were negatively correlated to the plasma GH concentrations but positively correlated to the body weight. It was concluded that the uterus is not only a target for different endocrine influences but contains biologically active, non-steroidal substances which have a complex effect on the endocrine system of adult, female rats.

Animals↗
PubMed1983

Mechanisms regulating hormone release and the duration of dioestrus in the lactating rat.

Lactation in rats nursing seven pups was associated with a period of dioestrus lasting for 3 weeks, reduced LH secretion, hyperprolactinaemia and increased serum progesterone levels. Removal of the litter resulted in increased LH secretion, a prompt return of oestrus and termination of the prolactin-dependent luteal phase. Administration of domperidone (2.5 mg/day), a dopamine receptor antagonist, to rats deprived of their litters on day 1 or 9 post partum maintained hyperprolactinaemia and delayed the reappearance of oestrus. Administration of bromocriptine (0.5 mg/day), a dopamine receptor agonist, to lactating rats with suckling pups suppressed prolactin secretion and advanced oestrus, females in the middle of lactation being considerably more sensitive to prolactin suppression than those in the early post-partum period. Cross-fostering experiments revealed that the greater sensitivity to bromocriptine of mothers in late lactation was due to their lactational age rather than to the age of the offspring. Similarly, the length of lactational dioestrus was not affected either by giving newborn pups to females in the middle of lactation or by giving 9-day-old pups to newly parturient females.

Animals↗
PubMed1983

Evidence that prolactin does not affect the induction of sexual behaviour by oestradiol and progesterone in ovariectomized rats.

Injection of 2.5 mg of the dopamine receptor antagonist domperidone raised serum prolactin concentrations within 3 h and high prolactin levels were maintained for 12 h in ovariectomized rats pretreated with 2 micrograms oestradiol benzoate (OB). This dose of domperidone stimulated the display of sexual behaviour in ovariectomized OB-treated rats within 3 h of administration. The behavioural effect of domperidone, but not its effect on serum prolactin concentrations, was blocked by adrenalectomy. Daily treatment with domperidone had no inhibitory effect on the subsequent induction of sexual behaviour by OB and progesterone in ovariectomized rats. A slight facilitation of the behaviour was noticed in OB-treated rats given daily domperidone injections, but this effect was cancelled by adrenalectomy. The results suggest that an acute increase in serum prolactin levels has no effect on the induction of sexual behaviour by OB in itself, but can stimulate the secretion of an adrenal product, perhaps progesterone, which facilitates the behaviour. Similarly, constant high levels of prolactin by themselves have no effect on the subsequent induction of sexual behaviour by OB and progesterone.

Adrenalectomy↗
PubMed1983

Inhibition of sexual behaviour in lactating rats.

Treatment with oestradiol benzoate (OB; 2-250 micrograms) and progesterone (0.5-25 mg) failed to induce sexual behaviour in lactating rats 6 days after parturition. Removal of pups permitted the induction of sexual behaviour by OB and progesterone and the inhibitory effect of the presence of pups was proportional to the number present. Ovariectomy of lactating rats or reduction of serum prolactin levels in intact lactating rats by daily treatment with the dopamine receptor agonist bromocriptine (0.5 mg/day) permitted the induction of sexual behaviour despite the presence of suckling pups. Removal of pups from lactating rats and subsequent maintenance of high prolactin levels by daily treatment with the dopamine receptor antagonist domperidone (2.5 mg/day) maintained the state of refractoriness to the behavioural effects of OB and progesterone provided that the ovaries remained in situ. Inhibition of sexual behaviour in lactating rats could be maintained after ovariectomy by implantation of progesterone-filled, but not androgen-filled implants at the time of ovariectomy. Removal of the pups or reduction of prolactin levels by bromocriptine treatment permitted the induction of sexual behaviour by OB in ovariectomized progesterone-implanted lactating rats. Inhibition of the behaviour in ovariectomized progesterone-implanted lactating rats could be maintained after pup removal by daily domperidone treatment. Continuously raised serum progesterone or prolactin levels have no effect on the induction of sexual behaviour in female rats but the present data suggest that during lactation progesterone and prolactin act in synergy to inhibit the behaviour.

Animals↗
PubMed1983

The effect of a prostaglandin synthetase inhibitor on the hormonal profile and the endometrium in women.

A prostaglandin synthetase inhibitor, naproxen, was given continuously throughout the menstrual cycle at a dose of 250 mg b.i.d. to 10 healthy fertile women. Blood samples were drawn three times a week during an earlier control cycle and during the treatment cycle and analyzed for LH, FSH, prolactin, estradiol and progesterone. Endometrial biopsies were taken in the secretory phase. Naproxen treatment did not suppress ovulation in any of the cycles and did not affect the corpus luteum function. In only one of the endometrial samples taken was the density of the lysosomes increased in the treatment cycle compared with the control cycle.

Endometrium↗
PubMed1983

Beta2-microglobulin, carcinoembryonic antigen and prostatic acid phosphatase in split ejaculates and urine voided before and after massage of the prostate.

Analyses of split ejaculates and urine voided before and after prostatic massage have been used to evaluate the origin of beta2-microglobulin (b2m) and carcinoembryonic antigen (CEA) in human semen. CEA and b2m were present in rather high concentrations in all the fractions of the split ejaculates. The urine voided after massage of the prostate also contained increased levels of CEA and beta2-microglobulin. Split ejaculates, selected from the electrophoretic pattern obtained for each fraction, revealed that b2m in seminal plasma originates from the prostate and seminal vesicles in equal amounts. Besides the "free" b2m in seminal plasma, human semen contains a sperm-bound b2m fraction. Carcinoembryonic antigen was found in the highest concentrations in the second fraction of split ejaculates indicating that it originates mainly from the prostate.

