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

This study addressed the possible coexistence of products of the proenkephalin and prodynorphin opioid peptide precursors in single neurons of the central nervous system of the rat. Antisera directed against met-enkephalin-arg-gly-leu and against Dyn B were used in immunohistochemical preparations of sections through the rat medulla. Examination of serial three micron frozen sections stained alternately with the two different antisera revealed that the majority of labelled neurons stain with only one of the two antisera. In specific area, however, immunoreactive m-enk and Dyn B could be detected in the same neuron. This was particularly true of the caudal ventrolateral nucleus of the solitary tract, where the two peptides were colocalized in most neurons. Other areas where the two peptides coexist include the midline raphe and the nucleus reticularis paragigantocellularis. These data provide the first evidence for colocalization of different opioid peptide families in single CNS neurons.
 ...
PMID:Colocalization of immunoreactive proenkephalin and prodynorphin products in medullary neurons of the rat. 639 21

Potential interactions between opiate peptides and catecholamines in mammalian heart were examined using isolated spontaneously beating rat atria as a test system. Methionine-enkephalin (ME), leucine-enkephalin (LE), phe-met-arg-phe amide (FMRFamide), D-ala2, N-methyl-phe4, met (O)5-ol-enkephalin (FK 33-834), methionine-enkephalin arg6 arg7 (ME arg6 arg7) and beta-endorphin had no effect on basal beating rate of isolated atria at all concentrations up to 10(-5) M. The positive chronotropic effect of norepinephrine (NE) on atrial rate is, however, significantly attenuated by enkephalin peptides. Thus, the maximal chronotropic effect of NE (an increase from 317 +/- 7.0 to 473 +/- 7.3 beats per minute (bpm) in 250 gm rats at a dose of 10(-5)M NE) is decreased by 42% in the presence of 10(-7)m ME. The action of ME is completely blocked by addition of 10(-7)M naloxone, which by itself has no effect on NE-induced positive chronotropy or basal beating rate. The dose-effect curve for ME attenuation of NE-induced positive chronotropy is bell-shaped, i.e., both 10(-8) M and 10(-5) M ME have no significant effect on NE positive chronotropy. Other enkephalin peptides acted in a similar manner to ME; LE (10(-7) M) and FK 33-834 (10(-8) M) decreased maximal NE-induced positive chronotropy 42 and 27%, respectively. The molluscan cardioexcitatory peptide FMRFamide (10(-7) M) also decreased maximal NE positive chronotropy, about 30%. In contrast, beta-endorphin did not significantly affect NE stimulation of atrial rate. We conclude that enkephalins can modulate the noradrenergic responsiveness of rat atria in vitro. The possible physiological relevance of this interaction is discussed.
 ...
PMID:Enkephalins modulate the responsiveness of rat atria in vitro to norepinephrine. 712 72

Immunocytochemical techniques applied to sections and whole-mount preparations of cercariae from two species of trematodes, Trichobilharzia ocellata and Schistosoma mansoni, revealed the occurrence of immunoreactivity (IR) to several neurosubstances in the nervous system (NS). Immunostaining was localized in cerebral ganglia, in the main commissure, in anterior and posterior nerve trunks, as well as in a pair of nerve fibres running along the tail. In T. ocellata, immunoreactivity (IR) was observed with antisera raised against: glutamate, FMRFamide, catch-relaxing peptide (CARP), small cardiac peptide B (SCPB), arg-vasotocin (AVT), arg-vasopressin (AVP), and substance P. In S. mansoni antisera raised against glutamate, FMRFamide, CARP, SCPB, alpha-caudodorsal cell peptides (alpha-CDCP), and cholecystokinin (CCK) showed neuronal IR. With the other 51 antisera tested no IR was observed. With anti-APGWamide, IR was observed outside the NS in cells of the wall of the daughter sporocyst and in flame cells of cercariae of T. ocellata. IR to FMRFamide was present in the escape glands of the intrasporocystic cercariae of T. ocellata and S. mansoni. IR to somatostatin was observed in subtegumental parenchymal cells of cercariae of S. mansoni. IR to met-enkephalin was present in cells of the cercarial embryos and in undifferentiated cells in developing cercariae. Trematodes are, together with cestodes, phylogenetically the oldest classes in which glutamate-like material and immunopositivity to a number of neuropeptides isolated from invertebrates has been demonstrated. The results are discussed in relation to immunocytochemical data obtained for other platyhelminths, to endogenous functions of the immunopositive materials, and to their possible role in parasite-host interactions.
 ...
PMID:Immunocytochemical study on biologically active neurosubstances in daughter sporocysts and cercariae of Trichobilharzia ocellata and Schistosoma mansoni. 802 56

