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Biomedical subjects

I Vermes

Publications and source records attributed to I Vermes.

At least 91 records · Page 5Linked to original sources
PubMed1985

Dopamine inhibits the release of immunoreactive beta-endorphin from rat hypothalamus in vitro.

Mediobasal hypothalamus tissue (MBH) from adult male rats was incubated in Krebs-Ringer bicarbonate medium (KRB). KRB was changed at 15 min intervals and the concentration of immunoreactive beta-endorphin (beta-ENDi) in the medium was measured by radioimmunoassay. Incubation of MBH tissue in normal KRB resulted in a constant release rate of beta-ENDi of approximately 1% of the tissue content per h. KRB containing 45 mM K+ causes a two fold increase in the release rate of beta-ENDi which was Ca2+ dependent. Dopamine (0.01-1.0 microM) inhibits both the spontaneous and the K+-stimulated release of beta-ENDi in a dose related manner. The dopamine receptor blocking agent haloperidol prevents this inhibitory effect of dopamine. The selective D-1 receptor agonist SKF 38393 does not affect the release rate of beta-ENDi; whereas the selective D-2 receptor agonist LY 141865 inhibits both the spontaneous and K+-stimulated release of beta-ENDi. The effects of LY 141865 can be blocked by (-)-sulpiride, a selective D-2 receptor antagonist. Norepinephrine only weakly inhibits the K+-stimulated release of beta-ENDi, an effect that can be blocked by haloperidol but not by the alpha-adrenoceptor blocker phentolamine. At concentrations tested (0.01-1.0 microM), isoproterenol, 5-hydroxytryptamine, carbachol and 8-Br-cAMP (1.0 microM) do not affect beta-ENDi release. It is concluded that dopamine can inhibit the release of beta-ENDi from hypothalamic neurons via a D-2 receptor mechanism.

Animals↗
PubMed1985

Stress-induced secretion of adrenocorticotropin in rats is inhibited by administration of antisera to ovine corticotropin-releasing factor and vasopressin.

Intact handled rats were pretreated with the immunoglobulin G fractions from normal rabbit serum or antisera to ovine corticotropin-releasing factor (CRF) and/or vasopressin and subjected to restraint or formalin stress. The formalin-induced rise in plasma ACTH was reduced to 28% in rats pretreated with anti-CRF, to 53% in those pretreated with antivasopressin, and to 16% in rats given both antibodies. Pretreatment of animals with anti-CRF, antivasopressin, or a combination of both antibodies also attenuated the ACTH response to restraint stress to 13%, 37%, and 12%, respectively, of those in normal rabbit serum-treated rats. Antiserum pretreatment did not reduce the restraint- or formalin-induced rise in plasma PRL in the same animals, however. We conclude, therefore, that both vasopressin and an ovine CRF-like peptide are physiologically relevant peptides involved in stress-induced ACTH release.

Adrenocorticotropic Hormone↗
PubMed1985

Role of epinephrine and vasopressin in the control of the pituitary-adrenal response to stress.

In addition to corticotropin-releasing factor (CRF) and structurally related peptides, arginine vasopressin (AVP), oxytocin, angiotensin II, vasoactive intestinal polypeptide, peptide histidine isoleucinamide, epinephrine (E), and norepinephrine induce secretion of adrenocorticotropin (ACTH) from corticotropic cells in vitro. The apparent affinity and intrinsic ACTH-releasing activity of these substances are lower than those of CRF. These substances can also act synergistically with CRF. In this paper the role of catecholamines and AVP in the control of ACTH release is discussed. Infusion i.v. of E increases plasma ACTH and corticosterone to levels that are normally found during stress. E-induced stimulation of pituitary-adrenal activity is mediated by beta adrenoceptors and involves release of CRF, because it can be prevented by beta-adrenoceptor blockers and by destruction of CRF neurons (hypothalamic lesions), blockade of CRF release (chlorpromazine, morphine, and Nembutal), or administration of CRF antiserum. Although stress can cause a vast increase in plasma E, circulating E is not essential for the acute stress-induced release of ACTH because blockade of beta (or alpha) adrenoceptors, administration of chlorisondamine, or extirpation of the adrenal medulla and sympathectomy do not prevent the pituitary-adrenal response to stress. In contrast, circulating E plays a major role in the release of intermediate-lobe peptides during emotional stress. Studies of the role of AVP in pituitary-adrenal control by the use of pressor receptor (V1) antagonists are not valuable because of the ineffectiveness of such antagonists in blocking AVP-induced release of ACTH from corticotropic cells in vitro. Treatment of rats with an antiserum to AVP reduces the ACTH response to stress. We conclude that AVP has an important role in stress-induced activation of the pituitary-adrenal system, possibly by potentiating the effects of CRF.

