Search PubMed⌕ Search

Biomedical subjects

G Wambach

Publications and source records attributed to G Wambach.

At least 55 records · Page 3Linked to original sources
PubMed1988

[Plasma ANP levels and its relation to electrolyte and water regulation in neurosurgical intensive care patients].

We examined the relation between plasma atrial natriuretic peptide (ANP) and the changes of the regulating hormones ADH and renin aldosterone in 20 neurosurgical intensive care patients. All patients suffered from elevated intracranial pressure due to severe head trauma or severe subarachnoidal hemorrhage of the anterior circulation. Under controlled mechanical hyperventilation (CMV) with PEEP, 15 patients without evidence of central dysregulation showed no change in plasma ANP, ADH and aldosterone. In five patients with severe central dysregulation of either electrolytes or blood pressure, increases of plasma ANP of various degrees could be observed together with a decline in serum aldosterone.

Aldosterone↗
PubMed1988

[Plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachycardia and concomitant polyuria (urina spastica)].

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.

Aged↗
PubMed1988

[Standardization of plasma determination of atrial natriuretic peptide (ANP)].

Comparison of normal values for plasma levels of atrial natriuretic peptide revealed a tremendous variability: the highest values being 10-times higher than lower mean values. We studied the impact of age, posture, sodium intake and the conditions of processing on the levels of ANP in normal control subjects. Middle-aged healthy subjects had p-ANP levels of 56 +/- 10 pg/ml compared to 25 +/- 10 pg/ml in 20-30-year-old students. Upright posture was followed by a decline in p-ANP of 20% whereas renin concentration rose 6-fold during upright posture. P-ANP increased during high sodium intake to 134 +/- 9 pg/ml, compared to 55 +/- 7 pg/ml during low sodium intake. We did not find a significant variability of p-ANP in the morning hours. Furthermore, when blood was stored at room temperature for 60 min, ANP levels remained unchanged. These variables should be taken into account when a control range is set up.

Adult↗
PubMed1988

[Atrial natriuretic peptide (ANP) in essential hypertension: a humoral marker for salt sensitivity and hypertensive heart disease at a clinically asymptomatic stage?].

Out of 32 patients (f = 10, m = 22; mean age: 46 +/- 3 years) with untreated essential (primary) hypertension (WHO-classification I-III) and without clinical signs of congestive heart failure or chronic renal failure, 19 showed plasma-ANP base levels above the normal range (greater than 100 pg/ml; normal range: 50 +/- 10 pg/ml). While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Plasma ANP levels were significantly correlated with the heart volume (r = 0.54; p less than 0.05; radiologically determined), the electrocardiographic signs of left ventricular hypertrophy (Sokolow-Lyon index; r = 0.62; p less than 0.05) and with the left atrial diameter (r = 0.34; p less than 0.05; determined by 2-D-echocardiography). We speculate that high levels of plasma ANP in patients with essential hypertension might be interpreted as a compensatory mechanism either for an insufficient excretion of sodium or for myocardial dysfunction.

Adult↗
PubMed1987

Plasma levels of atrial natriuretic peptide are raised in essential hypertension during low and high sodium intake.

Plasma levels of alpha-human atrial natriuretic peptide (hANP) were measured in 17 patients with primary hypertension (11 females, 6 males, aged 22-61; blood pressure systolic 154 +/- 7 mmHg, diastolic 92 +/- 4 mmHg) and in 9 normotensive controls (4 males, 5 females, aged 20-71; blood pressure systolic 117 +/- 4 mmHg, diastolic 76 +/- 2 mmHg) during unrestricted sodium diet, at the 4th day of a low sodium intake (40-60 mEq/day) and at the 6th day of sodium loading (280-320 mEq/day) both after an overnight rest and after 4 h of upright posture. In the controls, plasma levels of hANP at 8:00 a.m. were lowered from 73 +/- 11 to 49 +/- 7 pg/ml during low sodium diet and increased to 128 +/- 37 pg/ml after high salt intake. Plasma ANP levels were significantly lower after 4 h of upright posture during unrestricted, low and high sodium intake. In the hypertensive group, plasma ANP levels were elevated during unrestricted diet (203 +/- 43 pg/ml), during the low sodium period (139 +/- 31 pg/ml), and after high sodium intake (267 +/- 63 pg/ml) compared to the controls. All levels were lowered by upright posture. The absolute decrease was more pronounced compared to the normotensives, the relative decline was similar in both groups. In the hypertensives, plasma ANP levels significantly correlate with systolic and diastolic blood pressure (r = 0.468, r = 0.448, P less than 0.05) and with urinary aldosterone during unrestricted diet (r = 0.536, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Diminution by captopril of the diuretic, natriuretic and kallikrein stimulating action of furosemide by reduction in its renal secretion.