Acid Phosphatase↗
PubMed1983

Increased amine turnover in several hypothalamic noradrenaline nerve terminal systems and changes in prolactin secretion in the male rat by exposure to various concentrations of toluene.

Subacute exposure of rats to varying concentrations of toluene vapours leads to increases of amine levels and turnover in several types of hypothalamic noradrenaline nerve terminal systems. Furthermore, the exposure of toluene in concentrations ranging from 80-3000 ppm and benzene (1500 ppm) produced differential effects on dopamine and noradrenaline turnover within various parts of the hypothalamus. These regions are involved in neuroendocrine regulation and disturbances in the secretion of prolactin were demonstrated after exposure to toluene.

Animals↗
PubMed1983

Growth hormone: a regulator of the sexually differentiated steroid metabolism in rat liver.

Specific lesions in the periventricular area of the hypothalamus in male rats lead to a partial feminization of the liver steroid metabolism and a simultaneous reduction of the somatostatin level in the median eminence. Administration of an antiserum against somatostatin causes a similar degree of feminization of liver metabolism in male rats. Thus somatostatin could be the neuroendocrine regulator of the sexually differentiated metabolism of steroids in rat liver. A possible influence from the amygdaloid complex in regulating hepatic steroid metabolism is also indicated since large lesions in the amygdala cause a slight feminization of hepatic steroid metabolism in male rats. The female pattern of hepatic steroid metabolism is induced following frequent administration of hGH. The feminizing effect of hGH on hepatic steroid metabolism does not require the presence of gonads, adrenals, or thyroid. The somatogenic property of hGH seems to be responsible for the feminizing effect since purified rGH alone gives a complete feminization of hepatic steroid metabolism in hypophysectomized animals. rGH purified from male or female pituitary glands is equally efficient in feminizing hepatic steroid metabolism. Furthermore, male or female rGH have the same apparent molecular weight and isoelectric point. The mechanism whereby GH regulates hepatic steroid metabolism could be related to the sexually differentiated secretory profile of GH in the rat. A continuous presence of GH in the circulation seems to be a prerequisite for a female pattern of hepatic steroid metabolism. By analogy, it may be suggested that the high-peak, low-trough secretory pattern of GH characteristic of male rats causes a masculine type of liver steroid metabolism. Gonadal hormones affect both the secretory profile of GH and hepatic steroid metabolism. It is most probable that gonadal hormones affect liver steroid metabolism via modulations of the GH secretory profile. Possibly, estrogen exerts its effect directly on the pituitary by stimulating GH secretion. Androgen most probably has its primary site of action in the anterior hypothalamus or in extrahypothalamic areas. A plausible mechanism is that androgens stimulate the hypothalamic GH-inhibitory center. An overall view of the present hypothesis concerning hypothalamopituitary regulation of the sexually differentiated hepatic steroid metabolism in the rat is presented in Figure 2.

Androgens↗
PubMed1982

The regulation in vitro of placental release of human chorionic gonadotropin, placental lactogen, and prolactin: effects of an adrenergic beta-receptor agonist and antagonist.

An experimental model for the study of placental tissue release of hormones has been explored. It has been shown that the trophoblast in Ringer-glucose solution releases human placental lactogen (hPL) and chorionic gonadotropin (hCG) in a time- (10 to 180 minutes) and temperature- (4 degrees and 37 degrees C) dependent manner. The adrenergic beta-receptor agonist terbutaline caused an increase in hCG secretion but did not affect hPL. With a mixed trophoblast/decidua preparation, prolactin release was not found to be time and temperature related. Terbutaline increased prolactin release and timolol decreased it. The data suggest tha adrenergic mechanisms are involved in hCG and prolactin secretion from the placenta.

Chorionic Gonadotropin↗
PubMed1982

Interactions of nicotine and pentobarbitone in the regulation of telencephalic and hypothalamic catecholamine levels and turnover and of adenohypophyseal hormone secretion in the normal male rat.

The effects of single intraperitoneal injections of nicotine (1 mg/kg) and the sedative-hypnotic drug pentobarbitone (30 mg/kg) alone or in combination have been studied on catecholamine (CA) nerve terminal system of the hypothalamus and the forebrain and on the adenohypophyseal hormone secretion of the normal male rat. Nicotine produced discrete reductions of dopamine (DA) levels and increases of DA turnover in striatal and limbic areas of the forebrain and increases of amine turnover in different hypothalamic noradrenaline (NA) nerve terminal systems. These effects were all antagonized by simultaneous treatment with pentobarbitone. Pentobarbitone alone, however, did not modulate CA levels or turnover in the various parts of the hypothalamus and forebrain analyzed. On the other hand, pentobarbitone increased GH and prolactin secretion and in association with tyrosine hydroxylase inhibition markedly reduced corticosterone secretion. These effects were partly counteracted by nicotine in the case of GH and prolactin secretion. Furthermore, a positive interaction appears to exist between nicotine and pentobarbitone in their actions on LH secretion. The results suggest that pentobarbitone can antagonize the actions of nicotine on CA levels and turnover in various CA nerve terminal systems of the brain leading to possible reductions in nicotine induced arousal and positive reinforcement. The neuroendocrine actions of pentobarbitone do not seem to be greatly modulated through nicotinic cholinergic receptors.

Animals↗