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Biomedical subjects

A Grossman

Publications and source records attributed to A Grossman.

At least 289 records · Page 16Linked to original sources
PubMed1981

Studies off the opiate control of prolactin, GH and TSH.

Opiate peptides are known to influence the secretion of several anterior pituitary hormones under basal conditions. Further studies on prolactin, GH and TSH have therefore been performed in normal subjects, under basal and stimulated conditions, using an opiate agonist and antagonist. Sixteen mg naloxone had no effect on the basal release of prolactin or GH, but lowered TSH. An infusion of the met-enkephalin analogue DAMME (1 mg) increased GH, and produced an exaggerated response of both prolactin and TSH to 200 micrograms TRH i.v. The peak responses of both prolactin and GH to hypoglycaemia were unaffected by pretreatment with either low-dose (0.4 mg) or high-dose (25 mg) naloxone, or DAMME (0.25 mg). These results suggest that opiate peptides are unlikely to play a major role in the tonic or hypoglycaemia-stimulated release of prolactin and GH, although they may be of importance in the control of TSH.

Adolescent↗
PubMed1981

The effects of a met-enkephalin analogue on ACTH, beta-LPH, beta-endorphin and MET-enkephalin in patients with adrenocortical disease.

Thirteen patients with either Addison's disease, or Cushing's disease treated by bilateral adrenalectomy, were infused with the long-acting met-enkephalin analogue DAMME. In patients with Addison's disease significant and pronounced falls in ACTH and N- and C-terminal beta-LPH were seen; chromatography suggested that beta-endorphin fell concomitantly. Three out of four patients with Cushing's disease who had not received pituitary irradiation, also showed a decrease in plasma ACTH and N- and C-terminal beta-LPH; however, no change was seen in any of the irradiated patients. The changes were naloxone reversible. The levels of plasma met-enkephalin were normal and did not change after DAMME in any group of patients. These results are interpreted as suggesting that there are inhibitory opiate receptors controlling the release of ACTH, beta-LPH, and beta-endorphin.

Addison Disease↗
PubMed1981

Angiotensin II stimulates the release of ACTH from dispersed rat anterior pituitary cells.

In a rat anterior pituitary dispersed cell system, angiotensin II was found to stimulate the release of ACTH at concentrations ranging from 100 pmol/l to 1 mumol/l, with a maximal response being given by 10 nmol/l. The angiotensin II antagonist, saralasin, was able to block completely at a concentration of 1 mumol/l the stimulation of ACTH induced by 10 nmol/l angiotensin II, but had no effect on the basal release. The log dose-response curve for ACTH release by angiotensin II was shifted to the right in a parallel fashion by saralasin 10 nmol/l, suggesting competitive antagonism. The stimulation of ACTH release by a rat stalk-median eminence extract or by arginine vasopressin was unaffected by saralasin. The data are interpreted as suggesting that rat corticotrophs contain angiotensin II receptors, and that these may be involved in ACTH release in response to hypovolaemic stress.

Adrenocorticotropic Hormone↗
PubMed1981

GABA and muscimol inhibit the release of prolactin from dispersed rat anterior pituitary cells.

Prolactin release from columns of dispersed rat anterior pituitary cells was inhibited by GABA and the GABA agonist muscimol. The log dose-response curves for GABA and muscimol appeared to be parallel, but were not parallel to that for dopamine. Two GABA antagonists, bicuculline and picrotoxin, blocked the action of both GABA and muscimol, but the dopamine antagonists metoclopramide and perphenazine did not. The data suggest that there are specific GABA receptors on pituitary lactotrophs.

Animals↗
PubMed1981

Response of luteinizing hormone from columns of dispersed rat pituitary cells to a highly potent analogue of luteinizing hormone releasing hormone.

The response of LH from a perfused column of dispersed rat anterior pituitary cells to LH releasing hormone (LH-RH) and the analogue, D-Ser(But)6-desGly10-Proethylamide9-LH-RH (Hoe 766), was investigated. Dose-response curves showed non-parallelism between LH-RH and the analogue. but it was evident that the analogue was considerably more potent. After a single pulse of LH-RH, LH output returned to basal values in 8 min; this was prolonged to 20 min in the case of the analogue. During this 20 min the cells were refractory to pulses of LH-RH but pulses of the analogue maintained output of LH. During constant-dose perfusion with either synthetic LH-RH or the analogue, output of LH rapidly reached a peak and then gradually fell over several hours to approach baseline values. However, a pulse of 50 mmol potassium chloride/l was still able to release LH at this time. The data are consistent with the view that this analogue of LH-RH is highly potent and is strongly bound by the LH-RH receptor. Furthermore, since it desensitizes the LH-RH receptor, it appears that continued turnover of either LH-RH or the analogue at the receptor is necessary for output of LH to be maintained.

Animals↗
PubMed1980

Inhibition of vasopressin release in man by an opiate peptide.

The opiate control of vasopressin secretion in man was investigated with a long-acting analogue of met-enkephalin, DAMME (FK33-824, Sandoz). Infusion of 1 mg DAMME into water-deprived volunteers produced a diuresis which was attenuated by naloxone; there was no change in water excretion when subjects were hydrated. Plasma-immunoreactive-vasopressin failed to rise after DAMME administration, despite osmotic stimulation with hypertonic saline infusion. Opiates appear to be involved in mechanisms which suppress the osmotically mediated release of vasopressin, while opiate involvement in baroceptor-mediated release may be quite different.