The effect of furosemide (40 mg iv) on diuresis, natriuresis and renal kallikrein and kinin excretion was investigated without and with pretreatment by captopril (100 mg po). Furosemide stimulated markedly diuresis and natriuresis as well as urinary kallikrein and kinin excretion. Pretreatment by captopril (C) reduced the diuretic and natriuretic effect of furosemide significantly (UNaV pre-C: +15, 1 +/- 2.1 ml/min vs. post-C: 7.0 +/- 0.3 ml/min; p less than 0.001). Similar changes in urinary kallikrein and kinin excretion were observed after captopril pretreatment, but because of the great coefficient of variation these changes did not reach statistical significance. The reason for the reduced activity of furosemide after captopril pretreatment was the diminished proximal-tubular secretion of furosemide, as it could be shown by direct measurement of the drug in urine. After furosemide injection changes in plasma aldosterone concentration paralleled changes in renal kallikrein and kinin excretion. However, after captopril there was a sharp dissociation between aldosterone, which was diminished by captopril continuously, and renal kallikrein and kinins, which were still stimulated by furosemide. These results suggest that renal kallikrein-kinin system is stimulated by furosemide directly and independently of aldosterone secretion.

Adult↗
PubMed1987

[Increased concentrations of atrial natriuretic peptide in the plasma and heart atrium of patients with aortic and mitral valve diseases compared to patients with coronary heart disease].

Plasma levels of atrial natriuretic peptide (ANP) and tissue content of the peptide were measured simultaneously in 18 patients with coronary heart disease (group A) and 10 patients with aortic or mitral dysfunction (group B) undergoing open heart surgery. Plasma levels of ANP were significantly higher in patients with valvular heart disease compared to those with coronary heart disease (816 +/- 246 pg/ml versus 232 +/- 58 pg/ml, p less than 0.005). Similarly, tissue levels of ANP in the right atrium of group B doubled that of group A (227 +/- 46 micrograms/g versus 129 +/- 15 micrograms/g, p less than 0.025). Plasma levels and tissue content of ANP were not correlated. However, plasma ANP levels and mean pulmonary artery pressure were positively correlated (r = 0.688, p less than 0.05). Chronic stimulation of ANP secretion leads to a tissue accumulation of natriuretic peptide in heart atrium.

Aged↗
PubMed1987

Water immersion-induced endocrine alterations in women with EPH gestosis.

In 12 healthy pregnant women, 14 women with mild or moderate late pregnancy gestosis (EPH) and in 12 non-pregnant women, the influence of head out water immersion (WI) on mean blood pressure (MAP), the renin-aldosterone system, vasopressin (AVP) and atrial natriuretic hormone (ANF) was examined. WI induced a prompt fall in MAP in all examined groups. This decrease of MAP was maximal after 1 h WI, showing a tendency to rise later on in pregnant women. Simultaneously a decrease of plasma renin activity (PRA), plasma aldosterone, AVP and an increase of ANF was noted. The WI induced endocrine reaction pattern was qualitatively similar, but quantitatively different in the examined groups. In contrast to the response of non-pregnant women, healthy pregnant women and women with EPH gestosis showed a significantly smaller increase in ANF secretion induced by WI. No correlation was found between PRA, plasma AVP, aldosterone and ANF respectively. In addition changes in PRA, aldosterone, AVP and ANF did not correlate with WI-induced changes in MAP. From data obtained in this paper it seems, that WI-induced MAP changes are not related significantly to changes of the above mentioned hormonal factors.

Adult↗
PubMed1987

[Renal and adrenal function following acute administration of urapidil in hypertensive patients with normal and impaired renal function].

The effects of i.v. injection of urapidil (Ebrantil) (25 mg) on arterial blood pressure, renal function and renin-aldosterone system were studied in a group of patients with hypertension and normal renal function, in patients with hypertension and chronic renal failure and in normotensive controls. The pharmacokinetics of urapidil were evaluated simultaneously by measuring blood levels of the compound and its main metabolite. In the controls and in patients with hypertension, systolic and diastolic blood pressure were lowered few minutes after injection. Minimal blood pressure values were reached after 15-20 min. Hypotensive action was more pronounced in hypertensive patients as compared to controls. In contrast, increment in heart rate was greater in the controls. Despite the fall in blood pressure, renal plasma flow and glomerular filtration rate remained unchanged. Following the injection of urapidil, plasma renin activity increased with no change in plasma aldosterone levels. Plasma half-life of urapidil averaged 1.96 +/- 0.17 h in controls, 3.31 +/- 0.75 h in patients with hypertension and normal renal function and 2.52 +/- 0.46 h in patients with hypertension and chronic renal failure. Urapidil effectively lowers arterial blood pressure in patients with normal and impaired renal function with no deterioration in renal function.

