Biomedical subjects
Publications and source records attributed to S Czekalski.
This work shows that an intravenous infusion of atropine increases the concentration of atrial natriuretic peptide (ANP) in the plasma of healthy subjects. The effect is discussed in reference to the heart rate and the role of the autonomic nervous system in the control of ANP secretion by atrial cardiocytes.
The aim of the study was the search for the correlation between the degree of impairment renal function (measured by creatinine clearance) and plasma concentration of atrial natriuretic peptide (ANP) and urinary fractional sodium excretion (FENa) in patients with chronic renal diseases. Forty seven patients were studied: 10 with diminished renal reserve (group I), 10 with renal insufficiency (group II), 27 with renal failure (group III) and 10 chronically haemodialysed before dialysis (group IV). Control group consisted of 27 healthy persons. All patients and controls were on the diet containing 100-120 mmol sodium daily. Plasma ANP levels were significantly higher in all groups of patients (I--16.5 +/- 5.7; II--40.7 +/- 18.6; III--86.2 +/- 49.9; IV--196.1 +/- 51.3 pmol/l, respectively) than in controls (10.8 +/- 6.0 pmol/l). A significant correlation (r = 0.85; p less than 0.01) between plasma ANP concentration and FENa was found when the patients from all groups were pooled together. The results confirm the important role of ANP in the adaptation of reduced kidney mass to the excretion of sodium load.
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Atrial natriuretic peptide (ANP) is a hormone release into the circulation by atrial cardiocytes (Gutkowska et al. 1984). Extracellular fluid volume expansion acts as a powerful stimulus for ANP secretion and results in the augmentation of its plasma concentration (Lang et al. 1985). Patients with active acromegaly demonstrate the increased extracellular fluid volume (Falkheden et al. 1964), while a successful treatment of the disease results in the disappearance of hypervolemia (Strauch et al. 1977). We have recently demonstrated that in patients with active acromegaly the increased total body plasma volumes are accompanied by the elevated plasma ANP concentrations, whereas, in the successfully treated patients, both: total plasma volumes and plasma ANP levels do not differ significantly from these in healthy subjects (Czekalski et al. 1988b).
In twelve patients with acute renal failure, mean plasma levels of atrial natriuretic factor (ANF) and of its second messenger cGMP were found elevated at the early phase of the disease, but tended to return towards normal values at recovery. Variations of plasma ANF and cGMP were correlated significantly (p less than 0.05) with those of total blood volume. At the early phase of the disease, plasma ANF was also correlated with the excreted fraction of filtered sodium (FENa) (r = 0.95). Moreover, plasma ANF and FENa peaked concomitantly at the onset of the diuretic phase in the five patients who were not treated by diuretics or dialysis and were studied sequentially during the course of the disease. It is suggested that enhanced plasma ANF levels might reflect one of the mechanisms of adaptation controlling body fluid balance in acute renal failure.
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1. In order to examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the increased sodium excretion per nephron in chronic renal failure, we studied healthy subjects with normal renal function (group I) and patients with moderate (group II) or severe chronic renal failure (group III) before, during and after administration of an intravenous sodium load. All subjects had been on a controlled diet containing 120 mmol of sodium per day for 5 days before the study. 2. Under basal conditions, plasma ANP and fractional excretion of sodium (FENa) were highest in group III. Both parameters increased in response to the sodium load in the three groups studied (P less than 0.001). Changes with time differed from group to group (P less than 0.05), the more marked response for both parameters being observed in group III. After adjustment with respect to plasma ANP (analysis of covariance), FENa was no longer modified in response to the sodium load, whereas adjustment of FENa with respect to mean blood pressure was without consequence on the significance of its change with time. This demonstrates that plasma ANP, but not mean blood pressure, represents the main factor producing variation in FENa during and after the sodium load. 3. These results suggest an important role for plasma ANP in promoting adaptation of short-term sodium excretion in response to an acute sodium load in patients with chronic renal failure who ingest a normal sodium intake.
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To study the relation between plasma atrial natriuretic factor (ANF) and cardiac pressures, we measured plasma ANF in 24 patients with mitral stenosis 30 minutes before and 20 minutes after balloon mitral valvulotomy. All patients were without physical signs of congestive heart failure. Normal sinus rhythm was present in 15 (group 1), whereas the other nine (group 2) had permanent atrial fibrillation. There were no significant differences between groups for basal mean pressures in right atrium (RA), left atrium (LA), and pulmonary artery (PA). Valvulotomy resulted in a fall in both groups (p less than 0.001) in LA and PA mean pressures, whereas heart rate, cardiac index, and RA and aorta (AO) pressures did not change significantly. Basal ANF was not different in either group in RA (240 +/- 43 vs. 266 +/- 35 pg/ml) or AO (441 +/- 92 vs. 643 +/- 70 pg/ml) but tended to be higher in group 2 in LA (428 +/- 88 vs. 682 +/- 84 pg/ml; p = 0.059) and PA (488 +/- 93 vs. 759 +/- 92 pg/ml; p = 0.057). Plasma ANF was the highest in PA, and about 50% ANF was extracted in the systemic circulation. After valvulotomy, plasma ANF was greater (p less than 0.05) in group 2 (372 +/- 90, 755 +/- 152, 805 +/- 134, and 707 +/- 144 pg/ml) than in group 1 (206 +/- 36, 386 +/- 47, 429 +/- 66, and 421 +/- 49 pg/ml), regardless of the site of blood collection (RA, LA, PA, and AO, respectively). PA ANF was correlated with LA pressure (p less than 0.05) in group 1 before as well as after valvulotomy, whereas there was no such correlation in group 2. Cyclic GMP (cGMP) in LA was correlated (p less than 0.01) with PA ANF in group 1, and LA cGMP (10.0 +/- 1.2 and 9.1 +/- 1.8 pmol/ml in groups 1 and 2, respectively) was higher (p less than 0.05) than PA cGMP (9.1 +/- 1.0 and 8.0 +/- 1.5 pmol/ml in groups 1 and 2, respectively) before valvulotomy, which suggests the presence of ANF receptors in the pulmonary circulation. Taken together, these results indicate that in patients in sinus rhythm with mitral stenosis, there is an increase in ANF secretion depending on LA pressure. ANF secretion is also high in patients with mitral stenosis and atrial fibrillation but does not respond appropriately to changes in LA pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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Plasma atrial natriuretic peptide (ANP) was measured by radioimmunoassay in 10 patients with end-stage renal failure during two successive 150-min periods of ultrafiltration and perfusion of an identical fluid volume (1,800-2,400 ml). The patients were divided into two groups of 'denervated' and 'intact' patients based on three different tests for cardiac parasympathetic dysfunction. Plasma ANP was higher in the denervated group than in the intact group throughout all the study, but decreased with the volume ultrafiltered and increased with the volume perfused in both groups. The sensitivity of ANP response to perfusion was greater in denervated than in intact patients. These results demonstrate the close relationship between plasma ANP and stepwise decremental or incremental changes in extracellular fluid volume. They also suggest that cardiac parasympathetic innervation plays a role in modulation of ANP secretion in humans.
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