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Biomedical subjects

J F Bruni

Publications and source records attributed to J F Bruni.

17 recordsLinked to original sources
PubMed1982

Serotonergic mechanism in the control of beta-endorphin and ACTH release in male rats.

The role of the serotonergic mechanism in the regulation of beta-endorphin (beta-EP and adrenocorticotropin (ACTH)-like immunoreactivity in plasma was investigated. Increases in beta-EP and ACTH-LI produced by quipazine maleate (QPZ), a serotonergic agonist, 1 hr after injection could be completely prevented by the serotonin (5-HT) antagonist, cinanserin (CIN), which when injected alone, decreased basal plasma concentrations of both beta-EP-LI and ACTH-LI. Concurrent injections of L-5-HTP with the 5-HT reuptake inhibitor, fluoxetine, produced an additive increase in plasma beta-EP-LI 1 hr after injection. Injection of the 5-HT antagonist, cyproheptadine, significantly decreased plasma beta-EP-LI. Stress by immobilization for 30 min or exposing the rats to 40 degree +/- 1 degree C for 30 min produced an approximate 4-fold increase in plasma beta-EP-LI and ACTH-LI, which was potentiated by I.P. injections of fluoxetine. Furthermore, the stress induced increases in plasma concentrations of beta-EP-LI and ACTH-LI were significantly reduced by the serotonin antagonists metergoline and cinanserin. These results suggest that 5-HT is a potent stimulator of both beta-EP and ACTH release and the increase in plasma concentrations of ACTH and beta-EP induced by stress are probably mediated, at least in part, by central serotonergic mechanisms.

Adrenocorticotropic Hormone↗
PubMed1980

Beta-endorphin and somatostatin in the pancreatic D-cell colocalization by immunocytochemistry.

Utilizing highly specific antisera, beta-endorphin and somatostatin immunoreactivity were identified simultaneously in the D-cell of the pancreas of the rat, guinea pig, and man by the fluorescence-immunocytochemical technique. Our observations are consistent with a modulating role of beta-endorphin either within the D-cell or upon A and B cells, thereby regulating the secretion of insulin and glucagon.

Animals↗
PubMed1979

Effects of hypophysectomy, thyroidectomy, and thyroxine on specific prolactin receptor sites in kidneys and adrenals of male rats.

The effect of T4 on specific PRL binding in the kidneys and adrenals was measured in intact, hypophysectomized, and thyroidectomized male rats. PRL binding in the kidneys was reduced from 12.1 +/- 1.1% in the intact group to 4.5 +/- 0.5% after hypophysectomy; 4-day replacement with T4 returned PRL binding to intact values. T4 administered to intact rats significantly increased PRL binding above intact values. Thyroidectomy reduced PRL binding in the kidneys from 14.9 +/- 1.2% to 7.0 +/- 0.6%, and T4 treatment restored PRL binding to intact values. PRL binding was measured at 2, 3, 5, 7, and 10 days after thyroidectomy in kidneys and found to decrease progressively from 8.2+/-0.5% in the intact rats to 2.3+/-0.3% on day 10. A single injection of T4 doubled PRL recetor binding in kidneys of thyroidectomized rats at 12 h and returned binding to intact levels at 24 h. In contrast to the effects of T4 on kidney PRL binding, adrenal PRL binding was only slightly altered by thyroidectomy and T4. These results suggest that T4 has a specific role in regulating PRL receptors in the kidneys but not in the adrenals. Since PRL receptors in the adrenals were only slightly altered by thyroid status, it is believed that the changes in kidney receptors represent a specific rather than a general metabolic effect of T4.

Adrenal Glands↗
PubMed1979

beta-Endorphin in the human pancreas.

Using a specific antiserum, beta-endorphin was quantitated in 8 human pancreas obtained at autopsy by radioimmunoassay and localized by immunocytochemistry. The mean (+/- SE) concentration of beta-endorphin in pancreatic extracts of 5 non-diabetic adults was 13.5 +/- 9.8 ng/gm with a range of 2.1 to 52.8 ng/gm of tissue. Pancreatic beta-endorphin concentration in two premature infants were within the range found in adults. In one diabetic pancreas, there was no measurable beta-endorphin. Specific beta-endorphin immunofluorescence is localized within the pancreatic islets. This finding suggests that beta-endorphin may participate in intraislet regulation of pancreatic hormone secretion.

Adolescent↗
PubMed1979

Gonadotropin binding and testicular function in old rats.

Serum testosterone levels, testicular LH binding and the spermatogenic cycle were analyzed in rats 4 and 22 mo of age. With age, serum testosterone levels decreased from 3.2 to 0.63 ng/ml serum. There was no age related decline in testicular LH binding or changes in the spermatogenic cycle.

Aging↗
PubMed1978

Patterns of sex steroid and gonadotropin secretion in aging female rats.

