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Biomedical subjects

W Kaufmann

Publications and source records attributed to W Kaufmann.

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

Are calcium antagonists helpful in the management of primary aldosteronism?

The chronic effect of the calcium antagonist nitrendipine, a 1,4-dihydropyridine derivative, on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium was investigated in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA) (n = 3; age 44 +/- 4 years; PAC: 312 +/- 96 pg/ml; PRA: less than 0.1 ng/L/h; serum potassium: 2.8 +/- 0.3 mmol/L) or to bilateral idiopathic hyperaldosteronism (IHA): (n = 3; age 49 +/- 1 years; PAC: 212 +/- 32 pg/ml; PRA: 0.1 +/- 0.1 ng/L/h; serum potassium: 3.3 +/- 0.2 mmol/L). After withdrawal of antihypertensive medications 2 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40-60 mg. BP, PAC, PRA, and serum potassium were determined before and after 4 weeks of nitrendipine therapy. After 4 weeks, blood pressure was significantly reduced (178 +/- 10 to 165 +/- 6 mm Hg systolic, 109 +/- 7 to 101 +/- 6 mm Hg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings, we follow that calcium antagonists do not normalize BP, PAC, PRA, and serum potassium in patients with APA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Effect of atrial natriuretic peptide (ANP) on the renal kallikrein-kinin system in normotensive and spontaneously hypertensive rats].

Injection of atrial natriuretic peptide (ANP) induces marked diuresis, natriuresis and less marked blood pressure reduction. These effects are similar to those of renal kallikrein-kinin system (rKKS). In this study we investigated the influence of ANP on rKKS of rats. ANP was injected intravenously in male normotensive (WKy) and spontaneously hypertensive rats (SHRsp) as a bolus of 3.5 micrograms atriopeptin III. ANP induced, in both groups of rats, a marked increase in diuresis and natriuresis, while blood pressure decreased significantly. Renal plasma flow and urinary excretion of potassium increased only a little. The observed changes were similar in both strains of rats and there was no statistically significant difference except the lower potassium stimulation in the SHRsp than in the WKy (p less than 0.05). In regard to the basal activity of the rKKS there was a significant difference between the two strains of rats. The activity of renal kallikrein in urine and of kininase II in plasma was reduced in the SHRsp about 50%, while renal kinin excretion in urine was markedly enhanced in these rats, if compared to the WKy controls. In both groups of rats renal kallikrein and kinin excretion was stimulated by ANP for a short time and, simultaneously, total kininogen in plasma decreased after the injection of ANP. The increment of renal kallikrein excretion in urine was much less marked in the SHRsp than in the WKy rats. The reduced kallikrein stimulation was compensated by the reduced kinin degradation by kininase II in these rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

In vivo effects of camostat mesilate on plasma kallikrein, plasma kininase II and renal kallikrein of man.

N,N-Dimethylcarbamoylmethyl-4-(4-guanidino-benzoyloxy)phenylacetat e methanesulfonate (camostat mesilate) is reported to be an effective inhibitor of plasma kallikrein. It was shown in vitro to inhibit not only plasma kallikrein, but also renal kallikrein and plasma kininase II. These inhibitory activities, however, were very weak. The inhibition of plasma kallikrein in human plasma was limited in time, since a rapid reactivation of plasma kallikrein was noticed when samples were incubated at room temperature. In order to establish whether camostat mesilate was able to inhibit plasma kallikrein, kininase II and renal kallikrein also in vivo the inhibitory activity of camostat mesilate on these enzymes was studied in 5 healthy volunteers. After an oral intake of a single dose of 600 mg of camostat mesilate, plasma kallikrein was inhibited significantly, while kininase II in plasma was unaffected. Renal kallikrein activity determined by urinary excretion of active kallikrein remained unchanged after camostat mesilate intake. Thus, the results demonstrate that camostat mesilate in vivo inhibits only plasma kallikrein and has no effect on the activity of kininase II or renal kallikrein.

Adult↗
PubMed1986

Inhibition by FOY of kininase II in human plasma.

In this investigation we studied the inhibitory effect of FOY S 983 (gabexate mesilate) and FOY S 980 (camostate mesilate) on the kininase II activity in human plasma in vitro. Both compounds were able to inhibit kinase II, however, compared to captopril or EDTA only very weakly. The inhibitory effect of FOY S 983 or FOY S 980 could be diminished neither by NaOH-induced hydrolysis of the inhibitor nor by dialysis or ultrafiltration, but could be clearly reduced by dialysis against ZnCl2 solution. The inhibition of kininase II activity in human plasma by FOY S 983 was due to its 6-guanidinocaproate component probably acting as Zn2+-complexing agent. The ethyl 4-hydroxybenzoate component of FOY S 983 had no inhibitory effect.

Angiotensin-Converting Enzyme Inhibitors↗
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↗
PubMed1986

Evaluation of sinefungin for the treatment of Trypanosoma (Nannomonas) congolense infections in goats.

