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)

Neurointermediate lobes from amphibians (Rana pipiens) were incubated in Medium 199 containing dopamine, beta-endorphin or dopamine plus beta-endorphin. Dopamine inhibited melanocyte-stimulating hormone (MSH) secretion as measured by bioassay in hypophysectomized frogs, an effect which was transiently reversed by beta-endorphin. The effects of endorphin were in turn partially suppressed by the opiate antagonist, naloxone hydrochloride. Cells treated with all three agents exhibited expanded rough endoplasmic reticulum and decreased secretory granule content, indicative of peptide release and new synthesis. Beta-Endorphin alone did not stimulate MSH secretion above control levels, and at one time period was seen to reduce MSH secretion. The findings indicate a complex interaction between beta-endorphin and dopamine directly upon MSH secretion at the level of the neurointermediate lobe.
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PMID:Interaction of beta-endorphin, naloxone and dopamine: effects on melanocyte-stimulating hormone secretion of amphibian pituitaries in vitro. 628 39

The effects of synthetic corticotropin-releasing factor (CRF) and dopamine on immunoreactive beta-endorphin/beta-lipotropin (i beta-END/LPH) and alpha MSH release were studied in superfused human fetal pituitary glands. CRF (20 ng) stimulated the release of i beta-END/LPH in four anterior hemipituitaries from fetuses older than 20 weeks in gestation. There was no effect on three anterior hemipituitaries from fetuses of 19-20 weeks gestation. CRF had no effect on i beta-END/LPH or alpha MSH secretion from neurointermediate lobes regardless of fetal age. Dopamine (10(-6) M) had no effect on i beta-END/LPH or alpha MSH secretion from either anterior or neurointermediate lobes. The data suggest that anterior pituitary responsiveness to CRF develops at about 20 weeks gestation and that fetal neurointermediate lobe secretion of peptides is not regulated by CRF.
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PMID:Effects of synthetic corticotropin-releasing factor and dopamine on the release of immunoreactive beta-endorphin/beta-lipotropin and alpha-melanocyte-stimulating hormone from human fetal pituitaries in vitro. 629 May 22

A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
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PMID:Aldosterone suppression with dopamine infusion in low-renin hypertension. 630 9

Dopamine (DA) normally circulates in plasma. The plasma concentration of the free form of DA is approximately equivalent to that of epinephrine (E) and 20% that of norepinephrine (NE). The free form constitutes less than 2% of total plasma DA, and the remainder exists predominantly as sulfate or glucuronide conjugates. DA is found in adrenal medulla and cortex, peripheral nerves, sympathetic ganglia, carotid body, and kidney, but quantitatively the origin of circulating DA remains poorly understood. Plasma concentrations of free DA increase in association with events that increase sympathetic tone, although to a much lesser degree than seen for NE or E. Thus, upright posture, bicycle exercise, a variety of emotional and physical stresses, and hypoglycemia may be associated with increases in plasma free DA. Plasma DA decreases during the course of dietary sodium depletion in humans, in contrast to the plasma NE response, and consistent with a physiological role for DA in the regulation of aldosterone secretion. Plasma DA increases after administration of its precursor L-dihydroxyphenylalanine, together with the decarboxylase inhibitor carbidopa. Plasma NE and (in some studies) plasma DA decrease after administration of the DA receptor agonist bromocriptine. In contrast, plasma DA and one of its major metabolites, homovanillic acid, increase after administration of the DA receptor antagonist haloperidol. Administration of the endogenous opioid peptide beta-endorphin into the brain increases central sympathetic outflow, thus increasing plasma DA concentration, although to a lesser extent than for NE or E. Disordered basal concentrations of DA in plasma or disordered responses of plasma DA have been reported in a number of disease states. Clear understanding of physiological roles of DA in plasma and of its pathophysiology awaits definition.
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PMID:Plasma dopamine: regulation and significance. 641 58

