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)

Atrial natriuretic peptide (ANP), angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined in 12 healthy renal transplant donors before and 5, 12, 26, 54 days after uninephrectomy (Nx) in order to study the possible role of these hormones in functional adaptation to acute reduction in renal mass. Glomerular and tubular function was studied by measurements of the clearances of 51Cr-EDTA, lithium, sodium, potassium, and albumin. ANP was 7.4 +/- 3.1 pmol l-1 (mean +/- SD) before Nx and 8.7 +/- 6.1 pmol l-1 at 5 days after Nx and remained at this level through the observation period. Aldo showed a non-significant transient fall at 5 days after Nx. AII and AVP remained normal after Nx. At 5 days after Nx glomerular filtration rate (GFR) of the remaining kidney had risen from 45 +/- 7 ml min-1 before Nx to 57 +/- 8 ml min-1 (p less than 0.01), lithium clearance had risen from 13 +/- 2 ml min-1 before Nx to 20 +/- 7 ml min-1 (p less than 0.01), and sodium and water balance was normal. To conclude, plasma ANP, AII, Aldo and AVP do not appear to be responsible for the hyperfiltration and depression of fractional proximal sodium and water reabsorption observed in recently uninephrectomized man with normal sodium and water balance.
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PMID:Atrial natriuretic peptide and renal adaptation to contralateral nephrectomy in healthy man. 182 69

To evaluate the antiischemic effects of intravenous milrinone, 20 patients with angiographically proved coronary artery disease and stable angina were studied at rest and during exercise under control conditions and after an intravenous loading injection of milrinone (50 micrograms/kg/10 min) followed by an infusion with 0.5 micrograms/kg/min. Hemodynamic parameters, epinephrine, norepinephrine, and atrial natriuretic factor were assessed. Control ergometry revealed ischemia; however, during exercise with intravenous milrinone, ischemia was eliminated. Because of unloading effects, there was also a significant decrease in ST segment depression (p less than 0.001). Heart rate increased significantly (p less than 0.001) at rest but increased significantly less after exercise testing (p less than 0.001). The changes in mean arterial pressure, cardiac output, and myocardial oxygen consumption during exercise were not significantly different between the milrinone and control phase. Intravenous milrinone delayed the onset of angina (p less than 0.001) and significantly shortened the duration of anginal attacks (p less than 0.05); exercise duration in the milrinone phase was longer than in the control phase (p = 0.051). Because of vasodilatation, a mild secondary increase in norepinephrine was observed during the milrinone phase, and there was a significantly smaller increase in atrial natriuretic factor during exercise while receiving milrinone as a result of preload reduction (p less than 0.05). Intravenous milrinone produced beneficial hemodynamic and antiischemic effects in patients with coronary artery disease, stable angina, and reproducible ST segment depression probably by enhancing myocardial contractility and reducing preload and afterload.
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PMID:The use of intravenous milrinone in chronic symptomatic ischemic heart disease. 182 40

Atrial natriuretic factor (ANF) release is modulated by several haemodynamic factors, including ventricular and atrial wall stretch. Dipyridamole infusion, which is commonly used as a pharmacological stressor in patients with coronary artery disease, can acutely increase ventricular and atrial pressure via myocardial ischaemia. The aim of this study was to assess whether dipyridamole infusion (up to 0.84 mg kg-1 over 10') can affect ANF release in man. Nineteen patients (13 men, 6 women) with a history of chest pain were studied. Their drug regimen was interrupted and instead they were administered a dipyridamole infusion, combined with two-dimensional echocardiography and 12-lead ECG monitoring. Plasma ANF was measured by RIA while the patients rested, and after dipyridamole infusion. Eight patients had no evidence of myocardial ischaemia, as measured by electrocardiographic and/or echocardiographic criteria, during dipyridamole infusion: among them, ANF values were similar while they were at rest and at peak dipyridamole administration (23.9 +/- 9.5 vs 23.4 +/- 6.9 pg ml-1, P = ns). Eleven patients had dipyridamole-induced transient ischaemia (regional ventricular dyssynergy and/or ST segment depression): among them, ANF values rose significantly at peak dipyridamole administration (31.8 +/- 13.8 vs 65.5 +/- 36.4, P less than 0.01). We conclude that dipyridamole infusion does not increase ANF release in man in the absence of ischaemia. The induction of myocardial ischaemia acutely increases ANF release, probably through a rise in ventricular and atrial wall stress.
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PMID:Dipyridamole-induced myocardial ischaemia increases ANF release in man. 183 May 52

