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Biomedical subjects

E Stark

Publications and source records attributed to E Stark.

At least 73 records · Page 4Linked to original sources
PubMed1985

Structure-activity studies with ACTH/alpha-MSH fragments on corticosteroid secretion of isolated zona glomerulosa and fasciculata cells.

The steroidogenic action of ACTH/alpha-MSH fragments was studied on isolated zona glomerulosa and zona fasciculata cells dispersed by collagenase. ACTH-(4-7), ACTH-(6-10), ACTH-(4-10) and ACTH-(11-13) stimulated corticosterone production of the zona fasciculata and aldosterone production of the zona glomerulosa cells. ACTH-(7-10) was ineffective. ACTH-(4-7) appeared to be the most potent peptide of the tested fragments. None of the fragments affected the steroidogenic action of ACTH-(1-39). It is suggested that similar to the melanotropic effect of alpha-MSH two 'message' sequences for adrenocortical stimulation exist in the alpha-MSH part of the ACTH molecule.

Adrenal Cortex↗
PubMed1985

Sequelae of sural nerve biopsies.

Sequelae of sural nerve biopsy were examined in 24 patients. Fourteen subjects reported persisting pain or dysaesthesias for more than one year. In nine patients the symptoms were mild, in five severe. Hypaesthesia of the lateral aspect of the foot was found in 17 out of 18 patients with otherwise normal or only slightly impaired sensory function. In one patient sural nerve biopsy did not cause permanent sensory loss. Pain and dysaesthesia were not significantly related to post-biopsy or generalized hypaesthesia.

Adolescent↗
PubMed1985

Long-term suspension culture of isolated hypothalamic nuclei of the rat: morphological differentiation and release of substances influencing corticotropin and growth hormone secretion.

Individual hypothalamic nuclei were removed from 17-day-old rat embryos with 300 microns punches and maintained in suspension culture. Suspension culture of isolated nuclei appears to be suitable for studying morphological and functional differentiation of neural tissue and release of bioactivity influencing corticotropin and growth hormone release. During the 4 weeks in culture, neurons and glial cells differentiated well in each nucleus studied. The fine structure of the arcuate, periventricular, ventromedial and dorsomedial nuclei resembled that of the adult nuclei with many mature synapses; in contrast, in the neuropil of cultured preoptic, paraventricular and posterior hypothalamic nuclei mature synapses were very few or absent. The release of substances influencing corticotropin and growth hormone secretion by the cultured nuclei was tested in bioassays using anterior pituitary cell cultures and radioimmunoassay of hormones released into the medium. Corticotropin-releasing bioactivity was tested at weekly intervals. Cultured preoptic and paraventricular nuclei released corticotropin-releasing activity for up to 4 weeks whereas arcuate nuclei released corticotropin-releasing activity at 1 week only. The ventromedial and dorsomedial nuclei did not release corticotropin-releasing activity. The release of substances influencing growth hormone secretion was studied between 3 and 11 days in culture. After 3 days the medium of some hypothalamic nuclei stimulated growth hormone secretion, but after 7 and 11 days all cultured nuclei strongly inhibited it. The present findings demonstrate that hypothalamic nuclei can be cultured separately and suggest that neurons capable of releasing corticotropin-releasing activity(ies) are present in the preoptic and paraventricular nuclei of the rat whereas all hypothalamic nuclei studied contain intrinsic neurons capable of synthesizing and secreting somatostatin-like bioactivity.

Animals↗
PubMed1985

Study of the luteinizing hormone-induced increase of ovarian blood flow during the estrous cycle in the rat.

