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Biomedical subjects

J C Bedran de Castro

Publications and source records attributed to J C Bedran de Castro.

11 recordsLinked to original sources
PubMed1987

Role of opioid peptides in pulsatile release of gonadotropins and prolactin in the rat.

To determine the role of endogenous opioid peptides in the pulsatile release of gonadotropins and prolactin in the ovariectomized rat, the opiate receptor blocker, naloxone, was administered intravenously, and its effect on plasma FSH, LH and prolactin was determined by multiple sampling prior to and after injection. Naloxone produced a dose-related increase in plasma LH and to a lesser extent FSH and decreased prolactin levels in the experiment in which they were examined. Higher doses of naloxone produced a significant increase in plasma LH pulse amplitude and lengthened the interpulse interval with a consequent decrease in pulse frequency. Minimum values between pulses were also increased. There was no clear effect on FSH pulsations but pulses of prolactin were blocked. Intraventricular (third ventricle) injection of a specific anti beta endorphin antiserum (3 microliter) produced an initial decline followed by an elevation of LH but had no effect on plasma FSH. The normal rabbit serum control injections were without effect. It is hypothesized that initiation of LH pulses in the castrated rat may be related to a periodic removal of tonic beta endorphinergic tone.

Animals↗
PubMed1987

Beta-adrenergic blockers decrease levels of luteinizing hormone in plasma of orchidectomized rats.

The beta-adrenergic antagonists, propranolol and bornaprolol (FM-24), at greater than 2 mg/kg (as [-] form) significantly depressed plasma levels of luteinizing hormone (LH) in orchidectomized rats. This occurred in the absence of consistently significant changes in interpulse intervals or amplitudes of pulsatile LH release. Nadirs of plasma LH decreased significantly even at low blocker doses, with a clear dose dependence for both drugs. The highly significant decrease of plasma LH induced by blocker dosages causing greater than 93% inhibition of beta-adrenergic binding in the anterior pituitary gland was shown to occur without significant changes in binding of specific ligands at pituitary dopamine receptors and hypothalamic alpha 1-adrenergic receptors. The above evidence indicates that beta-blockers may lower LH release in vivo at the level of pituitary beta-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of unilateral decortication on beta-adrenergic receptors in the remaining cortex and in the hypothalamus of female rats.

Many experiments have been performed to evaluate the physiological role of catecholaminergic mechanisms in gonadotropin release. The purpose of the present study was to determine the concentration of beta-adrenoreceptors in the remaining (right) cerebral cortex and in right and left hypothalamic halves of hemi-decorticated female rats which exhibited elevated plasma gonadotropin levels as observed previously. The density of beta-receptors was measured using a high-affinity beta-adrenergic ligand, iodocyanopindolol (ICYP). Scatchard estimates were obtained for maximum binding (Bmax fmol/mg of tissues) from pooled cerebral cortical and hypothalamic tissue of animals under several experimental conditions after hemi-decortication and sham operation. There was an increase in beta-adrenoreceptor density in the remaining (right) cerebral cortex at all times examined in hemi-decorticate in comparison with the sham-operated animals (7 days, +10.9%; 21 days, +8.4%; 90 days, +22%; and 90 days plus ovariectomy, +34.8%). The number of beta-adrenoreceptors in the right hypothalamic half in hemi-decorticates decreased at 21 days (-42.20%) and then increased at 90 days (+76.63%) and 90 days plus ovariectomy (+51.75%) when compared with the left hypothalamic half. At the same time there were no significant changes in the sham-operated animals when comparing the receptor density in the right and left hypothalamic halves, respectively. Thus, our results suggest a direct or indirect adrenergic pathway by which the left cortex can influence the right cortex and a crossed pathway to the contralateral hypothalamus changing adrenergic activity which can alter the beta-adrenergic receptor binding capacity in the hypothalamus.

Animals↗
PubMed1986

The effect of unilateral decortication on the patterns of pulsatile follicle stimulating hormone (FSH) and luteinizing hormone (LH) release and on mean plasma prolactin (Prl) levels in the ovariectomized rat.

Previous experiments have shown that unilateral decortication is followed by an elevation in FSH and LH secretion, but there has been no study of the rhythms of release of gonadotropins in these animals. Consequently, this study was undertaken to determine if there are alterations in the pulsations of gonadotropins following hemi-decortication and also to measure plasma Prl in these animals to determine if it might also be under the influence of extrahypothalamic pathways. Our results show an increased mean plasma LH in unilateral decorticate animals that occurred because of an increase in pulse frequency without a significant increase in pulse amplitude. Mean plasma FSH was also elevated significantly in unilaterally decorticate animals, but there was no significant change in pulse frequency or amplitude. The length of the interpulse interval for LH release secretion decreased in unilateral decorticate animals, whereas the length of the cycle of FSH secretion increased in this circumstance. The mean levels of Prl were reduced in unilateral decorticate animals. These changes indicate that unilateral removal of cortico-rhinencephalic structures has an excitatory influence on gonadotropin secretion mediated by an increased frequency of LH and decreased frequency of FSH pulsations in the castrate, while at the same time there is a lowering of plasma Prl, probably due to removal of excitatory cortico-rhinencephalic pathways.