This study tests the hypothesis that atrial natriuretic factor (ANF) and C-ANF(4-23)-NH2 (C-ANF) augment cGMP generation and inhibit both cAMP generation and depolarization-induced catecholamine release in nerve growth factor treated pheochromocytoma cells by a pertussis toxin (PTX)-sensitive mechanism. Synthetic rat ANF(99-126) and the clearance receptor antagonist C-ANF (10(-12)-10(-9) M) inhibited basal and 5 microM vasoactive intestinal peptide (VIP)-induced cAMP generation in a concentration-dependent manner. These actions of ANF and C-ANF were blocked by 12-18 h pretreatment with PTX (100 ng/ml), suggesting ANF receptor coupling to adenylate cyclase via an inhibitory guanine nucleotide-binding protein. Both ANF (10(-11)-10(-9) M) and C-ANF (10(-11)-10(-8) M) also inhibited K(+)-induced catecholamine release in a concentration-dependent manner. ANF (10(-11)-10(-8) M) increased cGMP generation in a concentration-dependent manner but C-ANF did not. The accumulation of cGMP in response to ANF was not altered by treatment with PTX. Therefore, PTX dissociated the increased concentrations of cGMP from the ANF-mediated depression of evoked catecholamine release. C-ANF also dissociated elevations in cGMP concentrations from an ANF-mediated attenuation of evoked catecholamine release. The results of this study indicate that ANF inhibits adrenergic neurotransmission independent of guanylate cyclase.
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PMID:Neuromodulatory effects of atrial natriuretic factor are independent of guanylate cyclase in adrenergic neuronal pheochromocytoma cells. 197 29

The influence of positive end-expiratory pressure (PEEP) ventilation on plasma concentrations of atrial natriuretic factor (ANF) was studied in dogs anesthetized with sodium pentobarbital during normal cardiac function and during acutely impaired left ventricular function. Left ventricular impairment was induced by injecting repeated doses of polystyrene microspheres with a diameter of 50 microns into the main left coronary artery, causing a severe depression of left ventricular performance. This was accompanied by doubling of ANF concentrations measured in blood sampled from aorta. Application of PEEP (10 cmH2O (0.98 kPa] reduced plasma ANF in dogs both with normal and impaired left ventricular function. The decrease was significantly greater during left ventricular impairment compared to control, 31 and 19%, respectively. A positive correlation was observed between plasma ANF and transmural left ventricular end-diastolic pressure when all data were pooled, but not between ANF and transmural right atrial pressure. This implies that transmural left ventricular end-diastolic and hence transmural left atrial pressure probably is the principal determinant of acute ANF release in this model. Reduced plasma ANF in response to PEEP even during acute left ventricular impairment when ANF release was augmented, was probably due to diminished atrial distension during PEEP ventilation.
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PMID:Plasma concentrations of atrial natriuretic factor during positive end-expiratory pressure ventilation in dogs with normal or impaired left ventricular function. 253 Jul 46

Changes in arterial plasma levels of atrial natriuretic factor and catecholamine release were studied in 11 beagle dogs during pentobarbital anesthesia. Seven dogs were injected intravenously with Escherichia coli endotoxin, 0.5 mg/kg over 15 min. Four control dogs received only saline solution. The endotoxin injection resulted in cardiac depression,, hemoconcentration, acidosis and renal hypoperfusion. The central venous pressure remained relatively unchanged in both groups during the 2-hour study. The concentrations of epinephrine, norepinephrine and the norepinephrine metabolite 3,4-dihydroxyphenylglycol increased in arterial plasma during the acute hypodynamic endotoxin shock. In the control dogs the levels of these hormones remained very low and constant. Increased circulating levels of atrial natriuretic factor were observed in endotoxin shock with renal hypoperfusion, unchanged central venous pressure and no concomitant tachycardia.
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PMID:Plasma levels of atrial natriuretic factor and catecholamines in endotoxin shock in dogs. 253 42

The effects of cyclic nucleotide analogs and related agents on the Ca2+ dependent action potentials of cultured rat aortic smooth muscle cells (reaggregates) were examined. The action potentials were elicited by electrical stimulation in the presence of tetraethylammonium (TEA, 5-15 mM). Superfusion of the aortic cells with analogs of cyclic AMP (dibutyryl or 8-bromo-cyclic AMP, 1 mM), isoproterenol (1-10 microM) and forskolin (1-10 microM) depressed and abolished the TEA-induced action potentials. Abolition of the action potentials by these agents was reversible and was accompanied by some hyperpolarization of the membrane. Superfusion with 8-bromo-cyclic GMP (0.1-1 mM) also depressed or abolished the TEA-induced action potentials, whereas dibutyryl cyclic GMP (1 mM) and sodium nitroprusside (10 microM) had little effect. Synthetic atrial natriuretic factor (0.01-0.1 microM) had inhibitory effects in most experiments. Thus, depression of membrane excitability may be a contributing factor in the relaxation of aortic smooth muscle produced by some agents that increase intracellular levels of cyclic nucleotides.
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PMID:Cyclic nucleotides depress action potentials in cultured aortic smooth muscle cells. 283 Jan 20