Adrenocorticotropic Hormone↗
PubMed1984

Differential effects of various opioid peptides on vasopressin and oxytocin release from the rat pituitary in vitro.

Dynorphin (1-17), and to a lesser extent, beta-endorphin and [Leu]enkephalin (10(-6) M each) decreased the spontaneous release of vasopressin (VP) from the rat neurointermediate pituitary in vitro, whereas the oxytocin (OT) release remained unchanged. Naloxone, however, did not significantly alter the spontaneous VP and OT release. Dynorphin (1-17) (10(-7) M) increased the electrically evoked release of VP and OT, while 10(-6) M had a significant, somewhat less pronounced stimulatory effect only on VP, but not on OT release. The opiate inactive fragment [des-Tyr1]dynorphin (1-17) did not change the evoked VP and OT release, indicating that the dynorphin effect was mediated by opiate receptors. beta-Endorphin (10(-6) M and 10(-7) M) did not alter the evoked VP and OT secretion. 10(-6) M [Leu]enkephalin induced a stimulation of the evoked OT, but not VP release; 10(-7) M [Leu]enkephalin had no effect, neither on VP nor on OT release. The opiate antagonist naloxone (10(-5) M) induced an increase in the evoked VP and, even more pronounced, OT release. In a concentration of 10(-6) M, however, naloxone only increased the evoked OT release. When naloxone and dynorphin (1-17) were concomitantly applied, their stimulatory effects on the evoked VP and OT release were additive. Similarly to the effects of naloxone, addition of a monoclonal antibody which binds to the common N-terminal sequence of all endogenous opioid peptides, resulted in a marked increase in the evoked secretion of VP and, to an even more pronounced degree, of OT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The beta-adrenoceptor-blocking drug propranolol prevents secretion of immunoreactive beta-endorphin and alpha-melanocyte-stimulating hormone in response to certain stress stimuli.

Handled female Wistar rats were exposed to one of the following stress stimuli: restraint, electric foot shocks, passive avoidance situation, ether, or nembutal anesthesia followed by ip formalin or laparotomy. Trunk blood was collected 2-4 min after initiation of the stress stimulus for the determination of immunoreactive beta-endorphin (beta-ENDi), ACTH (ACTHi), and alpha-MSH (alpha-MSHi). All stressors evoked a rapid increase of circulating beta-ENDi to 0.75-2.10 ng/ml. All except passive avoidance situation also induced a rapid increase of plasma ACTHi to 0.45-0.70 ng/ml, whereas plasma alpha-MSHi increased after ether and restraint to 0.18-0.40 ng/ml but was not affected by formalin stress. To study the involvement of a beta-adrenoceptor mechanism in stress-induced peptide secretion, rats were treated with D-propranolol or L-propranolol 40 min before stress exposure. Propranolol did not prevent the increase of plasma ACTHi to any of the stressors studied. L-Propranolol but not its inactive D-isomer reduced (restraint, passive avoidance) or abolished (electric foot shocks) the increase in plasma beta-ENDi but did not affect the beta-ENDi response to other stressors (ether, formalin, laparotomy). Similarly, L-propranolol attenuated the alpha-MSHi response to restraint but not to ether stress. To discriminate between corticotroph or melanotroph origin of beta-ENDi released during stress, rats were treated with dexamethasone or were subjected to neurointermediate lobectomy (4 weeks). Neurointermediate lobectomy did not affect basal or stress-induced plasma ACTHi but resulted in undetectable alpha-MSHi levels. It largely prevented the beta-ENDi response to restraint stress (propranolol sensitive) but had little effect on the beta-ENDi response to formalin stress (propranolol insensitive). Conversely, dexamethasone prevented stress-induced ACTHi response without affecting plasma alpha-MSHi. The beta-ENDi response to restraint stress (propranolol sensitive) was not changed but the response to formalin stress (propranolol insensitive) was largely prevented by dexamethasone. These results show that the intermediate lobe is the main source of beta-ENDi secreted during exposure to stressors with a high emotional impact. Since intermediate lobe peptide secretion induced by such stimuli can be prevented by beta-adrenoceptor blockade, we speculate that stress-induced discharge of catecholamines, possibly from the adrenal medulla, is the trigger signal for peptide secretion from the melanotrophs during this type of stress.

