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)

Elucidation of the role of natriuretic peptides (NPs) in vertebrate adrenal steroidogenesis has been facilitated by the use of freshly dispersed adrenocortical cells. Our recent characterization of lizard adrenocortical cells [Carsia, R.V., John-Alder, H.B., 2003. Seasonal alterations in adrenocortical cell function associated with stress-responsiveness and sex in the Eastern Fence Lizard (Sceloporus undulatus). Horm. Behav. 43, 408-420] provided the opportunity to examine the influence of atrial natriuretic peptides (ANPs) and related NPs on reptilian adrenal steroidogenesis at the cellular level. In the present report, the action of NPs on lizard adrenal steroidogenesis was investigated using freshly dispersed adrenocortical cells derived from the Eastern Fence Lizard (Sceloporus undulatus). Basal production rates of aldosterone and corticosterone and maximal angiotensin II (ANG II)-induced production rates of these corticosteroids were inhibited with high efficacy (75-90%) by rat ANP at potencies of 0.4-0.7 nM. By contrast, rat ANP had no effect on maximal production rates of these corticosteroids in response to a maximal steroidogenic concentration of adrenocorticotropin (ACTH; 1 nM). However, rat ANP inhibited aldosterone and corticosterone production rates in response to a half-maximal steroidogenic concentration of ACTH (10 pM; approximately 50 pg/ml), albeit with less efficacy ( approximately 50%) and potency (approximately 6 nM) than for ANG II. Rat and eel ANP and rat and chicken brain natriuretic peptide (BNP) were equally efficacious at inhibiting maximal ANG II-induced aldosterone and corticosterone production but with different potencies. The order of inhibitory potency was rat ANP = chicken BNP > eel ANP > rat BNP. However, a specific peptide ligand for the NP clearance receptor was without effect. This study indicates that ANP and related NPs are efficacious inhibitors of lizard adrenal steroidogenesis by acting directly at the level of the adrenocortical cell.
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PMID:Natriuretic peptides are negative modulators of adrenocortical cell function of the eastern fence lizard (Sceloporus undulatus). 1621 63

Histopathological, ultrastructural and immunohistochemical investigations were conducted on 26 specimens of powan Coregonus lavaretus (L.) from Loch Lomond (Scotland). The hearts of all 26 powan (15 females and 11 males) investigated harboured metacercariae of the digenean trematode Ichthyocotylurus erraticus (Rudolphi, 1809). The vast majority of metacercariae were located either singly or as an aggregation of white cysts on the surface of the bulbus arteriosus. The intensity of infection ranged from 2 to 200 larvae heart(-1), although the number of metacercariae found on male powan did not exceed 13. Histochemically, the parasite cyst wall gave a strong positive reaction with periodic acid schiff (PAS) and a faint positive signal with Azan-Mallory stain. All the metacercariae cysts were embedded in a granulomatous proliferation of heart epicardium tissue, forming a reactive fibroconnective capsule around the parasite. The capsule enclosing the parasite (produced by the host's reaction to the parasite) measured 13.57 to 90.20 microm (37.43 +/- 3.56) in thickness. Within the capsule wall, eosinophilic granular cells (EGCs), granulocytes, melanocytes and, in some instances, partially degenerated or vacuolated epithelioid cells were observed in close proximity to the cyst wall. Pigment-bearing macrophages were scattered throughout the granulomatous host-tissue reaction and as macrophage aggregates (MAs) within the capsules surrounding parasites. Immunohistochemical tests were applied to infected heart sections using 12 different antisera. Nerve fibres immunoreactive to bombesin, substance P (SP), and atrial natriuretic peptide (ANP) antisera were observed in close proximity to the parasite larvae. The presence of a serotonin-like substance was also observed within host immune-cells surrounding trematode cysts. Large cells of the epicardium were found to be immunoreactive to met-enkephalin and vasoactive intestinal peptide (VIP) antisera but not immunoreactive to anti-protein gene-product 9.5 (PGP9.5) sera.
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PMID:Histopathology, ultrastructure and immunohistochemistry of Coregonus lavaretus hearts naturally infected with Ichthyocotylurus erraticus (Trematoda). 1626 40

It is generally accepted that the essential hypertension (EH) is caused by interactions among congenital gene, multiple pathogenetic pressor factors, and disorder of physiologic depressor factors. The central nervous system may play a key role in the development of EH. The underlying mechanisms, however, are not well understood. Studies show that peptidergic transmitters in the limbic forebrain are involved in long-term regulation of arterial pressure and in the pathogenesis of EH. In the limbic forebrain there are peptidergic pressor and depressor circuits. The former includes corticotropin releasing factor-, substance P-, and angiotensin II-circuits; and the latter includes beta-endorphin- and atrial natriuretic peptide-circuits. These circuits extensively interconnect and interact with each other. The altered functions of them may be the pathogenesis of EH. In this review, we focus on the roles of limbic peptidergic circuits in regulation of arterial pressure, relevant to the neurogenetic mechanisms in developing EH.
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PMID:Role of limbic peptidergic circuits in regulation of arterial pressure, relevant to development of essential hypertension. 1679 Feb 74