Using the isolated spinal cord of the frog, hemisected and further divided into two distinct quadrants, we studied electrophysiological changes produced by peptides present in the atrial natriuretic factor (ANF) preprohormone. ANF and related peptides (atriopeptin I and atriopeptin III) did not affect the frog spinal cord. The 1-16 fragment from cardiodilatin (10(-5) M) induced slow depolarization in ventral and dorsal nerve stumps. The depolarization was associated with an increase of the evoked dorsal root potentials and depression of the fast component of the reflex responses. When depolarization approached its maximum value, spontaneous slow potentials appeared progressively similar to the evoked potentials, and became rhythmic until they reached a frequency of one potential every 15-20 seconds. The effects of cardiodilatin 1-16 are localized at dorsal horn level. It is suggested that this substance exerts a modulatory effect on frog cord physiology.
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PMID:Electrophysiological study of the effects of cardiodilatin 1-16 on the frog spinal cord in vitro. 297 9

We recently showed that patients with compensated cirrhosis can dispose of their fluid overload while reclining. In contrast, patients with ascites fail to develop supine-induced natriuresis. To assess the effect of reclining on renal sodium handling in patients with advanced cirrhosis and the mechanisms blunting natriuresis in this situation, renal function and plasma concentrations of atrial natriuretic factor, aldosterone and norepinephrine were evaluated in 10 nonazotemic patients with cirrhosis and ascites and 10 healthy controls standing for 2 h and reclining for 2 h. While standing, all patients showed marked sodium retention and significantly elevated plasma atrial natriuretic factor levels, aldosterone and norepinephrine. Glomerular filtration rate did not differ from healthy controls. The reclining increased renal sodium excretion in both groups, but this change was far less marked in patients; natriuresis only rose to the control range in two of them. An increase in atrial natriuretic factor and a depression of plasma aldosterone and norepinephrine was seen in both controls and patients. In the latter, despite the greater change in atrial natriuretic factor and aldosterone, the aldosterone to atrial natriuretic factor ratio, which was inversely correlated with natriuresis during both standing and reclining remained significantly elevated. In the two patients who achieved normal natriuresis during reclining, reclining was associated with both the normalization of the aldosterone/atrial natriuretic factor ratio, and with an increase in glomerular filtration rate. The supine-induced increase in atrial natriuretic factor was not only preserved but was even enhanced in cirrhosis with ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal sodium handling in cirrhosis with ascites: mechanisms of impaired natriuretic response to reclining. 769 37

To compare the hemodynamic, antiischemic, metabolic, and neurohumoral effects of intravenous esmolol (beta 1 blocking agent) and gallopamil (verapamil-like calcium channel blocker), 14 patients with angiographically proven CAD and reproducible ST segment depression were studied at rest and during exercise under control conditions and after an intravenous bolus injection of esmolol (0.5 mg/kg/1 min, followed by an infusion with 0.2 mg/kg/min) or gallopamil (0.025 mg/kg/3 min). In contrast to gallopamil, esmolol significantly reduced systolic blood pressure (175.7 vs. 160 mm Hg) and heart rate (107.4 vs. 96.9 min-1) during exercise as well as cardiac output (11.57 vs. 9.38 l/min) and significantly enhanced systemic vascular resistance both at rest (1241 vs. 1479 dynes.s.cm-5) and during exercise (805 vs. 947 dynes.s.cm-5). On the other hand, exercise filling pressures and lactate levels (3.66 vs. 3.05 mmol/l) were significantly reduced by gallopamil only. Thus, the significant improvement of exercise tolerance by both esmolol and gallopamil is based on different mechanisms of action: esmolol improves myocardial ischemia by appreciably reducing myocardial oxygen consumption, whereas gallopamil primarily improves oxygen supply and ventricular performance. Plasma catecholamines, atrial natriuretic factor, and aldosterone levels as well as plasma renin activity were identically influenced by esmolol and gallopamil, respectively. A reflex activation of the sympathetic system did not occur.
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PMID:[Anti-ischemia effects of gallopamil and esmolol in an intra-individual comparison in patients with coronary heart disease]. 791 67


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