Caprine Trypanosoma (N.) congolense infections were treated with sinefungin, an antifungal antibiotic nucleoside. Single doses from 10 to 20 mg/kg bodyweight given intramuscularly were not curative for goats; single doses of 25 and 50 mg/kg were toxic, and caused death. Five and 7.5 mg/kg administered twice daily over a three-day period, resulted in a cure in 2 animals, while 2 others relapsed. All animals relapsed when given a single daily dose of 5 or 7.5 mg/kg for 4 consecutive days. When such doses were given twice a day, they caused death in 50% of the goats and the remainder were cured. Raised serum urea levels indicated the severe nephrotoxic side-effects of sinefungin even at subcurative levels. Histopathological examinations revealed an acute tubulonephrosis.

Adenosine↗
PubMed1986

Plasma levels of atrial natriuretic peptide (ANP) during mineralocorticoid escape in normal man.

A natriuretic factor has long been postulated to play a role in renal mineralocorticoid escape. We therefore investigated changes in plasma levels of atrial natriuretic peptide (ANP) during chronic treatment with 9 alpha-fluorohydrocortisone. Five normal subjects were studied on a constant diet (300 meq Na+ and 72 meq K+ per day) and received 0.8 mg 9 alpha-fluorohydrocortisone for up to 14 days. Sodium balance became positive and body weight increased between 1.0-4.5 kg maximally. Serum aldosterone was suppressed and plasma levels of ANP were stimulated up to 10-fold. Increment in plasma ANP was positively correlated with the gain in body weight (r = 0.666, p less than 0.001). Renormalization of sodium balance was seen in two subjects, however the maximum in plasma ANP did not occur during the time of renal escape. ANP-secretion is stimulated during sodium retention induced by mineralocorticoids, however ANP does not seem to trigger the escape mechanism.

Adult↗
PubMed1985

Na-K pump activity in erythrocytes of patients with endogenous and exogenous glucocorticoid excess.

The mechanism of glucocorticoid-induced hypertension is not clarified. Recent data suggest an alteration of active electrolyte transport systems by glucocorticoids. We therefore studied the activities of the Na-K pump by measuring the Na-K-ATPase activity in erythrocyte ghosts and the ouabain-sensitive uptake of rubidium in erythrocytes of patients with Cushing's syndrome and of patients with exogenous glucocorticoid excess after treatment with fluocortolone or ACTH. Na-K-ATPase activity was significantly increased in patients with Cushing's syndrome and in patients treated with ACTH compared to the controls. Similarly, total uptake of 86Rb and the ouabain-sensitive uptake in erythrocytes were found to be above the control range both in patients with Cushing's syndrome and in patients treated with fluocortolone. There was no difference in furosemide-sensitive uptake of 86Rb. The results demonstrate an increased maximal activity of the Na-K pump in patients with glucocorticoid excess.

Adrenocorticotropic Hormone↗
PubMed1985

Direct hypotensive action of intravascular bradykinin in man.

To investigate the cardiovascular effects of bradykinin (BK), the peptide was injected into 6 normotensive volunteers in the supine position. BK was given intravenously as a bolus in a dose of 0.001-7.5 microgram BK/kg body weight. Intraarterial blood pressure decreased dose related in a range of 0.25-1.0 microgram BK/kg body weight. Pretreatment with 2 X 50 mg indomethacin or 80 mg propranolol as well as changes in oral salt intake (from 10 to 300 mmol Na+/day) had no effect on the blood pressure-lowering effect of BK. Captopril (25 mg) potentiated the effect of BK 20- to 50-fold. In primary hyperaldosteronism, renal kallikrein activity and absolute vascular reaction to BK was increased. The results showed clearly that in man, similarly as in rats, BK lowers blood pressure by direct vasodilation and acts independently of prostaglandins, beta-receptors or salt intake.

Blood Pressure↗
PubMed1985

Haemorheology in adolescent hypertensives.

Fifty-three untreated borderline hypertensives and 73 normotensives were randomly selected from 1342 adolescents (age range 23-27 years) who were examined in 1975, 1976 and 1980 in an epidemiological study. Blood pressure was 127.2 +/- 1.0/79.0 +/- 0.8 mmHg in normotensives and 147.2 +/- 1.6/93.7 +/- 1.1 mmHg in hypertensives (P < 0.001). Erythrocyte deformability was measured with a positive pressure filter system (pore diameter 5 microns) at 37 degrees C. Erythrocyte deformability was significantly increased in hypertensives with a value of 1.77 +/- 0.05, compared with 1.64 +/- 0.04 in normotensives (P < 0.05). No difference in apparent whole blood viscosity, haematocrit and plasma fibrinogen was measurable between the groups. Although plasma noradrenaline and adrenaline concentration at rest and after 3 min standing were not different, excretion of urinary catecholamines was significantly elevated in hypertensives with 155.0 +/- 3.3 micrograms/24 h (normotensives: 100.7 +/- 5.3 micrograms/24 h; P < 0.001).

Adolescent↗