Adrenocorticotropic Hormone↗
PubMed1983

Mapping of CRF-immunoreactive nerve fibers in the medulla oblongata and spinal cord of the rat.

By use of an antiserum raised against Corticotropin Releasing Factor (CRF 1-41), nerve fibers can be stained in the medulla oblongata and spinal cord of rats. A dense plexus of CRF-immunoreactive (CRFi) nerve fibers is present in the nucleus tractus spinalis nervi trigemini from which fiber bundles enter the tractus spinalis nervi trigemini. Large numbers of CRFi fibers are present in the substantia gelatinosa of the spinal cord, while the tractus solitarius, the nucleus tractus solitarius and the nucleus ambiguus contain a low number of CRFi fibers. In rats treated with colchicine, CRFi cell bodies are found in the hypothalamus and occasionally in the nucleus tractus solitarius and the nucleus olivaris inferior. Posterolateral deafferentation of the hypothalamus did not result in a disappearance of the CRFi fibers in the medulla oblongata and spinal cord 7 days after surgery. These results indicate that CRFi fibers present in the spinal cord and medulla oblongata are part of a novel peptidergic neuronal system, which is different from the hypothalamo-infundibular CRF system.

Animals↗
PubMed1983

Vasopressin is not involved in the catecholamine-induced release of ACTH, alpha-MSH and beta-endorphin from the rat pituitary gland.

The effect of catecholamines on plasma levels of immunoreactive ACTH (ACTHi), alpha-MSH (alpha-MSHi), beta-endorphin (beta-ENDi), arginine-vasopressin (AVPi) and of corticosterone (B) was studied in female rats. Intravenous infusion of the specific beta-adrenoceptor-stimulating agent l-isoproterenol in Wistar rats under pentobarbital anesthesia resulted in a dose-dependent (dose range: 10-100 ng/kg . min) increase in plasma B. At higher concentrations, l-isoproterenol also caused a dose-dependent increase in plasma AVPi (dose range: 100-1,000 ng/kg . min). In addition to isoproterenol, also intravenous infusion of l-epinephrine caused a dose-dependent increase of plasma B (dose range: 100-1,000 ng/kg . min), whereas l-epinephrine was without effect on plasma AVPi, even at the highest dose tested (1,000 ng/kg . min). The effect of l-epinephrine or l-isoproterenol on plasma B was associated with a parallel and dose-related increase in plasma ACTHi, beta-ENDi and alpha-MSHi. The increase of plasma ACTHi, B and beta-ENDi in response to l-isoproterenol (300 ng/kg . min) was identical in Wistar, Long Evans and Brattleboro rats (Long Evans rats with a hereditary lack of vasopressin). Also the responses to l-epinephrine (1,000 ng/kg . min) were identical in Wistar and Brattleboro rats. We conclude that vasopressin does not mediate the catecholamine-induced release of ACTH, beta-endorphin and alpha-MSH.

Adrenocorticotropic Hormone↗
PubMed1982

Immunoreactive beta-endorphin in the hypothalamus of female rats: changes in content and release during prepubertal development.