To explore the roles of corticotropin and corticosteroids in the regulation of plasma lipoprotein concentrations, we investigated the effects of 4 days' administration of corticotropin 1-24 (Synacthen Depot, CIBA-Geigy, Basel, Switzerland) in healthy volunteers and compared them with those occurring during treatment with a synthetic glucocorticoid (dexamethasone). Corticotropin administration resulted in rapid decreases of apolipoprotein (apo) B, low-density lipoprotein (LDL) cholesterol, and plasma triglyceride concentrations of 20% to 30%, whereas dexamethasone treatment did not affect any of the apo B-containing lipoproteins. Lipoprotein (a) [Lp(a)] level was decreased by about 30%; in this case, a similar reduction was noted after dexamethasone treatment. High-density lipoprotein (HDL) concentrations increased with both treatments; however, apo A-I concentrations increased only with glucocorticoid treatment, whereas HDL cholesterol level was elevated after both regimens. The activity of hepatic lipase (HL) was significantly decreased after corticotropin, but not after glucocorticoid treatment. LDL receptor activity, studied in cultured Hep G2 cells, was upregulated by about 30% after incubation with corticotropin. We conclude that corticotropin exerts direct effects on lipoprotein metabolism in man, primarily on apo B-containing lipoproteins, which decrease probably due to a corticotropin-mediated upregulation of LDL receptor activity. The metabolism of Lp (a) seems to be primarily influenced by corticosteroids, which rapidly decrease Lp (a) concentrations. An inhibitory effect of corticotropin on HL activity seems to contribute, besides glucocorticoid effects on apo A-I metabolism, to the increase in HDL level.
 ...
PMID:Direct effects of corticotropin on plasma lipoprotein metabolism in man--studies in vivo and in vitro. 828 80

Decreased cardiac catecholamines were observed following incision and repair of the pericardium in sham-operated vs. unoperated control dogs. Animals were assigned to five groups: unoperated, sham-operated intact pericardia, open pericardia, sutured pericardia and complete ventricular sympathectomy. Hearts were collected four weeks after surgery. Sympathectomy decreased catecholamine content when compared to all other groups. Hearts with open/sutured pericardia contained significantly less catecholamines than controls. When the pericardium was intact or left open following incision, cardiac catecholamines were unchanged compared to unoperated controls. Since opioid peptides are colocalized with catecholamines, we measured met-enkephalin and met-enkephalin-arg-phe, proenkephalin A peptide products, in parallel samples. Similar to norepinephrine, met-enkephalin was decreased following both sympathectomy and pericardial repair. However, met-enkephalin-arg-phe, which may be more associated with the myocardium than its innervation, was not changed by any treatment. The sutured pericardium more than the stress of surgery apparently alters the tissue catecholamines and enkephalin. This may have resulted from the mechanical friction at the site of repair. Epinephrine and met-enkephalin contents in sympathectomized hearts were significantly lower than unoperated controls but were not significantly different from the intermediate values observed in the sutured group. The functional consequences of these changes on neuroendocrine status are unclear and will require further evaluation. The results also emphasize the need for careful attention to proper controls for surgical studies.
 ...
PMID:Pericardial repair depresses canine cardiac catecholamines and met-enkephalin. 857 36

