Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral, radiofrequency destruction of the hypothalamic paraventricular nucleus resulted in a pronounced depression in levels of immunoreactive (ir-) vasopressin (VP) in the medulla-pons of rats. The contents of ir-dynorphin1-17 (DYN), ir-DYN1-8 and ir-alpha-neo-endorphin (alpha-NE) therein were not, in contrast, affected. Exposure of naive rats to acute foot-shock stress was associated with an elevation in levels of ir-VP in the medulla-pons whereas those of ir-DYN, ir-DYN1-8 and ir-alpha-NE were not significantly altered. The data indicate that the paraventricular nucleus is a major source of ir-VP but not of ir-DYN, ir-DYN1-8 or ir-alpha-NE in the medulla-pons, and that these pools of ir-VP, in contrast to those of ir-DYN, ir-DYN1-8 and ir-alpha-NE, are involved in the response to stress. It is concluded that ir-DYN, ir-DYN1-8 and ir-alpha-NE exist in (a) neuronal network(s) independent of that of ir-VP in the medulla-pons of the rat.
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PMID:Independent origin and modulation of vasopressin as compared to dynorphin and alpha-neo-endorphin in the medulla-pons of the rat. 613 80

Vasopressin or alpha-adrenergic agents such as phenylephrine or adrenaline, but not glucagon, elicited an initial decrease in flux through pyruvate dehydrogenase assayed by 14CO2 production from [1-14C]pyruvate in perfused rat liver. This rapid decrease in 14CO2 production was maximal within 1-2 min of exposure, concomitant with a rise in effluent pyruvate concentration: a subsequent return towards initial values in both parameters was completed well before 5 min. This time course was superposed with Ca2+ efflux from perfused liver, maximal (at 116 nmol/min per g wet wt. of liver) at 1-2 min of exposure. The percentage of the active (dephospho) form of pyruvate dehydrogenase was not decreased at 2 min of exposure. The effect on flux through pyruvate dehydrogenase by phenylephrine was abolished by prazosine, phentolamine or phenoxybenzamine. Ionophore A23187 also caused a depression in 14CO2 production from [1-14C]pyruvate and a rise in effluent pyruvate concentration, but this effect was stable for longer times, and it was delayed when Ca2+ was omitted from the perfusion medium. Responses of phenylephrine and A23187 were not additive. The results demonstrate that under the experimental conditions employed in intact perfused liver, the mitochondrial multienzyme system of pyruvate dehydrogenase is sensitive to vasopressin, alpha-adrenergic agents and A23187. The similar time course in Ca2+ efflux may be indicative of the involvement of Ca2+ in mediating this effect.
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PMID:Decreased flux through pyruvate dehydrogenase during calcium ion movements induced by vasopressin, alpha-adrenergic agonists and the ionophore A23187 in perfused rat liver. 613 70

The effects of the calcium entry blockers nifedipine, (-)-verapamil and the dihydropyridine derivative PY 108-068 were evaluated on the increase in diastolic pressure of pithed normotensive rats caused by the selective alpha 1-adrenoceptor agonists cirazoline, (-)-phenylephrine, (+/-)-erythro-methoxamine, (-)-amidephrine and St 587 [(2-chloro-5-trifluoromethylphenylimino)-2-imidazolidine] as well as by the mixed alpha 1/alpha 2-adrenoceptor agonists clonidine and DPI [(3,4-dihydroxyphenylimino)-2-imidazolidine]. The calcium entry inhibitors (up to 3 mg/kg) caused 3- to 5-fold, parallel rightward shifts of the log dose-pressor effect curves to cirazoline, (-)-phenylephrine, (+/-)-erythro-methoxamine and (-)-amidephrine accompanied by only a slight depression of the maximal pressor response. In contrast, the calcium entry inhibitors produced a dose-dependent profound depression of both maximum and slope of the log dose-pressor response curves to St 587 and clonidine. For DPI about 10- and 100-fold parallel displacements to the right without reduction of the maximum were found following treatment with 1 and 3 mg/kg of nifedipine, respectively. Infusion of vasopressin to counteract the vasodilatory action produced by the calcium entry inhibitors did not significantly change the pattern of interference observed under the conditions of decreased baseline diastolic pressure. The results indicate that alpha 1-adrenoceptor-mediated vasoconstriction in the pithed normotensive rat, which is characterized by its sensitivity to blockade by prazosin and its relative insensitivity to antagonism by yohimbine or rauwolscine, can be subdivided into two distinct processes which are differentially influenced by blockade of calcium entry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effect of calcium entry blockers on alpha 1-adrenoceptor-mediated vasoconstriction in vivo. 614 29

