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Biomedical subjects

E Hartter

Publications and source records attributed to E Hartter.

At least 37 records · Page 2Linked to original sources
PubMed1991

Decrease of stimulated amylin release precedes impairment of insulin secretion in type II diabetes.

Amylin, a 37-amino acid polypeptide, has been identified as the major protein component of pancreatic amyloid deposits in patients with non-insulin-dependent (type II) diabetes mellitus. Amylin is stored and released together with insulin and has been proposed to play a major role in the pathogenesis of type II diabetes. To compare amylin release and its proportion to insulin secretion under different metabolic conditions, oral and intravenous glucose tolerance tests (OGTT and IVGTT, respectively) were performed in healthy, lean control subjects, obese patients with normal and impaired glucose tolerance (NGT and IGT, respectively), and obese type II diabetic patients. Compared with control subjects, basal and stimulated amylin secretion during OGTT was significantly higher in obese patients with NGT and IGT but not in type II diabetic patients. The integrated amylin response was significantly higher in obese patients with NGT than lean control subjects and type II diabetic patients matched for degree of obesity. The amylin-insulin ratio decreased slightly in obese subjects with NGT and IGT and significantly in type II diabetic patients. Amylin secretion was significantly stimulated during IVGTT in control subjects and obese patients with NGT and IGT but not in type II diabetic patients. These findings suggest that amylin is physiologically released by pancreatic beta-cells in a constant ratio to insulin in nondiabetic subjects. Glucose-stimulated amylin secretion is increased in obese subjects with NGT and IGT. In type II diabetes mellitus, amylin secretion relative to that of insulin is decreased, and amylin is not stimulated by IVGTT.

Adult↗
PubMed1991

[Role of amylin in the pathogenesis of type II diabetes mellitus].

Amylin, a peptide, which was isolated from the islet amyloid of type II diabetics, might play a potential role in the pathogenesis of type II diabetes mellitus. In in vitro and in vivo studies it has been shown that amylin has an effect on insulin secretion as well as on insulin sensitivity. From measurements of plasma amylin levels it is known that amylin is cosecreted with insulin and patients with hyperinsulinemia have also elevated amylin levels. In patients with impaired glucose tolerance and type II diabetes amylin levels are decreased compared to insulin. A secretory defect of amylin and its local accumulation in the islets of type II diabetics might be a cause for the insulin secretory defect in type II diabetes. Additionally, amylin can induce peripheral insulin resistance, which might also be a cause for type II diabetes mellitus. Amylin is a new pancreatic peptide, which might play an important role in the pathogenesis of diabetes mellitus.

Amyloid↗
PubMed1991

Radioimmunoassay of immunoreactive C-terminal big-endothelin(22-38).

Endothelin, a potent endogenous vaso-constrictor, is derived from its biosynthetic precursor by proteolytic degradation. The last step cleaves big-endothelin(1-38) to endothelin(1-21) and a C-terminal fragment. We have developed a radioimmunoassay for this peptide, based on an antiserum recognizing the C-terminal sequence big-endothelin(22-38) and cross-reacting with intact big-endothelin. To test for the presence of immunoreactive big-endothelin(22-38) in plasma, samples were extracted by passage through C18 silica cartridges, and desorption with methanol/water volume fraction 0.8. The yields of this purification and concentration procedure were about 70%. In 15 healthy persons we found concentrations of 1-11 pmol/l, which is about 10-fold higher than the reference levels reported for endothelin(1-21) or big-endothelin(1-38). Thus, endothelin-derived peptides containing the big-endothelin(22-38) sequence, but different from intact big-endothelin, do circulate in human blood. If a sufficiently tight correlation to levels of circulating endothelin(2-21) can be proven, this would facilitate studies on the physiological role of endogenous endothelin.

Endothelin-1↗
PubMed1990

Immobilization of alpha-human atrial natriuretic peptide on insoluble supports and affinity purification of specific antibodies from a polyclonal goat anti-alpha-human atrial natriuretic peptide serum.

alpha-Human atrial natriuretic peptide (alpha-hANP) was covalently coupled via single attachment onto two different insoluble matrices. Controlled-pore glass-alpha-hANP matrices were well suited for the purification of monospecific antibodies, whereas Enzacryl AA-alpha-hANP did not withstand the inevitable chemical and physical stresses during affinity purification.

Animals↗
PubMed1990

Determination of alpha-human atrial natriuretic peptide (alpha-hANP) in urine using combination HPLC with RIA strongly indicates non-immunoreactive metabolites.

Employing HPLC coupled with RIA, it was shown that alpha-human atrial natriuretic peptide is excreted in urine. Freshly collected urine had to be acidified to obtain reproducible results. When prepurified urine was subjected to HPLC (ion exchange and reversed phase) the subsequent quantification of alpha-hANP immunoreactive material in the eluate showed 10- to 30-fold greater amounts of alpha-hANP after treatment with HPLC; substances with the same elution parameters as synthetic alpha-hANP were detected, but they gave no response in the RIA.

