atrial-natriuretic-factor has been researched along with ibopamine* in 3 studies
2 trial(s) available for atrial-natriuretic-factor and ibopamine
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Renal function, neurohormonal activation, and survival in patients with chronic heart failure.
Because renal function is affected by chronic heart failure (CHF) and it relates to both cardiovascular and hemodynamic properties, it should have additional prognostic value. We studied whether renal function is a predictor for mortality in advanced CHF, and we assessed its relative contribution compared with other established risk factors. In addition, we studied the relation between renal function and neurohormonal activation.. The study population consisted of 1906 patients with CHF who were enrolled in a recent survival trial (Second Prospective Randomized study of Ibopamine on Mortality and Efficacy). In a subgroup of 372 patients, plasma neurohormones were determined. The baseline glomerular filtration rate (GFR(c)) was calculated using the Cockroft Gault equation. GFR(c) was the most powerful predictor of mortality; it was followed by New York Heart Association functional class and the use of angiotensin-converting enzyme inhibitors. Patients in the lowest quartile of GFR(c) values (<44 mL/min) had almost 3 times the risk of mortality (relative risk, 2. 85; P<0.001) of patients in the highest quartile (>76 mL/min). Impaired left ventricular ejection fraction (LVEF) was only modestly predictive (P=0.053). GFR(c) was inversely related with N-terminal atrial natriuretic peptide (ANP; r=-0.53) and, to a lesser extent, with ANP itself (r=-0.35; both P<0.001).. Impaired renal function (GFR(c)) is a stronger predictor of mortality than impaired cardiac function (LVEF and New York Heart Association class) in advanced CHF, and it is associated with increased levels of N-terminal ANP. Moreover, impaired renal function was not related to LVEF, which suggests that factors other than reduced cardiac output are causally involved. Topics: Aged; Aldosterone; Atrial Natriuretic Factor; Cardiac Output; Cardiotonic Agents; Catecholamines; Chronic Disease; Deoxyepinephrine; Dopamine; Epinephrine; Female; Glomerular Filtration Rate; Heart Failure; Humans; Kidney; Male; Middle Aged; New York; Norepinephrine; Predictive Value of Tests; Prognosis; Prospective Studies; Protein Precursors; Renin; Renin-Angiotensin System; Survival Analysis; Ventricular Dysfunction, Left; Ventricular Function, Left | 2000 |
[Renal effects of ibopamine in comparison with furosemide in patients with mild heart failure].
Ibopamine is a novel oral dopamine analogue with positive inotropy and diuretic effects. In a double-blind, randomized study, the drug was investigated in 10 patients (mean age 49 +/- 10 years, six male, four female) with mild heart failure (NYHA classes II: six patients, III: four patients). Effects of single oral doses of 200 mg ibopamine, of 40 mg furosemide, and of 200 mg ibopamine plus 40 mg furosemide were compared in each patient at 3-day-intervals. One h after application, systolic and diastolic blood pressure increased from 119 +/- 11 to 124 +/- 8, and from 75 +/- 4 to 80 +/- 6 mm Hg (p less than 0.01) in the ibopamine group, while changes in both other groups and changes of the heart rate were insignificant. During 2 h after drug ingestion urinary flow was raised from 124 +/- 81 to 227 +/- 166 ml/2 h in the ibopamine group (p less than 0.05), while the application of furosemide (with or without ibopamine) resulted in several fold increases of urinary flow. After ibopamine, the 2-h-creatinine-clearance rose from 123 +/- 73 to 130 +/- 85 ml/min (not significant). Sodium excretion remained unchanged by ibopamine, potassium excretion was increased from 2.9 +/- 1.7 to 4.0 +/- 3.3 mmol/h (p less than 0.05), while effects of furosemide were several fold of those of ibopamine. Atrial natriuretic factor concentrations in plasma increased significantly after ibopamine and after ibopamine plus furosemide (p less than 0.01), but remained constant after furosemide alone.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Atrial Natriuretic Factor; Blood Pressure; Cardiomyopathy, Dilated; Coronary Disease; Cyclic GMP; Deoxyepinephrine; Diuretics; Dopamine; Electrolytes; Female; Furosemide; Heart Failure; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Natriuresis; Urodynamics | 1990 |
1 other study(ies) available for atrial-natriuretic-factor and ibopamine
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Dopaminergic control of aldosterone secretion is not mediated by atrial natriuretic factor in patients with essential hypertension.
Both dopamine and atrial natriuretic factor (ANF) are known to suppress aldosterone secretion. Since it is possible that dopaminergic mechanisms facilitate ANF release, we investigated the relationship between these two inhibitory systems by comparing the increases in aldosterone induced by metoclopramide, a dopaminergic antagonist, with decreases in ANF. Aldosterone, ANF, prolactin, plasma renin activity, cortisol and potassium were measured before and after the intravenous injection of 10 mg metoclopramide, blood samples being collected at 15-min intervals up to 2 h after the injection. These studies were performed in patients with essential hypertension who were maintained on a constant sodium intake (100 mmol/day), before and after 5 days of treatment with ibopamine, an orally active dopamine analogue. Before ibopamine metoclopramide induced the expected, marked increases in aldosterone and in prolactin, but only minimal, non-significant decreases in ANF. All other humoral parameters, as well as blood pressure and heart rate, were unaffected by metoclopramide. After ibopamine treatment, which caused a transient natriuretic effect, the responses of aldosterone and of ANF to metoclopramide were similar to those observed in control studies, whereas that of prolactin was enhanced. Thus, it appears that the suppressive effect exerted by the dopaminergic tone on aldosterone secretion is independent of ANF both before and after dopaminergic stimulation. Topics: Aldosterone; Atrial Natriuretic Factor; Deoxyepinephrine; Dopamine; Humans; Hypertension; Metoclopramide; Prolactin | 1988 |