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)

Chronic renal failure was induced in male Wistar rats with 5/6 nephrectomy (group I) and sham-operation was carried in the controls (group II). The results showed that in group I, plasma ANP levels increased progressively as Scr elevated. The plasma levels of renin and angiotensin raised simultaneously as compared with the controls (P < 0.001). At the 20th week after operation, urine volume and Na decreased significantly (P < 0.05) and the number of glomerular ANP receptors decreased significantly at the 12th week (P < 0.05) and 20th week (P < 0.01). Our data suggest that in 5/6 nephrectomized rats: 1. The elevation of plasma ANP level might be partly caused by damage of glomerular receptors. 2. The elevated plasma ANP could not cause its diuretic, natriuretic, blood pressure depression and R-A inhibition effect due to the damage of kidney ANP receptors.
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PMID:[The relationship between plasma atrial natriuretic peptide (ANP) and glomerular ANP receptors in 5/6 nephrectomized rats]. 130 71

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

The purpose of this study is to determine whether the administration of the ACE inhibitor cilazapril can lessen the adverse effects of ventricular remodeling, including systolic and diastolic dysfunction, modulation of fetal gene expression, increase of collagen genes, and depression of the sarcoplasmic reticulum (SR) Ca2+ ATPase gene in a myocardial infarcted (MI) rat model. At 1 day after MI, the animals were randomly assigned to cilazapril treatment or no treatment. We performed Doppler-echocardiographic examinations and measured cardiac mRNA in rats at 1 month and 3 months after MI (each group n = 8). The weights of the right (RV) and left ventricles (LV) in 1- and 3-month MI rats were significantly larger than those of the control rats. Cilazapril significantly prevented the increase. The MI rats showed systolic dysfunction, as evidenced by decreased fractional shortening (control, 34 +/- 3% vs. MI, 17 +/- 3%; P < 0.01) and ejection fraction measured by the modified Simpson's method (control, 61 +/- 2% vs. MI, 36 +/- 3%; P < 0.01) in rats at 1 month after operation. MI rats showed diastolic dysfunction, defined as increased peak early filling velocity, increased deceleration rate of the early filling wave, decreased late filling velocity, and an increase in the ratio of early filling to late filling velocity. Cilazapril significantly prevented systolic and diastolic dysfunction in rats after MI. The increases in beta-MHC, alpha-skeletal actin, ANP, and collagen I and III mRNAs in the nonischemic LV and RV were significantly suppressed by treatment with cilazapril. Depressed SR Ca(2+)-ATPase mRNA (nonischemic LV, 0.7-fold, P < 0.05 vs. control; RV, 0.5-fold, P < 0.05 vs. control) at 3 months after MI was significantly restored to normal levels by cilazapril. Cilazapril improved the adverse remodeling process by attenuating the progression of systolic and diastolic dysfunction, and prevented abnormal cardiac gene expression following MI.
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PMID:Effect of cilazapril on ventricular remodeling assessed by Doppler-echocardiographic assessment and cardiac gene expression. 960 33

Membrane metalloendopeptidase EC 3.4.24.11 (Enkephalinase, neutral endopeptidase, NEP) is a cellular ectoenzyme, immunophenotypically identified as the leukocyte cluster of differentiation CD10 or CALLA (common acute lymphoblastic leukemia antigen). Immunological, biochemical and molecular biology techniques have identified tis cell membrane feature in various organs: brain, cardiovascular system, lung, placenta, kidney etc. The CD10 immunophenotype is a common feature of lymphoblasts in acute lymphoid leukemia not expressing the T- or B-markers. The enzymatic activity of CD10/NEP possibly influences normal lymphocyte ontogeny by proteolytic cleavage of the regulatory peptides. The substrates of CD10/NEP in the kidneys are (see the list of abbreviations) ANP, adrenomedullin and PAMP; in the brain, the substrates are enkephalins and oxytocin; in the lung, bombesin, BLP, GRP, neuromedin C, substance P and neurokinin A; in the cardiovascular system, angiotenisin II, bradykinin and CGRP; in the gut, VIP; on the neutrophil membrane, fMLP etc. Some substrates are not strictly tissue-specific, e.g. substance P. Preclinical and clinical trials explore possibilities of therapeutic application of the inhibitors of neutral endopeptidase, such as thiorphan in the management of pain, diarrhoea, depression, arterial hypertension and asthma. Other possibilities of application include the treatment of hyalinomembranous disease and prevention of neurotoxicosis in tetanus and botulism.
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PMID:[Membrane metalloendopeptidase (CD10/CALLA): distribution, physiologic and pathophysiologic functions and its inhibitors]. 974 92

