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

Somatostatin (SRIF) and vasopressin (AVP) were measured in hypothalamic and extrahypothalamic areas in normotensive Wistar-Kyoto (WK) and in spontaneously hypertensive, adult rats (SRH) under control conditions and after acute immobilization stress. Hypothalamic areas included the median eminence (ME) and the periventricular, suprachiasmatic, paraventricular, supraoptic, ventromedial and dorsomedial nuclei. Extra-hypothalamic areas included the striae medullaris, striae terminalis (N. Interst.), locus coeruleus, central gray, Areas 1 and 2 (NTS), and circumventricular organs. Under basal conditions, SHR and WK rats did not differ in their content of SRIF and AVP for most areas examined. After acute stress, however, striking differences were found in peptide content. Somatostatin content was not changed in SHR, but was significantly decreased in most areas in WK rats. On the contrary, generalized increases in AVP content were found in SHR after stress, with no changes in WK animals. An exception was the ME, which showed a decrease in peptide levels in both groups of rats. These results suggest that both hypothalamic and extra-hypothalamic AVP and SRIF are involved in the central stress response. The different changes in peptide levels observed for SHR and normotensive rats after acute stress further support the hypothesis of a role of both AVP and SRIF in central regulation of cardiovascular function.
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PMID:Changes in brain somatostatin and vasopressin levels after stress in spontaneously hypertensive and Wistar-Kyoto rats. 610 6

In the present work we have investigated to what extent somatostatin (SRIF) release from median eminence (ME) is affected by stress immobilization (IMO) in unanesthetized rats stereotaxically implanted with a push-pull cannula (PPC). One week after implantation, the ME was perfused with artificial cerebrospinal fluid for 1 hour in basal, stress and recovery conditions respectively. Samples were collected every 15 min and SRIF was measured by RIA. In another group of animals, a jugular cannula was inserted the day before and plasma samples were taken off simultaneously with the ME perfusate for GH and SRIF analysis respectively. SRIF release from the ME is rapidly (15 min) and significantly increased (58 +/- 11 vs 28 +/- 5 pg/15 min; n = 7; P < 0.01) in rats bearing only PPC. Intriguingly, animals bearing a jugular catheter plus a PPC showed no increase in SRIF release during the first 15 min of IMO in spite of a striking decrease of plasma GH (27.2 +/- 3.8 vs 3.6 +/- 1.3 ng/ml; n = 6; P < 0.001) observed at this time. However, in spite that the animals responded with a significant increase in SRIF, the response was later and more reduced than in animals without jugular cannula. Since our two rat groups--as result of jugular cannula surgery 24 hours before--showed differences such as a food intake, body weight gain, plasma GH levels and basal SRIF release, we think that these differences could explain the modifications in the regulatory mechanisms involved in GH control under acute stress.
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PMID:Role of somatostatin in the acute immobilization stress-induced GH decrease in rat. 809 30

Corticotropin-releasing factor (CRF) is the hallmark brain peptide triggering the response to stress and mediates-in addition to the stimulation of the hypothalamus-pituitary-adrenal (HPA) axis-other hormonal, behavioral, autonomic and visceral components. Earlier reports indicate that somatostatin-28 injected intracerebroventricularly counteracts the acute stress-induced ACTH and catecholamine release. Mounting evidence now supports that activation of brain somatostatin signaling exerts a broader anti-stress effect by blunting the endocrine, autonomic, behavioral (with a focus on food intake) and visceral gastrointestinal motor responses through the involvement of distinct somatostatin receptor subtypes.
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PMID:Activation of Brain Somatostatin Signaling Suppresses CRF Receptor-Mediated Stress Response. 2848 31