Adolescent↗
PubMed1980

Analysis of genetic variation affecting the relative activities of fast and slow ADH dimers in Drosophila melanogaster heterozygotes.

When AdhF/Adhs heterozygote homogenates are stained after electrophoresis, considerable variation is observed in the activity ration of the FF dimer to the SS dimer. Two AdhS strains showed a sharp, consistent difference when crossed to a common AdhF strain. Optical scanning and genetic analysis confirmed that this difference originates close to the Adh locus. Since the morphs varied concordantly in their activities on numerous alcohols, and since aging and heat treatment experiments failed to reveal a stability difference, it is proposed that the difference is regulatory in nature, affecting ADH synthesis and primarily cisacting. A survey of wild flies revealed additional variation in the FF/SS activity ratio. Further genetic analysis showed that the basis of this variation is not restricted to the second chromosome. Furthermore, modification of the activity ratio implies some degree of allelespecificity on the part of the modifiers.

Alcohol Oxidoreductases↗
PubMed1980

Secretion of ACTH, LPH and beta-endophin from human pituitary tumours in vitro.

Basal and stimulated secretion of immunoreactive ACTH, LPH and beta-endorphin from four human pituitary tumours has been studied in vitro using a superfused, isolated cell system. Chromatography of cell secretions under acid-dissociating conditions demonstrated that the human tumor cells released immunoreactive peptides with the elution profiles of alpha h (1-39) ACTH, beta h-LPH, gamma h-LPH and beta h-endorphin confirming that beta h-endorphin is secreted by human pituitary tumour cells and is not formed by enzymic cleavage from beta h-LPH in blood. No alpha- or beta h-MSH, nor any higher molecular weight forms of ACTH or LPH were detected. The cells from all four tumours responded to stimulation with rat stalk-median eminence extract (SME) and synthetic AVP with a concomitant release of ACTH, beta-LPH, gamma-LPH and beta-endorphin. In contrast to the isolated rat anterior pituitary cells, the pattern of responses to SME and AVP were indistinguishable and the release provoked by rat SME could be accounted for virtually entirely by its vasopressin content. No stimulation of release was observed when the cells were exposed to a variety of biogenic amines. Addition of hydrocortisone to the perfusion buffer of two tumours resulted in a slow inhibition of both basal and stimulated ACTH and LPH release. These data demonstrate that human pituitary tumour tissue from patients with Cushing's disease and Nelson's syndrome can be studied in vitro and that such studies may contribute to a greater understanding of the aetiology of these diseases.

Adrenocorticotropic Hormone↗
PubMed1980

Pituitary and testicular fibrosis in association with retroperitoneal fibrosis.

A patient is discussed who originally presented with retroperitoneal fibrosis, and subsequently developed both pituitary fibrosis and testicular fibrosis. Replacement of testicular tissue by fibrosis has not previously been described in this condition, while we have only been able to find a single previous report of pituitary fibrosis. Fibrous replacement of testis and pituitary should be considered as a further manifestation of the midline fibrosing syndrome.

Adult↗
PubMed1980

Two new dopamine agonists that are long acting in vivo but short acting in vitro.

The effects of two new ergolines, pergolide and CH29-717, on prolactin secretion in vitro and in vivo were compared with those of bromocriptine. Both ergolines had in vitro potencies similar to that of bromocriptine, but had a shorter duration of action. However, in vivo both were longer acting than bromocriptine after a single dose of 100 micrograms, and effectively suppressed prolactin secretion for greater than 24 h. It would appear that the pharmacokinetics of these ergolines are different to those of bromocriptine, and this may have considerable therapeutic importance.

Animals↗
PubMed1980

Metergoline and cyproheptadine suppress prolactin release by a non-5-hydroxytryptaminergic, non-dopaminergic mechanism.

A dispersed rat anterior pituitary cell system has been used to investigate the effects of cyproheptadine and metergoline on prolactin secretion. Both drugs were potent inhibitors of prolactin secretion. However, the inhibition was not antagonized by either 5-hydroxytryptamine or a variety of dopamine antagonists. We conclude that both drugs act through mechanisms that are neither 5-hydroxytryptaminergic nor dopaminergic.

Animals↗
PubMed1980

Chlorpromazine, haloperidol, metoclopramide and domperidone release prolactin through dopamine antagonism at low concentrations but paradoxically inhibit prolactin release at high concentrations.

1. The effects of chlorpromazine, haloperidol, metoclopramide and domperidone on the release of prolactin from perfused columns of dispersed rat anterior pituitary cells were studied. 2. Chlorpromazine, haloperidol, metoclopramide and domperidone antagonized the dopamine-mediated inhibition of prolactin release at low concentrations. 3. Each dopamine antagonist displaced the dose-response curve for dopamine-induced suppression of prolactin release to the right in a parallel manner. 4. At higher concentrations, the four drugs became less effective as dopamine antagonists. 5. At high concentrations in the absence of dopamine, chlorpromazine, haloperidol, metoclopramide and domperidone paradoxically suppressed prolactin secretion by an unknown mechanism.

Animals↗
PubMed1980

A comparison of the effects of four ergot derivatives on prolactin secretion by dispersed rat pituitary cells.

The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2.3; bromocriptine, 13; lisuride, 15; pergolide, 23. Ther dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.

Animals↗