Atrial Natriuretic Factor↗
PubMed1990

Interpretation of plasma concentrations of human atrial natriuretic peptide (hANP) in congestive heart failure.

The present study reports about novel findings concerning the interrelationship between release of human atrial natriuretic factor (hANP) and the clinical situation of patients suffering from congestive heart failure. Estimations of plasma hANP were done by specific and sensitive extraction-based RIA. The normal range was 5 to 80 ng/l, mean +/- SEM = 30 +/- 15 ng/l, n = 106. Influence of response to therapy on hANP-release was studied in altogether 14 patients. 12 of these patients had elevated plasma hANP at admittance, surprisingly peptide levels were normal in 2 patients throughout the study. 9 out of the 14 patients responded well to therapy (shift from NYHA IV/III to NYHA II within about 10 days), hANP-levels decreased to normal values: 235 +/- 104 ng/l vs. 65 +/- 13 ng/l; p less than 0.001. The 5 residual patients responded to therapy only partially (shift from HYHA IV to NYHA III within an observation interval of about 2 weeks). Plasma hANP values decreased from 225 +/- 94 ng/l to 137 +/- 22 ng/l (p less than 0.02), but were still supranormal. Atrial fibrillation, which persisted in 8 out of the 14 patients after therapy did not influence hANP levels: hANP levels paralleled clinical signs of improvement, irrespective of atrial fibrillation. Right heart catheterization revealed very high mean right atrial pressures in those 2 patients mentioned above, who had normal pretherapeutic hANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1989

Correlation between heart disorders and concentrations of directly measured atrial natriuretic peptide in plasma.

We used new commercially available direct radioimmunoassay to measure human atrial natriuretic peptide (h-ANP) in plasma from 48 individuals who were being evaluated for left and right ventricular function. For 13 healthy individuals with normal ventricular function these concentrations ranged up to 54 ng/L. Measurements of h-ANP clearly differentiated between normal subjects, patients with coronary artery disease, and patients who had undergone orthotopic heart transplantation (ANOVA P less than 0.0001, significant differences between all groups)--all showing normal ventricular function at rest. There was a strong negative correlation (r = -0.64, P less than 0.001) between left ventricular ejection fraction and h-ANP concentrations in plasma of patients with proven coronary artery disease, patients with cardiomyopathy, and healthy individuals. Results by the present method and methods involving extraction of the sample correlated well. Evidently the direct assay of h-ANP in plasma yields information that could be used to help evaluate heart disorders and other pathophysiological conditions causing increased h-ANP concentrations in plasma.

Adult↗
PubMed1988

Plasma atrial natriuretic factor in cirrhotic patients with ascites. Effect of peritoneovenous shunt implantation.

Human atrial natriuretic factor (ANF) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites, in whom sodium retention is a major clinical problem. The mean preoperative plasma level of ANF was 82 ng/L (normal range, 5-80 ng/L). Peritoneovenous shunting resulted in a significant rise in plasma ANF to 308 ng/L (p less than 0.0025) immediately after operation. This was followed by a constant fall until the seventh postoperative day, when mean plasma ANF was still significantly elevated (149 ng/L) compared with the preoperative value (p less than 0.01). Three months after shunt implantation mean plasma ANF had returned to the preoperative level (75 ng/L). Mean sodium excretion increased from 2.6 mEq/h preoperatively to 10.2 mEq/h at the second postoperative day (p less than 0.025). No direct relationship was noted between changes in plasma ANF level and changes in urinary sodium excretion after shunt implantation. These data demonstrate an intact ANF release response to intravascular volume expansion in cirrhotic patients with ascites, but exclude ANF as the diminished natriuretic factor as proposed by the overflow theory of ascites formation. Sodium excretion and fluid retention seem to be the result of vascular underfill and fluid maldistribution, and hormonal changes are likely to be secondary to them.

Aged↗
PubMed1988

Atrial natriuretic peptide decrease during spontaneous breathing with continuous positive airway pressure in volume-expanded healthy volunteers.

We examined the effect of spontaneous breathing with continuous positive airway pressure (CPAP) on the plasma concentrations of immunoreactive (ir) alpha-atrial natriuretic peptide (ANP). In three experiments, each of 11 healthy male volunteers performed CPAP at 20, 10 and 0 cm H2O for 2 h during continuous volume loading. Samples were drawn from a peripheral vein. Plasma concentrations of irANP were determined by a sensitive radioimmunoassay. Significantly lower concentrations of irANP were observed during 20 cm H2O CPAP than at 10 and 0 cm H2O. The concentrations of irANP did not differ significantly when individuals breathing with CPAP at 10 and at 0 cm H2O were compared. Our data suggest that CPAP at 20 cm H2O lowers the release of ANP in volume-expanded subjects. We hypothesize that this phenomenon may contribute to the fluid retention and renal dysfunction observed frequently during high CPAP levels. The decline in plasma concentrations of irANP may be the result of atrial compression by the distended lungs and of reduced venous return to the heart during CPAP.