We investigated whether plasma brain and atrial natriuretic peptide (BNP and ANP, respectively) levels could reflect left ventricular (LV) geometry and function in patients with mild to moderate essential hypertension. A positive correlation was found between LV mass index (LVMI) and plasma ANP levels in 84 untreated, hypertensive patients, but not between LVMI and plasma BNP levels. As compared with other geometric patterns, plasma BNP levels were increased in concentric hypertrophy, in which LVMI was increased and LV diastolic function was decreased. These data suggest that production of BNP was increased in hypertensive patients with concentric hypertrophy via LV overload or depression of diastolic function.
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PMID:Relation of plasma brain and atrial natriuretic peptides to left ventricular geometric patterns in essential hypertension. 1050 51

We performed an experiment within the project "RLF" (Russian long-term flight) on a cosmonaut onboard the space station MIR. For creating an analogue to orthostatic stress, we used lower body negative pressure (LBNP) as stimulus. Decrease in central and peripheral baroreceptor load by LBNP can be used as a cardiovascular countermeasure in cosmonauts or for inducing endocrine responses. Altered steady-state plasma concentration values of volume sensitive hormones have been observed inflight as well as postflight. Within this project we measured plasma ANP and cGMP as second messenger. Changes in plasma cGMP concentration are generally considered to be a good indicator of those in ANP activity. However, in our experiments depression of cGMP during space flight was more impressive than ANP decline. We are not aware of previous measurements of plasma cGMP under these conditions, and believe to be the first to report complete suppression of plasma cGMP during long-term stay in space.
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PMID:Diminished plasma cGMP during weightlessness. 1154 85

Cortical spreading depression (CSD) is characterised by slowly propagating waves of cellular depolarization and depression and involves transient changes in blood flow, ion balance and metabolism. In cerebral ischaemia, peri-infarct CSD-like depolarization potentiates infarct growth, whereas preconditioning with a CSD episode protects against subsequent ischaemic insult. Thus, many of the long-lasting molecular changes that occur in CSD-affected tissue are presumed to be part of a 'neuroprotective cascade.' 3',5'-Cyclic guanosine monophosphate (cGMP) has been shown to be a neuroprotective mediator and the nitric oxide system, which increases cGMP production by soluble guanylate cyclase, is up-regulated by CSD. Atrial and C-type natriuretic peptide (ANP/CNP) are present in cerebral cortex and their actions are mediated via particulate guanylate cyclase receptors and cGMP production. Therefore, in further efforts to characterise the role of cGMP-related systems in CSD and neuroprotection, this study investigated possible changes in cortical natriuretic peptide expression following acute, unilateral CSD in rats. Using in situ hybridisation, significant 20-80% increases in ANP mRNA were detected in layers II and VI of ipsilateral cortex at 6 h and 1-14 days after CSD. Ipsilateral cortical levels were again equivalent to control contralateral values after 28 days. Assessment of cortical concentrations of ANP immunoreactivity by radioimmunoassay revealed a significant 57% increase at 7 days after CSD. Despite using a sensitive signal-amplification protocol, authentic ANP-like immunostaining was readily detected in subcortical nerve fibres, but was not reliably detected in normal or CSD-affected neocortex, suggesting the presence of very low levels, and/or active or differential processing of the peptide. Cortical CNP mRNA levels are not altered by CSD, indicating the specificity of the observed effects.Overall, these novel findings demonstrate a prolonged increase in cortical ANP expression after an acute episode of CSD. The overlap between the described time course of CSD-induced protection against ischaemic insult and demonstrated increases in ANP levels, suggest that ANP (like nitric oxide) may contribute to CSD-induced neuroprotection, via effects on cGMP production and other signal-transduction pathways.
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PMID:Atrial natriuretic peptide expression is increased in rat cerebral cortex following spreading depression: possible contribution to sd-induced neuroprotection. 1271 Sep 79