Animals↗
PubMed1985

Ultrashort-loop positive feedback of corticotropin (ACTH)-releasing factor to enhance ACTH release in stress.

Previous experiments have shown that intraventricular injection of ovine corticotropin (ACTH)-releasing factor (oCRF) in doses too low to elevate plasma ACTH by direct action on the pituitary does not lower plasma ACTH, suggesting that the peptide lacks a negative ultrashort-loop feedback action to suppress its own release under resting conditions. The present study was performed to determine whether oCRF has any action to alter CRF release in stress. The peptide was injected into the third ventricle or external jugular vein of freely moving ovariectomized female rats 5 min prior to application of ether stress. When oCRF was injected into the third ventricle in doses of 500 pg (0.1 pmol) or less, there was no significant alteration in plasma ACTH prior to ether stress; however, there was a significantly enhanced increase in plasma ACTH 2 and 5 min after ether stress applied 5 min after intraventricular injection of oCRF at doses of 50 (0.01 pmol) or 150 pg (0.03 pmol). These results suggest that the peptide acts on structures adjacent to the third ventricle to augment stress-induced CRF release. To rule out the possibility that the sensitivity of the pituitary itself to CRF increases dramatically following stress, 10 or 100 ng of oCRF was injected i.v. These doses produced a significant dose-related increase in plasma ACTH at 2, 5, or 15 min. In other groups receiving the same doses of oCRF and ether stressed 5 min later, plasma ACTH was significantly higher 2 or 5 min after ether stress when compared with plasma ACTH in ether-stressed saline-injected animals. However, in contrast with the results of intraventricular injection of oCRF, the release of ACTH was no greater than that obtained by summing the independent effects of exogenous oCRF and the CRF released by stress. We conclude that CRF may have a positive ultrashort-loop feedback action to enhance stress-induced ACTH release and that this enhancement is not due to increased sensitivity of anterior pituitary corticotrophs to CRF.

Adrenocorticotropic Hormone↗
PubMed1985

Effects of intravenous and intraventricular injection of antisera directed against corticotropin-releasing factor on the secretion of anterior pituitary hormones.

To determine the physiological significance of corticotropin-releasing factor (CRF) in the control of pituitary hormone secretion, highly specific antibodies directed against the peptide were injected either intravenously or intraventricularly (third ventricle) and the effect on plasma levels of pituitary hormones was determined before and after application of ether stress for 1 min. The intravenous injection of CRF antiserum (0.5 ml) did not significantly alter basal corticotropin (ACTH) levels in freely moving ovariectomized rats but largely blocked the increase in plasma ACTH resulting from ether stress. These antibodies had no effect on the ether-induced decline in plasma growth hormone (GH), and they failed to modify plasma luteinizing hormone levels. In a second experiment, CRF antiserum (3 microliter) or normal rabbit serum was injected into the third ventricle. A blood sample was drawn 24 hr later and immediately thereafter another injection of CRF antiserum or normal rabbit serum was made. There was no modification in the level of any of the hormones 24 hr after the first injections, and they were similar in CRF antiserum and normal rabbit serum-injected animals. After imposition of ether stress, the response of plasma ACTH was nearly completely blocked by the intraventricular CRF antiserum, but the degree of blockade was slightly less than that obtained by intravenous injection. The decline in plasma GH after ether stress was blocked by the intraventricular CRF antiserum. There was no effect of the intraventricular injection of the antiserum on the levels of the other pituitary hormones. The results with intravenous injection of the antisera indicate that CRF plays an extremely important but probably not completely indispensable role in the release of ACTH after ether stress. The results of the intraventricular injection of the antiserum suggest strongly that endogenous CRF may also modify its own release in response to stress, augmenting it by a positive ultrashort loop feedback, and that the antisera against the peptide blocked this action; however, an action at the pituitary of these intraventricularly injected antibodies cannot be completely ruled out. The blockade of the stress-induced suppression of GH release by the CRF antibodies suggests that CRF released intrahypothalamically during ether stress brings about an alteration in the hypothalamic control of GH secretion such that the stress-induced inhibition of GH release is blocked.

Adrenocorticotropic Hormone↗
PubMed1985

Stress-induced secretion of alpha-melanocyte-stimulating hormone and its physiological role in modulating the secretion of prolactin and luteinizing hormone in the female rat.

