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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two breeds of commercial broiler chicks were used to investigate possible breed differences and to determine the effect of methionine and lysine on arginine requirements. Graded levels of arginine were added to a glucose-casein diet with or without added methionine and to a corn-soybean meal diet with and without added lysine and/or methionine. The arginine requirement of chicks receiving the glucose-casein diet with and without supplemental methionine was found to be 1.46 per cent and 1.55 per cent of the diet, respectively. No breed differences were found. When arginine was added to a corn-soy diet containing 1.53 per cent arginine, with or without supplemental methionine, no response was obtained indicating that this level of arginine was adequate. When this diet was supplemented with lysine to bring it up to the lysine level of the casein diet, a growth depression occurred which was overcome by the addition of 0.20 and 0.25 per cent arginine, respectively, in the absence and presence of supplemental methione. These levels of arginine exceeded the requirements determined for chicks fed the glucose-casein diet. In chicks fed the glucose-casein diet, muscle creatine increased with each level of added arginine with or without supplemental methionine. Creatinine excretion also increased with each level of added arginine in the absence of supplementary methionine but when methionine was added creatine excretion reached a plateau at the level of arginine which satisfied the chick's growth requirement.
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PMID:The effect of methionine and lysine levels on the arginine requirement of the chick. 116 68

The arginine homologues 2-amino-3-guanidinopropionic acid, 2-amino-4-guanidino-butyric acid and 2-amino-6-guanidinocaproic acid (= homoarginine) were synthesized and transformed into their methyl esters. The latter, together with arginine methyl esters. The latter, together with arginine methyl ester, arginine diethylamide and some guanidino compounds without the arginyl structure (agmatine, isopentyl-guanidine and n-butylbiguanide) were examined with regard to their behaviour on isolated fat cells, concerning the adrenalin-induced depression of the ATP level and the stimulation of glucose oxidation. The homoarginyl and arginyl derivatives counteracted the effect of adrenalin by re-elevating the ATP level, and thus they exerted an insulin-like activity. The esters were slightly active, whereas the arginine diethylamide and agmatine had a marked effect. The shorter homologues of arginine were totally inactive. However isopentyl-guanidine and butylbiguanide followed the effect of adrenalin: they additionally lowered the ATP level and therefore they acted in opposition to insulin. For comparative reasons the same compounds were tested with regard to their effects on glucose oxidation. The results were consistent with those quoted above: the homoarginyl and arginyl derivatives (agmatine included) forced the glucose oxidation similarly to insulin, the shorter homologues were inactive, isopentylguanidine and butylbiguanide decreased it.
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PMID:Effects of arginine homologous and other guanidino compounds on the ATP level and glucose oxidation in isolated fat cells. 118 Dec 75

The present study indicates that: (a) local administration of low concentrations of an analog of vasopressin, 1-deamino-[2-phenylalanine, 8-arginine]-vasopressin (DPAVP), constricts venules in the rat splanchnic terminal vascular bed of normal animals, unlike that seen for catecholamines; (b) maximal concentrations of DPAVP narrow but do not occlude both arterioles and venules: (c) microscopic muscular venules (31-39 mu i.d.) do not narrow more than 20% in response to the vasopressin analog DPAVP; and (d) terminal arterioles (17-23 mu i.d.) do not narrow more than 50% in response to DPAVP. Systemic administration of DPAVP to rats subjected to hemorrhage or bowel ischemia shock more than doubles survival rates over control rats receiving Ringer solution. Infusion of DPAVP produces a dose-dependent effect on arterial blood pressure, microscopic capacitance vessels, large arterioles and small arteries. In addition, i.v. administration of DPAVP: (a) returns arterial hematocrit towards normal after shock; and (b) regenerates and sustains vasomotion and venular tone, decreases microvascular hyperreactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes towards normal, predisposes to a splanchnic microbed virtually free of stasis, petechiae and leukocytic sticking, and restores capillary perfusion and outflow to near-normal. Further, DPAVP effectively restores the early reticuloendothelial system (RES) phagocytic depression, characteristic of shock syndromes, to normal; the latter eventuating in RES hyper-phagocytic activity. These findings indicate it is possible to synthesize vasoactive molecules which: (a) exert selective microvascular and RES phagocytic effects; and (b) are highly beneficial in the therapy of low-flow states, at least in rats.
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PMID:DPAVP: a vasopressin analog with selective microvascular and RES actions for the treatment of circulatory shock in rats. 127 38

Among the multiple biological activities of nitric oxide (NO) an immunoregulatory role consisting of the mediation of macrophage suppressive activity, has recently been evidenced. In the present work, we investigated whether NO was implicated in immunosuppression following burn injury. Thermal injury affecting 20-25% of the total body surface area in Wistar rats, provoked a biphasic depression of spleen cell proliferative responses to phytohemagglutinin (PHA) and concanavalin A (Con A). We show that these responses are fully restored on day 4 after burn and only by 55% on day 10 when spleen cells were stimulated in the presence of NG-monomethyl-L-arginine (NMMA), a potent inhibitor of the macrophage inducible NO synthase. Nitrite content in culture supernatant, as an indicator of NO release (in the absence of NMMA), was significantly augmented in Con A-stimulated spleen cells from burned rats as compared to normal spleen cells. These results show for the first time that NO is implicated, at least in part, in an immunosuppression state which is not linked to an infectious disease.
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PMID:Nitric oxide mediates the depression of lymphoproliferative responses following burn injury in rats. 130 64