Natriuretic peptides differentially modulate endocrine and behavioral stress responses in preclinical and human studies. While atrial natriuretic peptide inhibits the hypothalamic-pituitary-adrenocortical axis, C-type natriuretic peptide exerts stimulatory activity. In rodents, atrial natriuretic peptide reduces anxiety, whereas C-type natriuretic peptide has anxiogenic effects (mediated via corticotropin-releasing hormone). Patients with panic disorder show lower basal ANP plasma levels but a more pronounced release during experimentally induced panic attacks compared with controls. This could explain the absent pituitary-adrenocortical activation during panic anxiety and its paroxysmal nature. Furthermore, the effects of the panicogen cholecystokinin-tetrapeptide are attenuated by ANP pretreatment in panic patients, while C-type natriuretic peptide demonstrates anxiogenic action in healthy humans. Atrial natriuretic peptide agonists and C-type natriuretic peptide antagonists may have potential as a new class of antipanic and anxiolytic psychotherapeutic medication.
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PMID:Natriuretic peptides and panic disorder: therapeutic prospects. 1981 Sep 5

Recent studies have demonstrated a role for appetite- and volume-regulating neuropeptides in alcohol dependence, particularly in association with alcohol craving. The peptides leptin, ghrelin, adiponectin, vasopressin and the atrial natriuretic peptide (ANP) have been of particular interest because of their central effects on various brain circuits, including the hypothalamic-pituitary-adrenocortical (HPA) axis. In addition, pro-opiomelanocortin (POMC) plays an important role in linking appetite regulation with the HPA axis. Recent research has also demonstrated that the expression of these peptides in alcohol dependence is, at least partially, regulated by genetic and epigenetic mechanisms. These peptides and their associated circuits provide an intriguing new field for future pharmacological approaches for treating depression, anxiety and, potentially, addictive disorders such as alcohol dependence.
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PMID:Appetite- and volume-regulating neuropeptides: Role in treating alcohol dependence. 2087 12

Phagocytosis is an ancient cell function, which is similar at unicellular and multicellular levels. Unicells synthesize, store, and secrete multicellular (mammalian) hormones, which influence their phagocytosis. Amino acid hormones, such as histamine, serotonin, epinephrine, and melatonin stimulate phagocytosis, whereas peptide hormones, such as adrenocorticotropic hormone (ACTH), insulin, opioids, arginine vasopressin, and atrial natriuretic peptide decreased it, independently on their chemical structure or function in multicellulars. Macrophage phagocytosis of multicellulars is also stimulated by amino acid hormones, such as histamine, epinephrine, melatonin, and thyroid hormones, however, the effect of peptide hormones is not uniform: prolactin, insulin, glucagon, somatostatin, and leptin have positive effects, whereas ACTH, human chorionic gonadotropin, opioids, and ghrelin have negative ones. Steroid hormones, such as estrogen, hydrocortisone, and dexamethasone are stimulating macrophage phagocytosis, whereas progesterone, aldosterone, and testosterone are depressing it. Considering the data and observations there is not a specific phagocytosis hormone, or a hormonal regulation of phagocytosis neither unicellular, nor multicellular level, however, hormones having specific functions in multicellulars also influence phagocytosis at both levels universally (in unicellulars) or individually (in macrophages). Nevertheless, the hormonal influence cannot be neglected, as phagocytosis (as a function) is rather sensitive to minute dose of hormones and endocrine disruptors. The hormonal influence of phagocytosis by macrophages can be deduced to the events at unicellular level.
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PMID:Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review. 2885 1

The review discusses the hormonal changes during exercise stress. The exercise generally produces a rise of adrenaline (A), noradrenaline (NA), adrenocorticotropic hormone (ACTH), cortisol, glucagon, growth hormone, arginine vasopressine, etc., and a drop of insulin. The hormonal events during reestablishment of homeostasis due to exercise stress can be divided into a catabolic phase, with decreased tolerance of effort, and reversible biochemical, hormonal and immunological changes, and an anabolic phase, with a higher adaptive capacity, and enhanced performance. The two main hormonal axes activated in the catabolic phase are sympathetic-adrenal-medullary system and hypothalamic-pituitary-adrenal (HPA) axis, while in the anabolic phase, growth hormone-insulin-like factor I axis, and gonadal axes. The hormonal responses during exercise and recovery can be regarded as regulatory and integrated endocrine responses. The increase of catecholamines and ACTH is dependent on the intensity of exercise; a marked increase in plasma A occurs during exercises with high emotional content. The response of cortisol is correlated with the duration of exercise, while the effect of exercise duration on b-endorphin changes is highly dependent on the type of exercise performed. Cortisol and b-endorphin changes usually occur in phase, but not during exercises with high emotional content. Glucocorticoids and iodothyronines are involved in meeting immediate energy demands, and a model of functional interactions between HPA axis and hypothalamic-pituitary-thyroid axis during exercise stress is proposed. A modulation of coping responses to different energy demanding physical activities required for sport activities could be hypothesized. This review supports the proposed regulation of hypophysiotropic TRHergic neurons as metabolic integrators during exercise stress. Many hormonal systems (ghrelin, leptin, glucose, insulin, and cortisol) are activated to control substrate mobilizations and utilization. The cardiovascular homeostasis, the fluid and electrolyte balance during exercise are highly dependent on vasoactive hormones (antidiuretic hormone, atrial natriuretic peptide, renin-angiotensin-aldosterone, and prostaglandins) control.
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PMID:The different hormonal system during exercise stress coping in horses. 3263 78


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