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)

Glucocorticoids (GCs) are thought to regulate, in a permissive fashion, the basal activity of adrenal medullary phenylethanolamine N-methyltransferase (PNMT). However, it is unclear whether a large short-term increase in GC release, such as occurs during an acute stress response, may also play a role in PNMT regulation. The present study investigated how the GC influence over PNMT activity varies in relation to dynamic changes in the hormone-receptor signal. Using [3H]dexamethasone (DEX) and [3H]RU 28362 as radioligands, we have confirmed the presence of GC receptors in bovine adrenal medullary cells. A concentration-dependent decline in soluble GC receptor sites and an increase in nuclear uptake of [3H]DEX were found in response to GC levels as low as 5 x 10(-8) M. The loss of soluble sites plateaued between 5 x 10(-8) and 10(-6) M cortisol, with further losses occurring at 10(-5) and at 10(-4) M. The functional consequence of GC receptor binding was confirmed by measuring PNMT activity following 3-day exposure to cortisol. The pattern of PNMT induction was similar to that seen with GC receptor occupancy; at cortisol concentrations between 10(-8) and 10(-5) M, PNMT induction was at a plateau, with a further increase in activity at 10(-4) M. The increase in PNMT activity following 3-day exposure to low (10(-7) M) and high (5 x 10(-5), 10(-5) M) cortisol was blocked by the GC receptor antagonist RU 38486, suggesting a GC receptor-mediated event. Finally, a short (2 h) pulse of GC, which mimics the time course of physiological elevation of GC following acute stress, elevated adrenal medullary PNMT activity measured 3 days later. Therefore, our results provide novel evidence that short-term exposure of adrenal medullary cells to high cortisol levels can elevate PNMT activity.
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PMID:Adrenal phenylethanolamine N-methyltransferase induction in relation to glucocorticoid receptor dynamics: evidence that acute exposure to high cortisol levels is sufficient to induce the enzyme. 156 Feb 38

The present experiments were designed to test the hypothesis that adrenal epinephrine contributes to the development of hypertension in the Dahl salt-sensitive (DS) rat. All studies were carried out in conscious male DS and Dahl salt-resistant (DR) rats weighing 200-240 g. An indwelling femoral arterial catheter was placed for blood sampling and measurement of blood pressure. After 5 days of either a high salt (7% NaCI) or a normal salt (1% NaCl) dietary regimen, DS and DR rats were subjected to an acute stress paradigm (graded electrical footshock). There were no differences in basal plasma catecholamine concentrations or in the acute pressor responses to graded footshock between the four substrain/diet groups. However, in both DS and DR rats, plasma epinephrine responses to acute footshock were greater on a 7% than on a 1% NaCl diet. Additional groups of DS rats were treated with an inhibitor of adrenal phenylethanolamine N-methyltransferase, SK&F 29,661 (1-2 g/kg body wt/day) or with vehicle. Three days after placement of an arterial catheter, rats were placed on a 7% NaCl diet, and blood pressure was measured daily for an additional 3 weeks. Although SK&F 29,661 treatment was effective in reducing adrenal epinephrine content and apparent release by approximately 80%, treatment did not alter the time course of salt-induced changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of epinephrine in the development of hypertension in Dahl salt-sensitive rats. 239 87

The time course of regulation of rat adrenomedullary phenylethanolamine N-methyltransferase (PNMT) and tyrosine hydroxylase (TH) activity was studied after a single episode of 20-min restraint stress. Significant increases in PNMT and TH activity were observed 18 h after the beginning of the stress. The time course of acute stress-induced regulation of PNMT and TH was examined for the influence of neural and hormonal input. Unilateral denervation was performed, and the animals were exposed to a single episode of restraint. PNMT activity increased similarly in both the innervated and denervated adrenals, with a significant increase observed at 36 h after the stress. TH activity was similar in both denervated and innervated adrenals, with a significant increase observed at 24 and 36 h after stress. Finally, suppression of endogenous corticosterone with dexamethasone delayed the stress-induced increase in activity of PNMT but not TH. The present study indicates that increases in catecholamine biosynthetic enzymes can be observed after a single episode of mild, acute stress. In addition, glucocorticoids appear to be important in the time course of the stress-induced increase in PNMT but not TH activity, whereas neural input does not seem to affect the time course of these increases.
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PMID:Regulation of the adrenomedullary catecholaminergic system after mild, acute stress. 791 70