Dopamine-containing neurons directly innervate the intermediate lobe of the pituitary and dopaminergic compounds exert inhibitory effects on the secretion and the content of alpha-melanocyte-stimulating hormone and beta-endorphin in this tissue. In this study, we have investigated the effects of dopamine receptor agonists and antagonists on the level of pro-opiomelanocortin (POMC) mRNA in rat pituitary. RNAs isolated from neurointermediate pituitary (NIP) or anterior pituitary were spotted on nitrocellulose filters and the levels of POMC mRNA were quantified by hybridization to a POMC-specific complementary DNA probe coupled with autoradiography and densitometry. Administration of a dopamine receptor antagonist, haloperidol (2 mg/kg per day), to adult female rats resulted in a 3- to 5-fold increase in POMC mRNA level in the NIP. Treatment with the dopamine agonist 2-Br-alpha-ergocryptine (1 mg/kg per day) decreased significantly the content of POMC mRNA in the NIP. These drugs had no apparent effect on the POMC mRNA levels in the anterior pituitary. The effect of haloperidol and ergocryptine on POMC mRNA in the NIP is time- and dose-dependent. The elevation of POMC mRNA content in the NIP by haloperidol can be observed as early as 6 hr after treatment. These effects of dopaminergic compounds can also be demonstrated in adult male and ovariectomized female rats. The beta-endorphin content of the NIP, as measured by radioimmunoassay, and the de novo synthesis of POMC, as determined by radioactive amino acid labeling and two-dimensional gel electrophoresis analysis, also show negative regulation by dopaminergic compounds.
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PMID:Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds. 657 72

Morphine, met-enkephalin and leu-enkephalin (1 . 10(-5)M) rapidly, reversibly and in a naloxone-dependent manner depressed the amplitude of dopamine-induced depolarization in neurons of the snail Helix pomatia. Dopamine hyperpolarization and both types of responses to acetylcholine were not altered by morphine and enkephalins. A hypothesis of Zieglgansberger on a blockade of chemically excitable sodium channels by morphine and enkephalins is discussed. It is suggested that opiates block sodium channels when they are applied in high concentration (1 . 10(-4)-1 . 10(-3)M). Lower concentration of morphine and enkephalins (1 . 10(-5)M) modulate the neurotransmitter postsynaptic responses perhaps by means of affecting the cyclic nucleotide system.
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PMID:[Selective reduction by morphine and enkephalins of depolarization induced by application of dopamine to Helix pomatia neurons]. 683 23

The release of oxytocin from isolated posterior lobe of the hypophysis of untreated rats and rats pretreated with alpha-methyl-p-tyrosine (alpha-MPT) has been studied. The amount of oxytocin released under resting conditions, in response to ouabain was much higher in those preparations which had been pretreated with alpha-MPT. Dopamine failed to affect the resting release in tissue taken from control rats but it significantly reduced the secretion of oxytocin in tissue dissected from dopamine-deficient rats. Opioid peptides, beta-endorphin or D-Ala2-Pro5-enkephalinamide enhanced the release of oxytocin from isolated neural lobe of the hypophysis dissected from untreated rats, but they failed to enhance significantly the release from posterior lobe of rats which had been pretreated by alpha-MPT. Naloxone prevented the effect of the opioid peptides, and by itself significantly reduced the release of oxytocin. The data suggest that (i) dopamine stored in, and released from, the neural lobe may inhibit the secretion of oxytocin; (ii) the release of oxytocin may be continously controlled by an endogenous opioid peptide: opioid peptides may exert their effect via a disinhibitory phenomenon; they remove the inhibitory effect of dopamine on oxytocin release possibly by inhibiting the release of dopamine.
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PMID:Inhibition of dopamine of oxytocin release from isolated posterior lobe of the hypophysis of the rat; disinhibitory effect of beta-endorphin/enkephalin. 739 4

The amphibian Xenopus laevis is able to adapt the colour of its skin to the light intensity of the background, by releasing alpha-melanophore-stimulating hormone from the pars intermedia of the hypophysis. In this control various inhibitory (dopamine, gamma-aminobutyric acid, neuropeptide Y, noradrenaline) and stimulatory (thyrotropin-releasing hormone and corticotropin-releasing hormone) neural factors are involved. Dopamine, gamma-aminobutyric acid and neuropeptide Y are present in suprachiasmatic neurons and co-exist in synaptic contacts on the melanotrope cells in the pars intermedia, whereas noradrenaline occurs in the locus coeruleus and noradrenaline-containing fibres innervate the pars intermedia. Thyrotropin-releasing hormone and corticotropin-releasing hormone occur in axon terminals in the pars nervosa. In the present study, the neuronal origins of these factors have been identified using axonal tract tracing. Application of the tracers 1,1'dioctadecyl-3,3,3',3' tetramethyl indocarbocyanine and horseradish peroxidase into the pars intermedia resulted in labelled neurons in two brain areas, which were immunocytochemically identified as the suprachiasmatic nucleus and the locus coeruleus, indicating that these areas are involved in neural inhibition of the melanotrope cells. Thyrotropin-releasing hormone and corticotropin-releasing hormone were demonstrated immunocytochemically in the magnocellular nucleus. This area appeared to be labelled upon tracer application into the pars nervosa. This finding is in line with the idea that corticotropin-releasing hormone and thyrotropin-releasing hormone stimulate melanotrope cell activity after diffusion from the neural lobe to the pars intermedia. After anterograde filling of the optic nerve with horseradish peroxidase, labelled axons were traced up to the suprachiasmatic area where they showed to be in contact with suprachiasmatic neurons. These neurons showed a positive reaction with anti-neuropeptide Y and the same held for staining with anti-tyrosine hydroxylase. It is suggested that a retino-suprachiasmatic pathway is involved in the control of the melanotrope cells during the process of background adaptation.
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PMID:Involvement of retinohypothalamic input, suprachiasmatic nucleus, magnocellular nucleus and locus coeruleus in control of melanotrope cells of Xenopus laevis: a retrograde and anterograde tracing study. 752 68