Adult↗
PubMed1988

Human atrial natriuretic peptide secretion in precapillary pulmonary hypertension. Clinical study in patients with COPD and interstitial fibrosis.

Human atrial natriuretic peptide (hANP) is stored by granules of both human atria. Atrial distension appears to be a major stimulus for hANP secretion. Precapillary pulmonary hypertension increases right ventricular afterload and may thus cause right atrial distension. We therefore hypothesized that hANP plasma concentrations (1) are higher in the right atrium than in the peripheral vein, (2) are increased in patients with precapillary pulmonary hypertension, and (3) correlate with right atrial pressure. Thirty-three adult patients with chronic obstructive pulmonary disease (COPD) or interstitial fibrosis were examined by right heart catheterization. Mean pressures were measured in the right atrium, pulmonary artery, and pulmonary capillary wedge position, and blood was drawn from the right atrium and from a peripheral vein for determination of hANP levels. In general, hANP plasma levels in the right atrium were significantly higher than in a peripheral vein. Seventeen out of 33 patients had pulmonary hypertension, whereas 16 patients exhibited normal pulmonary artery mean pressures. In all patients, pulmonary arterial wedge pressure was normal. Plasma hANP concentrations were significantly higher in patients with pulmonary hypertension than in patients with normal pulmonary artery pressure. A strong correlation between central or peripheral hANP plasma levels (or both) and mean right atrial pressure could be observed (r = 0.75; p less than 0.001). From these data, we conclude that the increased secretion of hANP in our patients with precapillary pulmonary hypertension appears to be mediated by right atrial distension.

Adult↗
PubMed1988

[Methodological problems in the radioimmunologic measurement of ANP (atrial natriuretic peptide)].

Parameters influencing the measurement of hANP are designated and discussed on the basis of data from the literature and from our own results. Plasma hANP is dependent on the anatomical location of blood withdrawal, posture, state of hydration and salt load and medications. Interfering substances contained in plasma, management of samples and the type of assay used are of utmost importance. Direct RIA of hANP appears to be particularly sensitive to interferences. Preextraction of hANP from EDTA plasma by octadecylsilica cartridges, followed by RIA seems to be the most trustworthy method for measurement of hANP. Nevertheless, with this method too, we obtain different values for identical plasma samples if we use different antisera. Additionally, lipemia significantly lowers the ascertainable amount of endogenous, but not of exogenously added alpha-hANP. Therefore, it is reasonable to conclude that in preextracted samples too, hANP is not a homogeneous species. We observe a time-dependent increase in plasma hANP, reaching a final stable plateau value (about three times the initial values) after about 1.5 h, if EDTA blood samples are left on ice for prolonged time. Hemolysis interferes significantly with hANP determination. Readings of hANP values are reduced in dependence on plasma haemoglobin concentration. According to our experience, EDTA plasma can be stored for several months in either lyophilized form or deep frozen at -20 degrees C without the risk of reduction of hANP immunoreactivity. The data presented in this paper clearly show, that measurement of hANP is susceptible to faults in several details. Results should therefore be viewed critically.

Atrial Natriuretic Factor↗
PubMed1987

Atrial natriuretic peptide release due to physical exercise in healthy persons and in cardiac patients.

Plasma levels of human atrial natriuretic peptide were determined during different stages of a symptom-limited bicycle ergometer stress test. Eight healthy persons and three patients suffering from well-defined cardiac disorders were examined. Measurements of the peptide were performed before the exercise, at 75 watts, at maximal work load, and 10 and 30 min after ceasing the exercise. In healthy persons plasma levels of the peptide increased from preexercise levels of 4-41 ng/l to 16-59 ng/l at maximal work load, but remained in the normal range (10-70 ng/l). In contrast, in the cardiac patients, levels of the peptide were up to 8-fold higher at maximal physical exertion (154-270 ng/l) than at rest (34-86 ng/l). Within a recovery period of 30 min hormone concentrations returned almost to preexercise levels.

Aged↗
PubMed1987

Circadian variation and age dependence of human atrial natriuretic peptide levels in hospitalized patients.

Circadian variation of plasma levels of human atrial natriuretic peptide (hANP) was studied in 8 patients less than or equal to 65 a of age (mean +/- SD = 43.8 +/- 13 a; 5 females, 3 males) and in 15 patients greater than 65 years of age (mean +/- SD = 81.4 +/- 5.7 a; 9 females, 6 males). Intraindividual variation was up to 40% relative to the day's mean level in both groups. A significant elevation of hormone levels in the evening was observed in patients greater than 65 years of age (P less than 0.002), no circadian rhythm could be detected in patients less than or equal to 65 years of age. All patients except the two eldest had average plasma levels of hANP within our normal range of 3-75 ng/l (N = 106; mean +/- SD = 29.9 +/- 15.3), found in healthy persons up to 65 years of age. We propose, that in the elderly hANP levels rise during the day by edema because of latent renal and/or cardial insufficiency. At rest, in the evening and during the night edema is eliminated by the well known nycturia, which might well be facilitated or at least partially caused by elevated levels of hANP.

Adult↗