CYF rats were anesthetized on various days of the 4-day cycle and blood samples were collected at 5-min interals from the ovarian vein before and after i.v. administration of 5 micrograms/100 g BW of luteinizing hormone (LH). Ovarian venous outflow, blood pressure and hematocrit were continuously recorded, and from the blood samples progesterone (P) and 17 beta-estradiol (E2) were determined by radioimmunoassay (RIA). Ovarian blood flow and P secretion showed a parallel increase on Day 1 (estrus), on Day 2, and on the afternoon of Day 4 (proestrous). LH increased ovarian blood flow each day of the cycle together with P and E2 secretion; however, no relationship was seen between the initial value of hormone secretion and the LH-induced increase of ovarian blood flow. Inhibition of hormone secretion by cycloheximide prevented the LH-induced increase of ovarian blood flow; moreover, a decrease in ovarian blood flow parallel with the diminution of hormone secretion was observed. Indomethacin pretreatment abolished the hyperemic effect of LH and partially inhibited the LH-induced increase of hormone secretion. Propranolol blocked the LH-induced increase of ovarian blood flow and blunted the effect of LH on hormone secretion. It was concluded that in LH-induced hyperemia, cAMP, prostaglandins and other vasoactive metabolites released during the process of hormone synthesis, and also a beta-adrenergic mechanism, are involved in the regulation of ovarian blood flow.

Animals↗
PubMed1985

Vasopressin secretion as a possible target of the gamma-aminobutyric acid-mediated component of the corticosteroid feedback effect.

The inhibition of gamma-aminobutyric acid (GABA) synthesis did not interfere with the suppressive effect of dexamethasone on the stress-induced rise of plasma corticosterone levels in vasopressin-deficient homozygous Brattleboro rats. In dexamethasone-treated heterozygous rats corticosterone and vasopressin secretion increased after stress provided GABA synthesis was inhibited. The results indicate that inhibition of corticotrophin secretion by corticosteroids may in part be mediated by enhancement of GABA synthesis and a consequent inhibition of vasopressin release.

3-Mercaptopropionic Acid↗
PubMed1984

Growth hormone secretion of the neonatal rat pituitaries is stimulated by gamma-aminobutyric acid in vitro.

Growth hormone secretion from pituitaries of neonatal rats was stimulated by gamma-aminobutyric acid (GABA) and the GABA agonist muscimol in vitro. This response to GABA was absent after the 9th postnatal day. The stimulation of growth hormone secretion by GABA was antagonized by bicuculline-methiodide and by picrotoxin. Diazepam stimulated while baclophen had no effect on growth hormone secretion. This stimulatory GABA effect might be related to a certain developmental stage of the pituitary GABA receptors or to the lack of hypothalamic regulatory influence(s) in the newborn.

Aging↗
PubMed1984

Inhibition of growth hormone and prolactin secretion by a serine proteinase inhibitor.

The action of the tripeptide aldehyde t-butyloxycarbonyl-DPhe-Pro-Arg-H (boc-fPR-H), belonging to a family of serine proteinase inhibitors, on the release of immunoreactive prolactin (iPRL) and growth hormone (iGH) has been studied. In rat anterior pituitary cell cultures and pituitary quarters 1 mM boc-fPR-H inhibited basal iPRL and iGH release. Thyroliberin-induced iPRL release by cultured cells was also markedly inhibited with a concomitant accumulation of intra-cellular iPRL. During the short- and long-term exposure of cells to boc-fPR-H there no changes in total cell protein contents and in activities of some lysosomal marker enzymes. A wide scale of unchanged parameters characteristic for cellular metabolism indicated that the tripeptide aldehyde has no cytotoxic effect. The marked inhibition of basal as well as stimulated hormone release in the presence of the enzyme inhibitor might suggest that at least a portion of the hormones is released via a proteolytic enzyme-dependent process.

Animals↗
PubMed1984

Loss of sensitivity to morphine induced by prolonged ACTH treatment.

The effect of long term ACTH treatment on some actions of morphine were studied. The effect of ACTH administration was compared to that induced by acute dexamethasone injection. ACTH caused a delayed inhibition of the morphine induced increase in growth hormone secretion demonstrable 24 hr after the last hormone injection. The morphine induced increase of striatal DOPAC (3,4-dihydroxyphenylacetic acid) content was also inhibited by ACTH treatment, however, neither the analgesia, nor the hypermotility caused by morphine were affected. Dexamethasone did not alter significantly the responsiveness to morphine. It is concluded that the prolonged exposure to ACTH presumably causes a corticosterone-mediated loss of responsiveness of functionally restricted opiate sensitive mechanisms in the central nervous system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Decrease of morphine-induced prolactin release by a procedure causing prolonged stress.