Research has suggested that exogenous opioid substances can have direct effects on cardiac muscle or influence neurotransmitter release via presynaptic modulation of neuronal inputs to the heart. In the present study, multiple-labelling immunohistochemistry was employed to determine the distribution of endogenous opioid peptides within the guinea-pig heart. Approximately 40% of cardiac ganglion cells contained immunoreactivity for dynorphin A (1-8), dynorphin A (1-17) and dynorphin B whilst 20% displayed leu-enkephalin immunoreactivity. Different populations of opioid-containing ganglion cells were identified according to the co-existence of opioid immunoreactivity with immunoreactivity for somatostatin and neuropeptide Y. Immunoreactivity for prodynorphin-derived peptides was observed in many sympathetic axons in the heart and was also observed, though to a lesser extent, in sensory axons. Leu-enkephalin immunoreactivity was observed in occasional sympathetic and sensory axons. No immunoreactivity was observed for met-enkephalin-arg-gly-leu or for beta-endorphin. These results demonstrate that prodynorphin-derived peptides are present in parasympathetic, sympathetic and sensory nerves within the heart, but suggest that only the prodynorphin gene is expressed in guinea-pig cardiac nerves. This study has shown that endogenous opioid peptides are well placed to regulate cardiac function via both autonomic and sensory pathways.
 ...
PMID:Endogenous opioid peptides in parasympathetic, sympathetic and sensory nerves in the guinea-pig heart. 862 99

Within the lumbar sympathetic ganglia of guinea pigs, the endings of different populations of neuropeptide-containing preganglionic neurons form well-defined pericellular baskets of boutons around target neurons in specific functional pathways. We have used multiple-labelling immunofluorescence, confocal microscopy, and ultrastructural immunocytochemistry to investigate synaptic organisation within pericellular baskets labelled for immunoreactivity to calcitonin gene-related peptide (CGRP), substance P (SP), or the pro-enkephalin-derived peptide, met-enkephalin-arg-gly-leu (MERGL) in relation to their target neurons. Different functional populations of neurons, identified by their neurochemical profile, showed a significant degree of spatial clustering and predicted well the distribution of specific classes of pericellular baskets. Most of the boutons in a basket were completely surrounded by Schwann cell processes and did not form synapses. The synapses that were present were made mostly onto dendrites enclosed by the Schwann cell sheath surrounding the neuron within the basket. These dendrites probably originated from neurochemically similar neighbouring neurons. Nevertheless, some of the boutons in the baskets did form synapses with the cell body or proximal dendrites of the neuron they surrounded. Occasionally, cell bodies received a relatively high number of synapses and close appositions from boutons in a pericellular basket. Synaptic convergence of two immunohistochemically distinct types of preganglionic inputs was found in baskets of SP-immunoreactive or MERGL-immunoreactive, but not CGRP-immunoreactive, boutons. Taken together, our results show that the appearance of pericellular baskets is primarily due to the packing of the target neurons. The grouping of functionally similar classes of neurons with their pathway-specific projections of peptide-containing preganglionic neurons suggests that peptides could exert their effects in relatively well-defined zones within the ganglia.
 ...
PMID:Synaptic organisation of neuropeptide-containing preganglionic boutons in lumbar sympathetic ganglia of guinea pigs. 971 9

The following studies were conducted to determine if the ability of the intrinsic cardiac opioid, met-enkephalin-arg-phe to interrupt vagal bradycardia can be generalized to include the disruption of vagal effects on atrial contraction and coronary blood flow. Anesthetized dogs were instrumented to measure heart rate and left atrial contractile force or heart rate and coronary blood flow. The response of each variable was recorded at rest and during vagal stimulation. During the evaluation of vagal effects on contractile activity and coronary blood flow, heart rate was maintained constant by electrically pacing the hearts above their resting heart rate. In the first protocol, vagal stimulation reduced both heart rate and atrial contractile force in a frequency dependent fashion. When met-enkephalin-arg-phe (MEAP) was infused systemically for three min at 3 nmol min(-1) kg(-1), there were no observed changes in resting heart rate or atrial contraction. However, when the vagal stimuli were reapplied during the peptide infusion, the previously observed vagal effects on rate and contractile force were reduced in magnitude by one-half to two-thirds. The ability of MEAP to interrupt the vagal control of heart rate and contractile activity involves opiate receptors since the effect was eliminated in both cases by prior opiate receptor blockade with the high affinity antagonist, diprenorphine. In the second protocol, vagal stimulation produced a transient increase in coronary blood flow and an accompanying increase in myocardial oxygen consumption. These effects were reduced by approximately 80% during the systemic infusion of MEAP. A similar increase in coronary blood flow mediated by the direct acting muscarinic agonist, methacholine, was unaltered by the infusion of peptide. In summary, these data suggest that the intrinsic cardiac enkephalin, MEAP, is capable of inhibiting the vagal control of heart rate, contractile force and coronary blood flow and probably does so through a common opiate receptor located prejunctionally on vagal nerve terminals or within nearby parasympathetic ganglia.
 ...
PMID:Enkephalin inhibits vagal control of heart rate, contractile force and coronary blood flow in the canine heart in vivo. 1041 30