The present study examines the relationship of the hypothalamic paraventricular nucleus (PVN) to discrete brain and pituitary pools of immunoreactive (ir) vasopressin (VP), oxytocin (OT) and particular opioid peptides in the rat. Selective, bilateral destruction of the PVN resulted in a parallel depression in levels of ir-VP, ir-OT, ir-dynorphin (DYN), ir-DYN and ir-alpha-neo-endorphin (alpha-NE) in the neurointermediate lobe of the pituitary, whereas in its anterior counter-part no decrease in the content of any of these peptides was seen. In contrast, the content of ir-beta-endorphin (beta-EP) in the neurointermediate lobe was not significantly altered. Further, a rise in levels of ir-beta-EP in the anterior lobe, together with a fall in these in systemic plasma, was found. In the hypothalamus, in distinction to ir-met-enkephalin (ME), a diminution in the content of ir-VP, ir-OT, ir-DYN, ir-DYN, ir-alpha-NE and, in addition, ir-beta-EP was observed. In the septum, midbrain and medulla/pons, however, a selective depression in levels of ir-VP (and, as measured in the medulla/pons, of ir-OT) was seen: the content of ir-DYN, ir-DYN, ir-alpha-NE, ir-beta-EP and ir-ME was unchanged in these tissues. These data indicate that: (1) the PVN is an important contributor to neurointermediate lobe, but not anterior lobe, pools of ir-VP, ir-OT, ir-DYN, ir-DYN and ir-alpha-NE in contrast to ir-beta-EP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hypothalamic paraventricular nucleus: relationship to brain and pituitary pools of vasopressin and oxytocin as compared to dynorphin, beta-endorphin and related opioid peptides in the rat. 614 57

The present study examines the influences of selective destruction of the locus coeruleus (LC) or of the ventral noradrenergic bundle (VB) upon discrete CNS and pituitary pools of vasopressin, dynorphin and related opioid peptides in the rat. The selectivity of the lesions was indicated by the fact that destruction of the LC strongly depressed levels of noradrenaline in the cortex in contrast to the hypothalamus, whereas destruction of the VB decreased noradrenaline in hypothalamus but not cortex. Rats sustaining VB lesions displayed a parallel depletion in neurointermediate, but not anterior, lobe levels of immunoreactive-(ir-dynorphin (DYN), ir-DYN, ir-alpha-neo-endorphin (ir-alpha-NE) and ir-vasopressin (ir-VP) whereas those of ir-Met-enkephalin (ir-ME) were unaffected. In the hypothalamus, the content of ir-DYN and ir-VP tended to rise and that of ir-DYN and ir-alpha-NE was significantly elevated, whereas that of ir-ME was not altered. LC destruction failed, in contrast, to modify levels of ir-VP, ir-DYN, ir-DYN, ir-alpha-NE or ir-ME in any of the above structures. It was found to, however, result in a depression in levels of ir-DYN and ir-alpha-NE, but not of ir-ME or ir-VP, in both the hippocampus and striatum whereas VB lesions were, in this respect, ineffective. Further, in the spinal cord, LC lesions resulted in a significant elevation in levels of ir-DYN and ir-alpha-NE in comparison to those of ir-DYN, ir-VP and ir-ME. Neither type of lesion significantly altered the content of any opioid peptide examined in thalamus, cortex, septum or midbrain. These data indicate that: the LC as compared to the VB interact differently with discrete pools of ir-DYN, ir-DYN, ir-alpha-NE and ir-VP in brain, pituitary and spinal cord; it is the VB rather than the LC which modulates the activity of magnocellular neurones projecting to the neural lobe of the pituitary; ir-DYN, ir-DYN and ir-alpha-NE are, in all tissues, regulated independently of ir-ME; levels of ir-DYN, ir-DYN and ir-alpha-NE are co-regulated with those of ir-VP in the hypothalamus-neural lobe axis but not in extrahypothalamic brain tissues nor the spinal cord; and DYN, DYN and alpha-NE might, in certain cases, be modulated differentially of one another, possibly reflecting alterations in precursor processing.
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PMID:Contrasting interactions of the locus coeruleus as compared to the ventral noradrenergic bundle with CNS and pituitary pools of vasopressin, dynorphin and related opioid peptides in the rat. 614 61