The effects of morphine and fentanyl on plasma prolactin levels in rats have been measured. It was found that a prolonged immobilization stressful procedure for 5 h inhibited the response to morphine and fentanyl to increase prolactin secretion, but did not influence the increase in plasma prolactin caused by haloperidol. The injection of a large dose of cortisol (25 mg/kg, s.c.) also evoked an inhibition of morphine-induced prolactin release. The inhibition was maximal 24 h after the administration of the glucocorticoid. These results indicate that stress may induce prolonged alteration in endogenous opioid-mediated neuromodulation via a prolonged release of glucocorticoids.

Animals↗
PubMed1984

[Glucocorticoid hormones and the immune response].

The level of glyco- and mineralcorticoids in the blood and correlations between functional activity of hypothalamo-hypophyseal--adrenocortical system and antibody production, were investigated. The role of glycocorticoids in the immune system responses to antigen on the cellular and molecular levels including the changes in glycocorticoid binding sites and cyclo-nucleotides level, was shown. The role of glycocorticoids in actualization of the immune responses depending on the intensity and duration of hormonal changes, is considered from the standpoint of different sensitivity of the individual clones of immunocompetent cells to hormones.

Adrenal Cortex↗
PubMed1983

Long-term ACTH induced diminished responsiveness of prolactin secretion to morphine.

The effect of morphine on plasma prolactin level and on dopamine turnover in the median eminence was studied using adult male rats chronically treated with ACTH. It was found that the ACTH pretreatment caused a decrease in the effect of morphine on prolactin secretion and prevented the inhibitory effect of morphine on dopamine turnover measured in the median eminence. The prolonged ACTH administration did not influence the prolactin content of the pituitaries and the in vitro dopamine sensitivity of lactotroph cells. Acute dexamethasone injection did not change the morphine-caused prolactin release. These results suggest that chronic ACTH treatment (possibly via corticosterone hyperproduction) elicits an opiate-tolerance like state of tuberoinfundibular dopaminergic neurons.

Adrenocorticotropic Hormone↗
PubMed1983

Responsiveness of adenohypophysial corticotrophs to hypothalamic (SME) extract remains unchanged in rats with hypothalamic lesions inhibiting CRF release.

The corticotrophin-releasing activity of stalk-median eminence (SME) extract was studied using incubated quarters of anterior pituitary glands obtained from rats with long-term anterolateral deafferentiation or complete surgical lesion of the medial basal hypothalamus, as well as with the lesion of the paraventricular nuclei. These hypothalamic interventions are known to cause a complete or partial but significant deficiency in hypothalamic corticotrophin-releasing factor (CRF) release, however, such lesions failed to alter the sensitivity of the ACTH response from incubated pituitary segments towards the SME extract. These results suggest that the specific responsiveness of adenohypophysial corticotrophs is maintained when hypothalamic CRF supply is decreased for a long period of time.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of arginine-8-vasopressin and 1-deamino-8-D-arginine-vasopressin on ACTH secretion in rats.

The corticotropin-releasing effect of arginine-8-vasopressin (AVP) has been compared to that of 1-deamino-8-D-arginine-vasopressin (dDAVP) in male rats of R-Amsterdam strain. AVP increased the level of ACTH and corticosterone in the peripheral blood in a dose-dependent manner. In contrast to AVP, a very potent antidiuretic agent dDAVP which is devoid of pressor activity had no effect on ACTH release and did not stimulate the secretion of corticosterone. It is concluded that CRF activity of vasopressin in vivo is related to its pressor activity. These data are in agreement with the previous findings of these authors demonstrating that dDAVP shows a very low affinity for vasopressin receptors of the cell membranes in the adenohypophysis.

Adrenocorticotropic Hormone↗
PubMed1982

Electrical stimulation in the rat of the supraoptic nucleus: failure to alter plasma corticosterone after surgical lesioning of the paraventricular nucleus.

Electrical stimulation of the supraoptic nucleus (SON) for 3 min in dexamethasone-morphine-pentobarbital-pretreated rats raised the plasma level of corticosterone; 4 days after placing a surgical lesion in the hypothalamic paraventricular nuclei (PVN) electrical stimulation of the SON failed to change the plasma level of corticosterone. We suggest that nerve fibres originating in or near the PVN that pass near the SON are likely to contain corticotropin releasing factor and elicit and release of ACTH following electrical stimulation.

Animals↗