Nardilysin (N-arginine dibasic convertase, EC 3.4.24.61) was first identified on the basis of its ability to cleave peptides containing an arginine dibasic pair, i.e., Arg-Arg or Arg-Lys. However, it was observed that an aromatic residue adjacent to the dibasic pair (i.e., Phe-Arg-Lys) could alter the cleavage site. In this study we determined whether nardilysin can cleave peptides at a single basic residue. Nardilysin cleaves beta-endorphin at the monobasic site, Phe(17)-Lys(18), with a k(cat)/K(m) of 2 x 10(8) M(-)(1) min(-)(1). This can be compared to a k(cat)/K(m) of 8.5 x 10(8) M(-)(1) min(-)(1) for cleavage between a dibasic pair in dynorphin B-13. Nardilysin also cleaves calcitonin at His-Arg and somatostatin-14 at Cys-Lys. We examined the hydrolysis of fluorogenic peptides based on the beta-endorphin 12-24 sequence, Abz-T-P-L-V-T-L-X(1)-X(2)-N-A-I-I-K-Q-EDDnp. Nardilysin hydrolyzes the peptides when X(1)-X(2) = F-K, F-R, W-K, M-K, Y-K, and L-K. The kinetics of cleavage at F-K and F-R are similar; however, K-F is not hydrolyzed. Nardilysin cleaves at two monobasic sites M-K and F-R of the kallidin model peptide Abz-MISLMKRPPGFSPFRSSRI-NH(2), releasing desArg(10) kallidin (KRPPGFSPF). However, nardilysin does not release desArg(10) kallidin from the physiological precursor low molecular weight kininogen. These studies extend the range of potential substrates for nardilysin and further substantiate that nardilysin is a true peptidase.
 ...
PMID:Nardilysin cleaves peptides at monobasic sites. 1259 Jun 13

Sympathetic axons in the upper eyelid and in tissues in the superior retro-orbital space were examined for NPY immunoreactivity. Sympathetic nerve terminals containing co-localised NPY were associated with blood vessels, the conjunctiva and the Meibomian glands. The acini of the Harderian gland completely lacked sympathetic innervation. Sympathetic axons lacking NPY were only found in the tarsal muscle. In addition, a minority of terminals, located in the more proximal part of the tarsal muscle, contained weak immunoreactivity to NPY. Injections of the retrograde tracer, Fast Blue, into the eyelid or retro-orbital space labelled postganglionic somata in the superior cervical ganglion. While many retrogradely labelled somata were immunoreactive for NPY, around half lacked NPY immunoreactivity and so are likely to project to the tarsal muscle. Most of the retrogradely labelled postganglionic somata lacking NPY were surrounded by terminals immunoreactive for met-enkephalin, leu-enkephalin and met-enkephalin arg-gly-leu which were all found to be present in the same nerve terminals. Sectioning the cervico-sympathetic trunk eliminated all enkephalin-immunoreactive pericellular baskets. Many enkephalin-immunoreactive pericellular terminals contained co-localised VAChT, calretinin and calbindin immunoreactivity, but completely lacked nitric oxide synthase immunoreactivity. A second population of nerve terminals that were immunoreactive for nitric oxide synthase also surrounded tarsal muscle-projecting neurons, but these terminals lacked immunoreactivity to enkephalin. Thus, postganglionic neurons projecting to the tarsal muscle are of at least two chemical phenotypes (with or without NPY) and they receive convergent input from at least two populations of preganglionic neurons with distinctive chemical phenotypes.
 ...
PMID:Chemical coding of sympathetic neurons controlling the tarsal muscle of the rat. 1279 4


<< Previous 1 2 3 Next >>