Serum estradiol, progesterone, LH, and FSH were determined by RIA in 20- to 30-month-old constant estrous (CE), irregular pseudopregnant (PP), and anestrous (AS) female rats and from 4- to 5-month-old cycling female rats. Disruption of the estrous cycle in aging rats was associated with major changes in secretion of pituitary gonadotropins and ovarian steroids. None of the old rats, in contrast to the young rats, showed cyclic changes in any of the hormones studied. Serum progesterone was much higher in the PP than in the other two old groups, serum estradiol averaged somewhat higher in the CE than in the other two aged groups, and all four hormones were lower in the AS rats than in any other group. Basal serum FSH values were higher in the old CE rats than in either of the other old age groups and were slightly higher than in young rats on the afternoon of proestrus or morning of estrus. Serum FSH values were lower in the old PP and AS rats than in young rats on the afternoon of proestrus or morning of estrus. Serum FSH values were lower in the old PP and AS rats than in young rats on the afternoon of proestrus or morning of estrus. Serum values in the old CE rats were about the same as in young rats on the morning of proestrus or estrus, about the same in old PP rats as in young rats during diestrus, and were undectable in old AS rats. Since the ovaries of old rats are capable of near normal function under appropriate gonadotropic stimulation, it is concluded that the major cause for cessation of regular estrous cycles in old rats lies in altered hypothalamo-pituitary function.

Aging↗
PubMed1976

Serum and pituitary TSH and response to TRH in developing male and female rats.

Serum and pituitary thyroid-stimulating hormone (TSH) was measured by radioimmunoassay in male and female Sprague-Dawley rats from 21 through 80 days of age. In males, serum TSH levels increased progressively from days 30 through 50, and were found to be lower on days 60, 70, and 80. In females, serum TSH levels were elevated on days 40 and 50, compared with day 30, but declined on days 60-80. A sex difference in serum TSH levels, with those of the male higher than those of the female, appeared by day 30 and was maintained through day 80. The anterior pituitary (AP) content of TSH in males increased from days 21 through 50 and remained constant through day 80; in females the AP content increased between days 25 and 60 and remained constant through day 80. In males, thyrotropin-releasing hormone (TRH) induced a significant elevation in serum TSH at all ages tested, but was less effective in increasing serum TSH on day 25 than on days 15 or 40 or in 3-4-month-old rats. The response to TRH appeared to be sustained longer in adults than in all other age groups. These observations indicate that serum TSH levels increase in both male and female rats at about the time of puberty and then decline, and that changes in the response to TRH may account in part for the increase in serum TSH levels during development.

Age Factors↗
PubMed1975

Effects of hyper- and hypothyroidism on serum LH and FSH levels in intact and gonadectomized male and female rats.

The effects of hypo- and hyper-thyroidism on serum LH and FSH were determined in both intact and castrated male and female rats. Thyro-parathyroidectomy (Tx) for 30 days in rats with intact gonads resulted in a significant reduction in serum LH and FSH, and also in a decrease in serum testosterone in males. Administration of 2.5 mug thyroxine (T4)/100 g BW to Tx rats of both sexes returned serum LH and FSH levels to those of intact rats, and in males also restored normal serum testosterone levels. Tx superimposed upon castration resulted in a significantly greater increase in serum LH and FSH than produced by castration alone. Administration of 2.5 mug T4/100 g body weight to castrate-Tx rats reduced serum LH and FSH values to those of castrate rats, whereas 10 mug T4/100 g BW evoked a further decrease in serum LH but no additional reduction in serum FSH. When both 2.5 mug T4/100 g BW and 2 mug estradiol benzoate were injected into Tx-ovariectomized rats, the decrease in serum LH and FSH was much greater than produced by T4 alone. These observations indicate that hypothyroidism results in decreased release of LH and FSH in rats with intact gonads, and in increased release of LH and FSH in castrate rats of both sexes. Administration of a replacement dose of T4 can restore LH and FSH release to normal in Tx rats with intact gonads, and to castration levels in Tx-castrate rats.

Animals↗
PubMedDate not supplied

Improved screening for benzodiazepine metabolites in urine using the Triage Panel for Drugs of Abuse.

Screening for benzodiazepines is an important component of many drug testing programs. Current immunochemical methods are limited by a lack of sensitivity to many of the 35 forms of benzodiazepines available and because the antibodies used are insensitive to the glucuronic acid conjugates that constitute the major metabolites in urine. The Triage Panel for Drugs of Abuse (Biosite Diagnostics), a new screening device, is a competitive immunoassay containing monoclonal antibodies directed against glucuronide metabolites of benzodiazepines. We tested this device on 326 urine specimens, which were also tested by two other immunoassay methods (FPIA and EMIT) and by GC/MS. We found a sensitivity of 97.5% and a specificity of 94.3% for the Triage assay when it was applied to a population in which approximately 50% of the specimens were positive; a distribution of eight different benzodiazepines was found in the positive samples. Other immunoassays performed with lower sensitivity or specificity or both. We found no significant difference between two analysts using the Triage test. We conclude that the Triage method represents a superior method for benzodiazepine screening when compared with other immunoassay methods.

Anti-Anxiety Agents↗