1. Melanostatin, a thirty-six amino acid peptide recently isolated from the frog brain due to its ability to inhibit alpha-melanocyte-stimulating hormone (alpha-MSH) release, is the amphibian counterpart of mammalian neuropeptide Y (NPY). The effect of synthetic melanostatin on the bioelectrical activity of cultured frog melanotrophs was studied in 124 cells by using the whole-cell patch-clamp technique. 2. In current-clamp experiments, melanostatin (1 microM) provoked a reversible hyperpolarization and a suppression of spontaneous action potentials. In some cells the hyperpolarizing response was absent, but an arrest of spike firing still occurred. 3. Melanostatin-induced hyperpolarization was associated with a decrease in membrane resistance. In voltage-clamp experiments, melanostatin induced an outward current at a constant command potential. This hyperpolarizing outward current appeared to be carried by potassium ions. 4. Cell dialysis with the non-hydrolysable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) sustained the outward current produced by melanostatin. Dopamine (1 microM), which generates a similar hyperpolarizing outward current in frog melanotrophs, was not capable of increasing the current provoked by melanostatin and sustained by GTP gamma S. 5. Melanostatin also modulated voltage-operated currents. The amplitude of voltage-activated potassium current was increased by 30%. 6. Melanostatin reduced the fast sodium current. This inhibitory effect was rather persistent compared to the other modulated currents. 7. Melanostatin markedly scaled down high voltage-activated N- and L-like calcium currents. The activation kinetics of these two calcium currents were not altered by the peptide. 8. Pretreatment of melanotrophs with pertussis toxin (1 microgram ml-1) blocked melanostatin-induced inhibition of N- and L-like calcium currents. 9. It is concluded that the NPY-related peptide melanostatin generates a very complex pattern of electrical responses in frog melanotrophs, including hyperpolarization and modulation of voltage-activated currents underlying action potentials. G proteins appear to mediate at least part of these effects.
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PMID:Melanostatin (NPY) inhibited electrical activity in frog melanotrophs through modulation of K+, Na+ and Ca2+ currents. 791 31

It has previously been shown that dopamine plays a pivotal role in the regulation of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion from the intermediate lobe of the pituitary. In the present study, we have investigated the various intracellular mechanisms that are associated with the action of dopamine on frog pituitary melanotrophs. Dopamine reduced forskolin-stimulated cyclic adenosine monophosphate (cAMP) production and the inhibitory effect of dopamine was blocked by the dopaminergic D2 receptor antagonist sulpiride. The D2 receptor agonist apomorphine inhibited incorporation of [3H]inositol into membrane phospholipids. Dopamine also inhibited the formation of inositol trisphosphate and provoked accumulation of phosphatidylinositol bisphosphate. The inhibitory effect of dopamine on inositol trisphosphate production was mimicked by D2 receptor agonists and blocked by sulpiride. Using a double-wavelength microfluorimetric approach, we found that dopamine caused a rapid and transient decrease in K(+)-evoked stimulation of intracellular calcium concentration. The time-courses of the responses of the various intracellular messengers indicate that blockage of voltage-dependent calcium channels is the primary event associated with activation of dopamine D2 receptors, while inhibition of polyphosphoinositide breakdown, related to blockage of voltage-dependent calcium channels, and reduction of cAMP production are secondary events which may contribute to the sustained inhibitory effect of dopamine on alpha-MSH release.
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PMID:Effect of dopamine on adenylate cyclase activity, polyphosphoinositide metabolism and cytosolic calcium concentrations in frog pituitary melanotrophs. 838 14


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