Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Ca2(+)-mobilizing hormone angiotensin II (AII) dose-dependently inhibited the K(+)-induced sustained increase of cytoplasmic Ca2+ concentration in adrenal glomerulosa cells and caused a rapid decrease of cytoplasmic Ca2+ when added to cells already stimulated with K+. These effects of AII on the K(+)-induced Ca2+ signal were mimicked, although less effectively, by other Ca2(+)-mobilizing agonists such as [Arg8]vasopressin (AVP) and thapsigargin. Phorbol esters did not show such effects, nor did corticotropin (ACTH), a secretagogue acting via cyclic AMP. The K(+)-stimulated initial 45Ca2+ uptake, a measure of Ca2+ entry into glomerulosa cells, was also prevented by AII pretreatment, and was inhibited by AVP, but not by ACTH. The stimulatory effect of K+ on aldosterone production, however, was not inhibited by AII, and the AII-induced aldosterone production was further increased by increasing K+. These data indicate that AII is able to inhibit static increases in cytoplasmic Ca2+ by inhibiting Ca2+ entry through voltage-sensitive Ca2+ channels and, possibly, by activating Ca2+ extrusion from the cells. It is also concluded that the Ca2+ signal evoked by AII is very efficient in stimulating hormone secretion, and the secretory response of the cells becomes more sensitive to any further increase of Ca2+ entry through voltage-sensitive Ca2+ channels.
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PMID:Angiotensin II inhibits K(+)-induced Ca2+ signal generation in rat adrenal glomerulosa cells. 184 39

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

A 62-year-old man was admitted because of nausea and vomiting. Severe hyponatremia with renal sodium loss was found. Endocrinological studies revealed that the patient had isolated adrenocorticotropin (ACTH) deficiency and secondary adrenocortical insufficiency. Furthermore, an inappropriate secretion of antidiuretic hormone (ADH) in relation to the low plasma osmolality was observed at an early stage of hyponatremia. Hydrocortisone therapy effectively corrected his hyponatremia. Following the correction of hyponatremia, the value of free water clearance increased and the level of the plasma ADH decreased. Thus, the present case indicates that ACTH deficiency can cause the syndrome of inappropriate secretion of ADH.
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PMID:Inappropriate secretion of antidiuretic hormone in isolated adrenocorticotropin deficiency. 185 May 79

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.
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PMID:[Current findings in the regulation of formation of corticoliberin, pro-opiomelanocortin and ACTH as well as the efficacy of these compounds]. 196 5

The role of central angiotensin II (AII) in the shaking stress-induced adrenocorticotropic hormone (ACTH), plasma catecholamine secretion and pressor response were investigated using conscious rats. We also studied whether or not vasopressin (VP) is involved in the shaking stress-induced pressor response. The shaking stress caused significant elevations in plasma ACTH, catecholamine, and systolic blood pressure. Intra-third ventricular administration of the AII antagonist, Sar1, Ile8-angiotensin II (saralasin) significantly attenuated pressor response and plasma noradrenaline elevation but not plasma ACTH elevation. Pretreatment with the vascular-type VP receptor (V1) antagonist, d(CH2)5Tyr(Me)AVP, did not attenuate pressor response nor plasma catecholamine elevation. These results indicate that the central angiotensinergic pathway at least partly mediates the shaking stress-induced activation of the sympathetic nervous system without VP involvement, and that central AII does not mediate the ACTH secretion evoked by shaking stress.
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PMID:Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion. 196 26

Bilateral simultaneous blood samples were taken from the inferior petrosal sinuses of nine patients with Cushing's disease for measurement of adrenocorticotropin (ACTH), vasopressin (AVP), prolactin, growth hormone, luteinising hormone (LH), and follicle stimulating hormone (FSH). Inter-sinus gradients for ACTH (range 3.3-18.2) and AVP (2.0-375) correctly lateralised the microadenoma in seven of these patients. One additional patient showed an increased gradient for AVP but not ACTH on the side of the tumour. The correlation between the AVP and ACTH concentrations in the petrosal sinus draining the microadenoma was significant. Petrosal sinus plasma concentrations of prolactin and growth hormone were also significantly higher on the side of the tumour than on the non-tumour side. Evidence against a non-specific tumour effect on the secretion of all pituitary hormones was the fact that in most cases the gradients for LH and FSH were not significant. It is proposed that increased delivery of AVP to part of the pituitary may result from an aberrant blood supply, and that AVP may interact with corticotropin releasing factor to promote tumour growth and ACTH release.
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PMID:Arginine vasopressin in Cushing's disease. 197 Jan 7

Because of the large number of cell phenotypes in the nervous system, it has been difficult to characterize each as to specific electrophysiological properties. We have developed a technique that allows the identification of central and peripheral nervous system neurons following intracellular recording. We use electrodes that contain 2% biocytin to do current- and voltage-clamp recordings; the recorded neurons are revealed with streptavidin-fluorescein isothiocyanate labeling and identified through immunohistochemical staining for specific antigens. Presently, we report on the use of this technique to identify four cell types--dopamine, beta-endorphin, vasopressin and oxytocin--in the hypothalamus of the mammal. This technique should have widespread applicability for electrophysiologists.
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PMID:A method for immunocytochemical identification of biocytin-labeled neurons following intracellular recording. 197 96

Plasma levels of beta-endorphin, vasopressin and cortisol during head-up tilt were measured in tetraplegic patients and in normal healthy subjects. In tetraplegic patients rapid tilt from the horizontal to 30 degrees or 60 degrees head-up induced orthostatic hypotension and increased plasma levels of cortisol, beta-endorphin and vasopressin. In control subjects head-up tilt failed to alter plasma levels of these hormones. These data show that the head-up position in tetraplegics causes various endocrine reactions.
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PMID:Release of vasopressin, cortisol and beta-endorphin in tetraplegic subjects in response to head-up tilt. 202 76


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