Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to find out whether beta-endorphin (beta-E) is involved in the development of hypertension, we performed two series of experiments. Firstly, spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) were submitted to ether stress. Plasma concentrations of beta-endorphin-like immunoreactivity (beta-EI), adrenocorticotropin (ACTH) and alpha-melanotropin (alpha-MSH) were measured by radioimmunoassay. The basal concentration of beta-EI was similar in WKY and SHR, whereas WKY had higher levels of ACTH and lower levels of alpha-MSH than SHR. In both strains acute stress enhanced the plasma concentration of beta-EI to the same extent and with a similar time-course. The increase of plasma beta-EI coincided with a rise in ACTH but not alpha-MSH. Gel chromatography of beta-EI revealed that plasma extracts contain similar amounts of beta-lipotropin- (beta-LPH) and beta-E-sized immunoreactive components, and that acute stress elevated both forms of beta-EI. Secondly, isolated tail arteries of SHR and WKY were perfused and field stimulated with two pulses at 1 Hz. beta-E depressed stimulation-evoked vasoconstriction with the same potency in both strains. Thus, basal and stress-induced levels of beta-EI did not differ in SHR and WKY. Moreover, in the tail artery of both strains the sensitivity of presynaptic opioid receptors towards beta-E was almost identical. If the beta-E sensitivity of these receptors in other arteries of WKY and SHR is also similar a major role of the circulating peptide in the development of hypertension is rather unlikely.
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PMID:Plasma concentration and vascular effect of beta-endorphin in spontaneously hypertensive and Wistar Kyoto rats. 303 90

The opioid peptide methionine-enkephalin (Met-enkephalin) was measured in plasma and cerebrospinal fluid (CSF) of sheep in which the cisterna magna, carotid artery, and jugular vein were chronically cannulated. Venous blood plasma and CSF were collected before and after stress treatment and in control studies in conscious animals. Plasma and CSF were extracted with octadecylsilica and oxidized, and Met-enkephalin was measured as its Met-sulfoxide derivative by specific RIA. The molecular form of immunoreactive Met-enkephalin was characterized by peptide size exclusion chromatography of an octadecylsilica extract of sheep plasma through Bio-Gel P2, followed by reverse phase liquid chromatography, and was identical to Met-enkephalin and Met-sulfoxide-enkephalin. Insulin-induced hypoglycemia produced an elevation of plasma cortisol and an increase in the plasma concentration of Met-enkephalin. Acute hemorrhage led to an earlier and greater rise in plasma cortisol than that associated with insulin-induced hypoglycemia, but did not increase the concentration of Met-enkephalin in plasma. Neither form of acute stress increased the concentration of Met-enkephalin in CSF. These studies confirm that secretion of Met-enkephalin into blood can be dissociated from stimulation of the pituitary-adrenocortical system. They also show that circulating Met-enkephalin is elevated in conscious sheep during acute hypoglycemic stress, but plasma Met-enkephalin is unlikely to exert effects on the opiate receptors of periaqueductal or spinal nociceptive neurons under these conditions, since it does not enter cerebrospinal fluid in significant amounts.
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PMID:Immunoreactive methionine-enkephalin in cerebrospinal fluid and blood plasma during acute stress in conscious sheep. 327 39

Exercise or acute stress can exert significant effects on immune system as well as cardiovascular and respiratory systems through catecholamines. In this study, we investigated effects of norepinephrine (NE), a catecholamine neurotransmitter on human immunodeficiency virus type-1 (HIV-1) infection. NE inhibited in vitro HIV-1 infection of peripheral blood mononuclear cells (PBMC) from healthy donors and ex vivo HIV-1 replication in patients' PBMC. In transient expression assays, NE downregulated HIV-1 long terminal repeat, but site-directed mutagenesis on NF-kappaB-binding sites or cotreatment with H89 (a protein kinase A inhibitor) abrogated the NE-mediated effect. Gel-shift assays showed suppression of NF-kappaB activity in NE-treated cells. NE increased cytoplasmic levels of IkappaB-alpha, a natural inhibitor of NF-kappaB. Thus, NE apparently inhibits HIV-1 infection, at least in part through NF-kappaB inactivation.
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PMID:Norepinephrine inhibits human immunodeficiency virus type-1 infection through the NF-kappaB inactivation. 1627 22