The authors have investigated the hypothesis that loss of endothelium-derived relaxing factor (EDRF) activity contributes to cerebral vasospasm after subarachnoid hemorrhage. Adventitial exposure to hemoglobin was studied angiographically by injecting purified hemoglobin solution or autologous whole blood into the cisterna magna of anesthetized pigs. Both interventions induced intra- but not extracerebral vasoconstriction, which persisted for 2 and 7 days, respectively. Cyclic guanosine monophosphate (cGMP) levels were measured in isolated buffer-perfused pig intrathecal arteries to quantify inhibition of basal EDRF activity by hemoglobin. Adventitial exposure was less effective than intimal exposure, 10 microM hemoglobin applied adventitially for 30 minutes having an effect equivalent to that of 1 microM applied intraluminally for 5 minutes. The depression of cGMP levels by hemoglobin was reversible and equivalent to the effect of endothelial denudation or incubation with NG-nitro-L-arginine methyl ester, so that the effects of hemoglobin can be attributed to a specific action on EDRF rather than interaction with a nitric oxide-like substance produced by vascular smooth muscle or adventitial nerves. Cyclic GMP levels in isolated arteries were unchanged after in vivo exposure to hemoglobin for either 2 or 7 days or to whole blood for 2 days, and were reduced by intraluminal perfusion with 1 microM hemoglobin. In contrast, after 7 days of in vivo exposure to whole blood, cGMP levels were already depressed, and not further reduced by intraluminal perfusion with 1 microM hemoglobin. The findings support the view that adventitially applied hemoglobin can inhibit basal EDRF activity and that in vivo adventitial exposure to whole blood leads to a reduction in basal cGMP levels in association with vasoconstriction of intrathecal arteries. Both mechanisms could contribute to the clinical syndrome of cerebral vasospasm after subarachnoid hemorrhage.
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PMID:The effect of chronic subarachnoid hemorrhage on basal endothelium-derived relaxing factor activity in intrathecal cerebral arteries. 131 93

ProELH is the prohormone to the bag cell egg-laying peptide of Aplysia. In addition to containing the structure of the hormone (ELH) itself, proELH also contains several other secreted peptides: AP (acidic peptide) and alpha-, beta-, and gamma-bag cell peptides (BCPs). The BCPs, ranging in length from 5 to 9 amino acids, are structurally similar in that they all contain the sequence Arg-Leu-Arg-Phe. An additional peptide from the atrial gland, Atrial A, also contains this sequence. The BCPs previously have been reported to have direct feedback (autocrine) effects on the bag cells, including electrophysiological excitation and inhibition. Moreover, some of these effects are temperature-dependent. The autocrine functions of these peptides were explored here by investigating their effects on bag cell cAMP levels. In addition, we monitored the effects of Atrial A, as well as ELH and AP, which are proELH products that do not have sequence homology with the BCPs. While ELH and AP have no effect on bag cell cAMP levels, the other peptides fall into two functional classes. alpha- and gamma-BCP produce an elevation of cAMP levels at 20 degrees and a depression at 15 degrees C. The elevation in cAMP is sensitive to low Ca2+/high Mg2+. beta-BCP and Atrial A elevate cAMP levels independently of temperature, and are insensitive to low Ca2+/high Mg2+. Our results suggest that there may be multiple bag cell receptors for these peptides with the Arg-Leu-Arg-Phe sequence representing a receptor-recognition motif.
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PMID:ProELH-related peptides: influence on bag cell cAMP levels. 133 78

NG-Methyl-L-arginine (NMA), an inhibitor of nitric oxide synthesis by vascular endothelium, depresses cardiac function and causes systemic vasoconstriction in vivo. The mechanism of cardiac depression is unclear. Since cGMP inhibits one isoform of myocardial phosphodiesterase (PDE), we hypothesized that a decrease in cGMP might increase PDE activity and lower myocardial cAMP levels, resulting in decreased contractility. Experiments were conducted in isolated, paced, Langendorff-perfused (constant flow) rat hearts under control or isoproterenol-stimulated conditions. In non-stimulated hearts, a 15 min infusion of 30 microM NMA had no effect on cAMP content or on left ventricular dP/dt; however, myocardial cGMP content was decreased. Infusion of 0.01 microM isoproterenol caused dP/dt to increase and caused coronary resistance to fall; myocardial cAMP levels increased while cGMP remained unchanged by isoproterenol. In this stimulated condition, infusion of 30 microM NMA decreased dP/dt and myocardial cGMP and cAMP concentrations. NMA caused coronary resistance to increase to similar maximal values in isoproterenol-stimulated and non-stimulated hearts. Although coronary flow was kept constant during NMA administration, NMA depressed cardiac contractility in isoproterenol-stimulated hearts, but not in non-stimulated hearts, and the depressed contractility in isoproterenol-treated hearts was associated with a decrease in myocardial content of cGMP and cAMP. Therefore, these results are consistent with the hypothesis that NMA may decrease myocardial contractility by decreasing cGMP which leads to increased PDE activity and decreased cAMP.
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PMID:NG-methyl-L-arginine decreases contractility, cGMP and cAMP in isoproterenol-stimulated rat hearts in vitro. 133 73