Female Wistar rats of different ages (1-45 days) were used. Extracts were made of the mediobasal hypothalamus (MBH) and beta-endorphin immunoreactivity (beta-ENDi) was quantitated by radioimmunoassay. Low but significant amounts of beta-ENDi (6.5 ng/MBH) were present on the first postnatal day. Hypothalamic beta-ENDi content did not change during the first week but decreased during the second week to a minimum (4.5 ng/MBH) on day 14. Thereafter, beta-ENDi increased rapidly to 13 ng/MBH on day 28 and remained at this level. Gel filtration showed that beta-ENDi substances with chromatographic characteristics identical to those of beta-END and beta-LPH were present in MBHs of 14-, 20- and 45-day-old rats. A beta-ENDi substance, possibly representing beta-END1-27, was nearly absent on day 14, but represented a major component of the MBH of the 45-day-old rat. In vitro incubation of MBH resulted in spontaneous release of beta-ENDi. Depolarization of neuronal membranes by incubation in medium containing 45 mMK+ stimulated beta-ENDi release. Both the spontaneous and K+-stimulated release of beta-ENDi were low on day 10 but reached postpubertal levels on day 20. These observations lead us to propose that the beta-ENDi-containing neurons in the hypothalamus of developing female rats rapidly mature between 14 and 20 days after birth. This may be causally related to the rapid decrease in circulating FSH levels that occurs during this period.

Aging↗
PubMed1982

Effect of hypothalamus lesions on the presence of CRF-immunoreactive nerve terminals in the median eminence and on the pituitary-adrenal response to stress.

By use of an antiserum raised against conjugated ovine corticotropin releasing factor (CRF1-41), nerve fibres can be stained immunocytochemically in the external zone of the median eminence of rats. The presence of CRF-immunoreactive (CRFi) nerve fibres and the plasma corticosterone response to ether stress were studied in rats 6-7 days after making various types of lesions in the hypothalamus. Complete anterolateral deafferentation of the mediobasal hypothalamus caused complete disappearance of CRFi fibres from the median eminence and blocked the corticosterone response to stress. Incomplete anterolateral hypothalamic deafferentation did not prevent the stress-induced increase of corticosterone and in these rats, part of the CRFi nerve fibres remained intact. A horizontal cut placed ventral to the paraventricular nuclei, completely prevented the corticosterone response in those rats that showed a complete disappearance of CRFi nerve fibres from the median eminence. Some rats however, still exhibited CRFi nerve fibres and these animals responded to stress with increased corticosterone levels. A similar horizontal cut made just dorsal to the paraventricular nuclei affected neither the corticosterone response to stress nor the appearance of CRFi nerve fibres in the median eminence. We conclude that the presence of CRFi nerve fibres in the median eminence is a prerequisite for rats to show a pituitary-adrenal response to ether stress and therefore represents the first functional evidence for the role of these hypothalamic CRFi-neurons.

Adrenal Glands↗
PubMed1982

In vitro release of LHRH from the hypothalamus of female rats during prepubertal development.

In this study changes in serum FSH concentration, hypothalamic LHRH content and in vitro release of LHRH from hypothalami of female Wistar rats during prepubertal development are described. The concentration of FSH in serum was determined by radioimmunoassay. Extremely high levels (1.800 ng/ml) were found between 12 and 16 days of age. Thereafter, FSH levels rapidly fell to low levels (135 ng/ml) on day 32. LHRH was measured by radioimmunoassay in extracts of mediobasal hypothalami (MBH) and showed a gradual increase during the first 10 days of life. Between 10 and 16 days of age, hypothalamic LHRH content did not change. After day 16, LHRH content sharply increased to a maximum found on day 32. The release of LHRH from MBH of developing rats was studied during in vitro incubation in Krebs-Ringer bicarbonate buffer. LHRH in the medium was measured by radioimmunoassay. The spontaneous release rate of LHRH was maximal from MBH of 12-day-old rats and minimal from those of 32 days. Depolarization of neural membranes, by medium containing 45 mM K+ induced a stimulation of LHRH release. This K+ -induced release of LHRH was also most prominent on day 12. These observations are consistent with the hypothesis that the high circulating FSH levels found in female rats between 12 and 16 days of age are at least in part caused by a high secretion rate of LHRH during this period.

Animals↗
PubMed1981

Hypothalamic deafferentation in the rat appears to discriminate between the anterior lobe and intermediate lobe response to stress.