The pattern of alpha MSH release during immobilization stress in ovariectomized rats was determined and correlated with that of plasma PRL and LH. Stress induced a marked elevation in plasma immunoreactive alpha MSH, with a time course identical to that of plasma PRL. The increment in plasma PRL was greater than that in plasma alpha MSH. Plasma LH was markedly lowered by stress. Analysis of pituitary and hypothalamic alpha MSH indicated a significant (P less than 0.05) increase in the neurointermediate lobe and anterior lobe content of alpha MSH. The alpha MSH content in the hypothalamus was lowered by stress when expressed as tissue content (P less than 0.025), although no significant differences in content in this area were detected when the results were expressed in terms of tissue protein. Stress induced a marked increase (P less than 0.01) in the median eminence levels of alpha MSH. Intraventricular (third ventricle) injection of the gamma-globulin fraction of a specific antiserum raised against alpha MSH increased basal PRL levels (P less than 0.025) and prevented the decline in plasma PRL that occurred 60 min after the onset of stress in the normal rabbit serum-injected rats. The stress-induced suppression of plasma LH was attenuated and delayed by the administration of alpha MSH antibodies. In conclusion, alpha MSH of brain origin is released during stress and is involved in lowering plasma PRL to basal levels and producing a partial suppression of plasma LH.

Animals↗
PubMed1985

Possible negative ultra-short loop feedback of luteinizing hormone releasing hormone (LHRH) in the ovariectomized rat.

To determine if LHRH might act within the brain to modify its own release, repeated blood samples were removed from conscious ovariectomized rats and minute doses of LHRH were injected into the third ventricle (3V). The effect of these injections on plasma LH and FSH was measured by radioimmunoassay (RIA). The higher dose of intraventricular LHRH (10 ng in 2 microliter) induced an increase in plasma LH within 10 min after its injection. Plasma LH decreased for the next 60 min. This was followed by restoration of LH pulses characteristic of the ovariectomized rat. This dose of LHRH slightly elevated plasma FSH concentrations. In stark contrast, a 10 fold lower dose of 1 ng of LHRH injected into the ventricle resulted in a highly significant decrease of plasma LH at 10 min following injection, followed by return of LH pulsations. There was no effect on the pulsatile release of FSH. The results are interpreted to mean that at the higher dose, sufficient LHRH reached the site of origin of the hypophyseal portal vessels in the median eminence so that it diffused into portal vessels and was delivered to the gonadotrophs to induce LH release. In contrast, the lower dose provided sufficient hypothalamic concentrations of the peptide to suppress the discharge of the LHRH neurons, thereby leading to a decline in plasma LH, indicative of an ultrashort-loop negative feedback of LHRH to suppress its own release.

Animals↗
PubMed1984

Physiological role of alpha-melanocyte-stimulating hormone in modulating the secretion of prolactin and luteinizing hormone in the female rat.

Long-term ovariectomized (OVX) rats were injected in the third cerebral ventricle with 5 microliter of the globulin fraction of an antiserum raised against alpha-melanocyte-stimulating hormone (alpha-MSH) or an equal volume of the globulin fraction of normal rabbit serum (NRS). Immunoneutralization of brain alpha-MSH produced an increase in the area under the secretion curve of prolactin (Prl), the amplitude of Prl pulses, and mean plasma Prl (P less than 0.01). In animals that had received two injections of NRS or anti-MSH and were subjected to a 2-min ether stress, Prl levels significantly increased within 5 minutes in the NRS-injected rats, whereas Prl levels in the antiserum-injected rats did not increase any further from the initially high baseline levels. The administration of antibodies against alpha-MSH produced a small increase (P less than 0.05) in the area under the secretion of luteinizing hormone (LH) and mean plasma LH; however, the number of LH pulses was unaffected. We conclude that endogenous alpha-MSH of central origin is a physiological neuromodulator of release of Prl and LH in the OVX rat and is involved in the stress-induced release of Prl.

Animals↗
PubMedDate not supplied

The effect of the estrous cycle and estrogen on the release of immunoreactive alpha-melanocyte-stimulating hormone.

Circulating levels and tissue content of alpha-MSH were measured on the morning of various days of the estrous cycle, and on the afternoon of proestrus in freely moving conscious rats. No surges of alpha-MSH were detected by RIA in the morning of various days of the cycle. The neurointermediate lobe content of alpha-MSH was slightly elevated on diestrus 1 as compared to the levels on diestrus 11 and proestrus but not to estrous levels. No changes in alpha-MSH content were detected in the anterior pituitary, the median eminence, mediobasal hypothalamus and the preoptic area at various stages of the estrous cycle. Plasma alpha-MSH levels were slightly elevated at 1500 hr of proestrus which was followed three hours later by a decline. This profile of plasma alpha-MSH on the afternoon of proestrus was reproduced by the SC administration of estradiol benzoate to long-term ovariectomized rats. These data suggest that, contrary to the results obtained by bioassay of alpha-MSH no surges of alpha-MSH occur on any day of the cycle, although a slight elevation on the afternoon of proestrus was detected. The altered pattern of release of this peptide on the afternoon of proestrus may be induced by estrogen.

Animals↗