To determine whether diabetes predisposes rats to hypertension, tail-cuff systolic pressures were measured in male rats made diabetic by pretreatment with streptozotocin. From Weeks 2 through 7, diabetic rats weighed less but had higher systolic pressures than nondiabetic ones. Further comparisons made while the rats were anesthetized with urethane showed that pressor and sympathetic nerve responses to ventromedial hypothalamic stimulation, as well as pressor responses to injected vasopressin, were significantly reduced in the diabetic group. A generalized reduction of cardiovascular reactivity was considered unlikely because systemic pressor responses to norepinephrine and tyramine were unimpaired. Yet reflex bradycardia elicited by norepinephrine was enhanced indicating that baroreceptor resetting had not occurred. Thus, diabetic rats were characterized by hypertension, narrowed pulse pressure, bradycardia with increased reflex responses to norepinephrine, and reduced pressor responses to hypothalamic stimulation and to vasopressin. The successful induction of diabetes was confirmed not only by the presence of hyperglycemia, hypoinsulinemia, glycosuria, and abnormal glucose tolerance, but also by reductions in pancreatic weight, insulin, and beta-cell content. Although our results suggest that diabetic rats are predisposed to become hypertensive, other mechanisms such as hypothalamic depression may be activated to restrict further elevations in blood pressure.
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PMID:Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness. 621 80

Tissue from histologically confirmed ACTH cell adenomas in Cushing's disease (CD) and Nelson's syndrome (NS) was gained by transsphenoidal surgery. Combined enzymatic and mechanic agitation of tumor tissue yielded a cell suspension. Aliquots of the cell suspension were transferred to superfusion chambers immediately after isolation and investigated for ACTH and beta-endorphin production. Feedback action of cortisol (CO) and dexamethasone on basal hormone production and on lysine vasopressin (LVP) induced ACTH secretion were studied. Adenomatous tissue and anterior lobe tissue from the same patient in CD could be investigated simultaneously in 4 cases. The paraadenomatous tissue showed depression of basal and LVP-induced ACTH secretion. In all adenomatous tissues investigated there was missing or reduced suppression of basal ACTH secretion by physiological levels of CO. CO not only failed to suppress LVP-induced ACTH secretion but also seemed to enhance LVP stimulation in some experiments. This study confirms former results, that a missing or inversed feedback action or glucocorticoids in adenoma cells is a mechanism involved in the pathological ACTH secretion in CD and NS. Bioassayable and immunoreactive ACTH from media of superfusion and short-term static incubation were compared with beta-endorphin and beta-LPH in an assay detecting these two peptides with equimolar sensitivity. Secretory patterns were basically parallel but great differences showed in quantities of hormones secreted. In addition, Sephadex G-50 gel chromatography was performed to separate beta-endorphin from beta-LPH and to calculate the ratios. These profiles show great variations between different adenomas.
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PMID:In vitro secretion of ACTH, beta-endorphin and beta-lipotropin in Cushing's disease and Nelson's syndrome. 626 13

The hormonal responses to insulin-induced hypoglycemia were studied in 15 abstinent alcoholics with varying degrees of central and peripheral nerve damage and in six normal controls. Blood samples were taken at intervals after the injection of soluble insulin (0.1 U/kg of body weight). Growth hormone responses were significantly depressed (p less than 0.05) in nine alcoholics with severe central nerve damage (Korsakoff's psychosis) as compared to other alcoholic subjects. The alcoholic subjects with Korsakoff's psychosis also showed significant depression (p less than 0.01) of glucose recovery from hypoglycemia as compared with controls. However, responses of vasopressin, cortisol, and catecholamines (epinephrine and norepinephrine) were generally normal in the Korsakoff patients. Our results do not support previous suggestions that impairment of memory in alcoholism may be related to altered vasopressin secretion, even though the reduced growth hormone secretion in brain-damaged alcoholics does indicate some hypothalamic-pituitary dysfunction.
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PMID:Growth hormone, vasopressin, cortisol, and catecholamine responses to insulin hypoglycemia in alcoholics. 637 19

The effect of humid heat (Ta = 43 degrees C, Pa = 32 Torr) on sweat rate, plasma renin activity and plasma levels of aldosterone and antidiuretic hormone (ADH) was studied in four male subjects before and after repeated heat exposures. Over-sweating and sweat drippage followed by hidromeiosis were observed in three subjects during initial heat exposure. With repeated humid heat exposures increased sweat rates were accompanied by a more intense sweat depression (hidromeiosis) in all four subjects. In our conditions, no changes in plasma levels of aldosterone and ADH or plasma renin activity were observed with hidromeiosis. Plasma renin activity was slightly depressed by repeated exposures, whereas plasma volumes were enhanced, with no significant changes in plasma Na or K. The results suggest that neither ADH nor the components of the renin-angiotensin aldosterone system are involved in the hidromeiotic phenomenon.
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PMID:Endocrine concomitants of sweating and sweat depression. 637 Jun 92

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
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PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79


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