Cyclic GMP (cGMP) is synthesized by guanylyl cyclase (GC) in response to nitric oxide (NO) and carbon monoxide (CO) or natiuretic peptides (NPs); atrial, brain and C-type (ANP, BNP and CNP). cGMP is degraded by several cGMP-specific phosphodiesterases (PDEs). Guanylate cyclases (GC) are differentiated into: membrane-bound/particulate (pGC) and cytosolic/soluble (sGC). In recent years evidence has accumulated that NO is the main activator of sGC and NO/cGMP plays important role in glutaminergic, cholinergic and dopaminergic signaling pathways. cGMP in the nervous system is involved in long term potentiation and depression (LTP, LTD) suggesting its participation in learning and memory mechanism. cGMP regulates calcium homeostasis and phototransduction. Its level is regulated by PDEs and their specific inhibitors protect cGMP level in cells and are very important from clinical point of view.
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PMID:Cyclic GMP metabolism and its role in brain physiology. 1607 88

Altered pituitary-thyroid (PT) function (TSH, FT4, FT3 plasma levels) was correlated with symptoms of Eating Disorders (ED) in 137 patients (65 ANR, 12 ANP, 19 ANBP, 26 BN, 8 EDNOS-AN, 7 EDNOS-BN) and 30 controls. PT hormone concentrations were assessed by immunofluorimetry and psychopathology by EDI-2 and HSCL-90. Values of TSH were decreased in ANP, BN, EDNOS-AN, of T4 in ANR, ANP, AN-BP, of T3 in ANR, ANP, ANBP, BN, EDNOS-AN, EDNOS-BN. TSH values correlated negatively with ineffectiveness in BN and EDNOS-AN, and with depression in EDNOS-AN. FT4 values correlated positively with perfectionism in ANR, ANP and ANBP, with interoceptive awareness in EDNOS-AN, and negatively with depression in EDNOS-AN and with body dissatisfaction in EDNOS-BN. FT3 values correlated positively with perfectionism in ANBP and BN, with ineffectiveness in ANR and ANP, with depression in EDNOS-AN, with hostility in ANR and EDNOS-BN, with interpersonal sensibility in ANP, with somatization in EDNOS-BN, and negatively with interpersonal distrust in EDNOS-AN. Prospective studies are needed to confirm whether or not altered PT parameters correlate with ED symptoms during the course of the diseases.
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PMID:Disorders of eating behavior: correlation between hypothalamo-pituitary-thyroid function and psychopathological aspects. 1611 94

Our objective was to investigate the plasma levels of brain and atrial natriuretic peptides (BNP and ANP, respectively) in patients with septic shock/severe sepsis and to study the association of BNP and ANP levels with hemodynamic parameters, severity of the disease, and prognosis of those patients. This is a prospective case series study of 22 patients with septic shock, 11 patients with severe sepsis, and 20 healthy volunteers at the Department of Emergency and Critical Care Medicine, Nara Medical University Hospital, Japan. Blood collection was performed on admission and on days 1, 2, and 4. Plasma BNP and ANP levels were measured by radioimmunoassay. Right atrial pressure, mean pulmonary arterial pressure, pulmonary arterial wedge pressure, and left ventricular stroke work index were determined using a thermodilution catheter. Acute Physiological and Chronic Health Evaluation II scores were calculated. Plasma levels of BNP and ANP were markedly elevated in patients with septic shock/severe sepsis compared with controls (BNP, 7 +/- 0.3 pg mL; ANP, 13 +/- 1 pg mL). In patients with septic shock, both BNP and ANP peaked on day 2 (BNP, 987 +/- 160 pg mL; ANP, 103 +/- 17 pg mL). Plasma levels of BNP on day 2 in patients with septic shock significantly correlated with right atrial pressure (r = 0.744, P < 0.01), mean pulmonary arterial pressure (r = 0.670, P < 0.01), pulmonary arterial wedge pressure (r = 0.709, P < 0.01), left ventricular stroke work index (r = -0.552, P < 0.05), Acute Physiological and Chronic Health Evaluation II score (r = 0.581, P < 0.01), and poor prognosis (P < 0.05). The optimal cutoff point for predicting mortality in patients with septic shock was a BNP level of 650 pg mL on day 2, in which sensitivity and specificity were 92% and 80%, respectively. Increased plasma levels of BNP may reflect not only the severity of myocardial depression but also the disease severity and could be of prognostic value in patients with septic shock.
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PMID:Prognostic value of increased plasma levels of brain natriuretic peptide in patients with septic shock. 1687 20


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