Adrenal Glands↗
PubMed1986

Androgen receptors in experimentally induced colon carcinogenesis.

Sex hormones may play a role in colonic carcinogenesis, as evidenced by epidemiologic and experimental data showing different tumor rates in males and females. We investigated the effects of hormonal manipulation on tumor development and on androgen receptor binding in both colonic wall and experimentally induced tumors in male rats. Five of six groups, each with 40 animals, were given 10 weekly s.c. injections of azoxymethane (AOM), 7.5 mg/kg body weight. Group-I served as normal controls. Group-II received AOM only. Group-III was castrated 2 weeks prior to carcinogen treatment. Group-IV was castrated similarly and then hormone substituted with testosterone propionate. Group-V was chemically castrated with the anti androgen cyproterone acetate. Group-VI was castrated and given hormone vehicle. Scatchard analysis for androgen receptors in cytosol from normal colonic wall and tumor was performed with 3H-methyltrienolone as the ligand. Androgens were found to have an inhibitory effect on carcinogenesis: chemical castration increased colonic tumor development (P less than 0.05 for multiplicity), and testosterone administration produced a borderline statistically significant reduction in tumor incidence in surgically castrated rats (P less than 0.053), particularly in the right colon. Specific binding sites for androgen with high affinity and low capacity were found in the colonic wall of all groups. Receptor density was not altered by AOM administration, but increased after surgical castration. Receptor density was markedly lower in tumors than in normal colonic wall. Receptor binding sites in tumors were not altered by the various hormonal manipulations. Our study demonstrated that although cytoplasmic androgen receptors are present in colonic wall and in experimental tumors, AOM-induced colonic carcinogenesis appears to be only mildly affected by manipulation of androgens.

Animals↗
PubMed1986

Sodium loading raises urinary cortisol in man.

It has been suggested that cortisol secretion is modified by sodium intake. We therefore studied the pituitary-adrenal axis by measuring diurnal rhythms of ACTH and cortisol levels in serum of 10 normal control subjects after 4 days of low sodium diet (intake 40 mEq/day) and after 6 days of high sodium diet (intake 320 mEq/day). Urinary excretion of aldosterone-18-glucuronide and free cortisol were determined at the end of each diet. Urinary aldosterone excretion declined from 17.9 +/- 2.6 to 2.8 +/- 1.1 microgram/day and urinary cortisol increased from 26.2 +/- 6.2 to 36.8 +/- 13.8 micrograms/day during low and high sodium intake. In contrast, plasma ACTH and serum cortisol measured every two hours for a 24-h period were similar both during low and high sodium intake. The results suggest an altered handling of cortisol by the kidney during high salt intake.

Adrenocorticotropic Hormone↗
PubMed1986

Blood viscosity: a pathogenetic factor in the development of essential hypertension?

Inhibition of the ouabain-sensitive Na-K-ATPase by digoxin significantly decreases erythrocyte deformability (5). Since first a decrease in this transport system has been discussed as a pathogenetic factor in the development of essential hypertension and second an increase in blood viscosity, due to an increased hematocrit has been observed in elderly hypertensives, hemorheology and sodium transport systems were examined in adolescent hypertensives and compared with age-matched normotensive controls. 73 normotensives (N; mean blood pressure 127/80 mmHg) and 53 hypertensives (H; mean blood pressure 147/94 mmHg) aged 23-27 yrs were randomly selected from an epidemiological survey, covering 1342 adolescents. While apparent whole blood viscosity at different shear rates, hematocrit, plasma fibrinogen were not significantly different, erythrocyte deformability, measured with a positive pressure filter system (pore phi 5 mu) and expressed as Q = delta P/ery.susp.Hct 10%/delta P/plasma was significantly attenuated with Q = 1.77 +/- 0.05 in H, compared to 1.64 +/- 0.04 in N (p less than 0.05) The decrease in erythrocyte deformability was not accompanied by an inhibition of the Na-K-pump nor of total K+-uptake in erythrocytes, both measured with the 86Rb uptake. There was only a slight increase in Na+-excretion in urine of 184.4 + 12.2 mval in H, compared to 162.0 +/- 10.4 mval in N (n.s.). K-/+-excretion and serum electrolytes did not show any difference. Whether the decrease in erythrocyte deformability may contribute to an increase in peripheral vascular resistance in essential hypertension has to be further clarified.

Adult↗