Anterolateral deafferentation of the mediobasal hypothalamus prevented the increase of the plasma corticosterone concentration induced by ether, histamine and electric footshock. Hypothalamus deafferentation also prevented the ether stress-induced increase of the plasma levels of ACTH and beta-endorphin immunoreactivity (ACTHi, beta-ENDi). Infusion of isoproterenol evoked an increase of the plasma levels of corticosterone, ACTHi, beta-ENDi and alpha-MSH immunoreactivity (alpha-MSHi) in sham-operated rats. In rats with a deafferented hypothalamus, the responses of plasma corticosterone and ACTHi to isoproterenol were blocked but the responses of plasma beta-ENDi and alpha-MSHi remained intact. We conclude that circulating beta-ENDi after exposure to ether is of anterior lobe origin while circulating beta-ENDi after infusion of isoproterenol is of intermediate lobe origin.

Adrenocorticotropic Hormone↗
PubMed1981

Epinephrine as a potent releaser of immunoreactive beta-endorphin in rats.

The intravenous infusion of catecholamines to rats induced a dose dependent increase of immunoreactive beta-endorphin (beta-Endi) in plasma. The ED50 values of 1-epinephrine and 1-isoproterenol were 110 and 100 ng/kg X min respectively. 1-Propranolol, but not d-propranolol prevented the effect of 1-epinephrine. Infusion of 100 ng/kg X min of 1-epinephrine increased plasma epinephrine to 11 pmol/ml, a concentration that can occur during stress. We conclude that circulating catecholamines can stimulate beta-Endi secretion via a beta-adrenergic receptor mechanism and may play a role in the response of beta-Endi to stress.

Animals↗
PubMed1981

Release of beta-lipotropin and beta-endorphin from rat hypothalami in vitro.

Hypothalamic tissue extracts of rats were chromatographed and beta-endorphin immunoreactivity (beta-Endi) was measured. The two major peaks of beta-Endi co-eluted with beta-lipotropin (beta-LPH) and beta-End respectively. Hypophysectomy caused a local decrease of beta-LPH and beta-End concentrations in the mediobasal hypothalamus. During superfusion of hypothalamic tissue blocks in vitro, membrane depolarization by electric stimulation or 45 mM k+ induced a Ca2+-dependent release of both beta-LPH and beta-End.

Animals↗
PubMed1980

Studies on the prolactin response induced by electroconvulsive therapy in schizophrenics.

Electroconvulsive therapy (ECT) and simulated ECT (SECT)-induced prolactin response has been studied in 14 schizophrenic males. Cortisol, growth hormone, and thyroid stimulating hormone (TSH) changes have been measured simultaneously. The prolactin rise was significantly higher after ECT than after SECT. Cortisol increase after ECT did not exceed significantly the elevation after SECT. Changes in growth hormone and TSH concentrations were inconsistent and non-significant. On the basis of the results it may be assumed that ECT-induced prolactin response is a consequence of specific transmitter changes in the CNS and not a result of stress reaction or generalized neuronal discharge. ECT-induced prolactin response was negligible in two cases. Both patients were chronically hospitalized schizophrenics resistant to therapy. Whether the prolactin response or its absence is of predictive value with respect to prognosis or effect of ECT remains to be seen.

Adult↗
PubMed1980

Maturation of the circadian rhythm of the adrenocortical functions in human neonates and infants.

The cortisol levels in the peripheral blood were measured radioimmunologically at 08.00, 12.00,. 16.00, 20.00, 24.00 and 04.00 h in human neonates and infants with ages of 1, 2 and 3 days, 1, 2 and 4 weeks, 2, 3 and 6 months and 1 and 3 years. During the first 2 days of extrauterine life the neonates had high plasma cortisol levels without a circadian rhythm. During the first 2 months there were decreased cortisol levels in the infants, but the diurnal rhythms were still absent, and free-running fluctuations were observed. The typical circadian rhythms of the plasma cortisol levels were present in infants aged 3 months; these rhythms were identical with the diurnal changes of 1- and 3-year-old infants. In the groups of patients studied the data suggest that the circadian rhythm of the adrenocortical function may develop to the adult-type pattern already during early infancy.

Adrenal Cortex↗