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)

A yin-yang hypothesis is presented linking noradrenergic activity, thromboxane, melatonin, left hemisphere functioning, and cyclic AMP on the one hand, and dopamine, beta-endorphin, calcium, right hemisphere functioning, and cyclic GMP on the other. It is further suggested that there is a yoking of NA, TXA2, serotonin and melatonin in the left hemisphere, and a similar yoking of DA, BE, calcium and cGMP in the right. Evidence is presented to support the hypothesis that each element (NA, TXA2, etc.) on one side can modulate or balance a corresponding element (DA, BE, etc.) on the other. It is suggested that thromboxane is the key element in noradrenergic overactivity and that not taking this into consideration has confounded much prior research. This theory takes into account information processing models as well as pharmacological data and neurochemical theory on coupling of adenylate cyclase to its hormone receptors. Inhibiting noradrenergic overactivity can be obtained by inhibiting thromboxane and concomitantly activating opiate receptors. This protocol may have clinical utility in treating a wide range of disorders such as: anxiety, depression, schizophrenia, sleeplessness, withdrawal states, enuresis, Gilles de la Tourette syndrome, Parkinsonism, Alzheimers, dementia, anorexia, infant ruminations, essential tremor, spasticity of spinal cord injury, diarrhoea, ulcerative colitis, extrapyramidal symptoms, akathisia, neuroleptic malignant syndrome, attention deficit disorder, hyperhidrosis, and possibly AIDS.
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PMID:Inhibiting noradrenergic overactivity by inhibition of thromboxane and concomitant activation of opiate receptors via dietary means. 254 22

Arachidonic acid metabolites have been shown to modulate the secretion of various hormones, including luteinizing hormone, growth hormone and adrenocorticotropin. In this paper we describe the effect of a series of eicosanoids on hypothalamic secretion of corticotropin-releasing hormone (CRH) in vitro. Explanted rat hypothalami in culture were exposed to prostaglandins (PG) F2 alpha or E2, thromboxane (TX) B2, the TXA2 receptor agonist U-49,619 and leukotrienes (LT) B4, C4 and D4 at concentrations ranging from 10(-15) to 10(-5) M. PGE2, LTD4 and TXB2 did not alter hypothalamic CRH secretion. On the other hand, the remaining eicosanoids tested induced a significant increase of hypothalamic CRH secretion (p less than 0.05). The concentration of 10(-11) M dexamethasone inhibited the effect of stimulatory eicosanoids on CRH secretion. The CRH response to U-49,619 was completely prevented by the TXA2 receptor antagonist SQ-29,548. The latter also inhibited serotonin (5-HT)-, acetylcholine (ACh)- and PGF2 alpha-induced CRH release. Indomethacin was capable of blocking the secretion of CRH induced by 5-HT and ACh. In addition, PGE2 inhibited the increase of CRH secretion induced by PGF2 alpha, 5-HT and ACh. These findings suggest that eicosanoids may be involved in the regulation of hypothalamic CRH secretion, either as autocrine/paracrine or as endocrine factors.
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PMID:Arachidonic acid metabolites modulate rat hypothalamic corticotropin-releasing hormone secretion in vitro. 255 44

This study was performed to test the hypothesis that thromboxane A2 stimulates increases in fetal adrenocorticotropic hormone (ACTH), vasopressin, or renin secretion and affects fetal cardiovascular function by an action on the fetal central nervous system. We infused a stable synthetic analogue of thromboxane A2, U-46619, into one common carotid artery or inferior vena cava or infused saline into one common carotid artery in chronically catheterized fetal sheep between 127 and 140 days gestation. We found that intracarotid but not intravenous infusions of U-46619 at a rate of 750 ng/min stimulated increases in fetal plasma ACTH concentration. Infusions of U-46619 at both sites increased fetal blood pressure; the infusion into the carotid arterial blood produced a more rapid increase in blood pressure and a significant decrease in central venous pressure. None of the infusions altered plasma vasopressin concentration or plasma renin activity, blood gases, hematocrit, or plasma cortisol concentration. We conclude that thromboxane A2 stimulates fetal ACTH, but not vasopressin or renin, secretion via an action within the area perfused by carotid arterial blood. Thromboxane A2 increases blood pressure via an action at the fetal central nervous system, as well as via a direct vasoconstrictor action in the systemic circulation.
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PMID:Fetal ACTH and blood pressure responses to thromboxane mimetic U-46619. 823 57

Thromboxane A2 (TxA2), well known as a vasoconstrictor and activator of platelets, also stimulates reflex cardiovascular, pituitary, adrenocortical, and blood gas responses, although the site of action is unknown. Previously we determined that the site of these actions is perfused by the carotid vasculature. The purpose of the present study was to test the hypothesis that TxA2 stimulates these responses by acting at the carotid sinus. The TxA2 mimetic U46619 (1 microgram.kg-1.min-1) or saline was infused into the carotid artery (CA) or vena cava in conscious, chronically instrumented carotid sinus denervated (CSD) or sham-operated sheep. Mean arterial pressure increased in all groups receiving U46619. Heart rate increased only in the CSD group receiving CA infusions of U46619. Adrenocorticotropic hormone (ACTH) and cortisol increased in the sham and CSD groups receiving CA U46619, and responses were not different between sham and CSD groups. PaCO2 values were higher in all CSD treatment groups compared with sham treatment groups. Arterial pH increased and PaCO2 decreased in both the sham and CSD groups in response to CA U46619. Although PaCO2 values were higher overall in the CSD group, the magnitude of change in response to U46619 infusions was similar in sham and CSD animals. There was no difference in pHa between CSD and sham groups. Hematocrit and PaO2 did not change. We conclude that TxA2 does not act at the carotid sinus, as responses to U46619 infusions in CSD animals were not different in the cases of ACTH, cortisol, and blood gases, or were enhanced rather than diminished in the case of heart rate. These findings support a hypothesis that TxA2 acts at the brain to mediate cardiovascular, pituitary, adrenocortical, and blood gas responses.
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PMID:Thromboxane A2 does not act at the carotid sinus to mediate cardiovascular, adrenocorticotropin, cortisol, or blood gas responses. 963 49