Experiments were performed to investigate whether balloon injury induces nitric oxide synthase activity in the blood vessel wall. Contractions to phenylephrine were compared in left carotid arteries of the rat, previously injured by balloon catheterization and excised either immediately (t = 0), 6, or 24 hours after the procedure, with those in control right carotid arteries (with and without endothelium). Phenylephrine evoked comparable concentration-dependent contractions in balloon-injured (t = 0) and control carotid arteries without endothelium, whereas those in control arteries with endothelium were depressed. In the balloon-injured carotid arteries (6 and 24 hours), the concentration-contraction curves to phenylephrine were shifted to the right compared with those observed in balloon-injured arteries (t = 0). In balloon-injured carotid arteries (6 hours), the hyporeactivity to phenylephrine was enhanced by superoxide dismutase. In balloon-injured carotid arteries (24 hours), nitro-L-arginine and methylene blue restored full contractions, whereas superoxide dismutase potentiated the hyporesponsiveness to phenylephrine. The depressed contractions were associated with a concomitant increase in the basal level of cGMP; this production was abolished by nitro-L-arginine. The depression of the concentration-contraction curves to phenylephrine and the increase of the tissue level of cGMP induced by interleukin-1 beta (4 hours) were more pronounced in balloon-injured arteries (24 hours) than in control arteries without endothelium. The effects of interleukin-1 beta were inhibited by nitro-L-arginine. These observations indicate that in vivo endothelial injury of the rat carotid arteries induces the production of nitric oxide from L-arginine in the blood vessel wall, an effect which is potentiated by interleukin-1 beta.
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PMID:Balloon injury and interleukin-1 beta induce nitric oxide synthase activity in rat carotid arteries. 137 60

The most fundamental aspect of the cerebral circulation is the well-described coupling of cerebral metabolic activity and cerebral blood flow. A number of substances have been proposed to link flow and metabolism, including K+, pH and adenosine. In the alpha-chloralose anaesthetised cat we studied simultaneously cerebral neuronal activity and local blood flow to attempt to dissociate the two and thus determine the coupling substance. Neuronal activity was determined by monitoring unit firing in the parietal cortex with tungsten in glass microelectrodes while local cerebral blood flow in the same area was monitored continuously using laser Doppler flowmetry. To initiate an increase in metabolic activity and, pari passu, blood flow spreading depression was elicited by needle stick injury. Spreading depression when initiated causes a wave of depolarization, measured as an increased firing rate and associated marked (400 +/- 95%) increase in local cerebral blood flow. Intravenous administration of NG-nitro-L-arginine methyl ester (1-NAME), a potent nitric oxide synthase inhibitor, produced a complete blockade of the hyperemia associated with spreading depression but no change in either resting cell firing or spreading depression-evoked increases in firing rate. These data demonstrate at least for spreading depression-elicited increases in metabolic activity, that nitric oxide (NO) is a key coupling compound that links changes in cerebral blood flow and metabolism. These data imply that NO may have a more general role in flow/metabolism coupling and further studies in other situations are required to determine the extent to which NO is responsible for this fundamental cerebrovascular phenomenon.
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PMID:Nitric oxide synthesis couples cerebral blood flow and metabolism. 146 53

We investigated whether increased nitric oxide (NO) synthase activity within cardiac myocytes contributes to the depressed cardiac contractility observed in endotoxic shock. Isolated ventricular myocytes were studied to examine the effects of substrates and inhibitors of NO synthase on myocyte contractility. When stimulated electrically, the resting length of myocytes from control animals shortened by 5.3 +/- 0.3% (means +/- SE, n = 32). Baseline contraction of myocytes from endotoxin-treated animals was reduced to 3.0 +/- 0.3% (n = 17, P < 0.001). The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) had no effect on myocytes from control animals, but it increased the contraction of myocytes from endotoxin-treated animals by 40% (fractional shortening increased to 4.3 +/- 0.4%, P < 0.01). Similar results were obtained with NG-methyl-L-arginine. The effect of L-NAME could be reversed by excess L-arginine, but not D-arginine. The effect of endotoxin was abolished by dexamethasone pretreatment. Methylene blue also reversed the effects of endotoxin but had toxic effects on myocytes. Agents that either prevent synthesis or the effects of NO reverse the depression of myocyte contraction seen following endotoxin treatment.
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PMID:Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia. 148 19


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