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Biomedical subjects

F Krück

Publications and source records attributed to F Krück.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Aldosterone and renin in liver cirrhosis with ascites].

Supine plasma aldosterone and plasma renin activity were determined in patients with cirrhosis of the liver and ascites (n = 10). Most of the patients initially showed an increase in plasma aldosterone and plasma renin activity. However, values within the normal range were observed (plasma aldosterone, n = 3; plasma renin activity, n = 4). In the ascitic fluid renin activity could not be detected, whereas aldosterone concentrations correlated significantly with the respective plasma levels (r = 0.8, p less than 0.01). During therapy with spironolactone alone (n =2) or in combination with furosemide (n = 4), diuresis and natriuresis showed no correlation with changes in plasma aldosterone and/or plasma renin activity. Our results suggest that other factors than renin and aldosterone secretion may be important in the formation of ascites in patients with cirrhosis of the liver. In addition, the inverse correlation between mean arterial blood pressure and plasma renin activity (r = -0.65, p less than 0.05) found in our patients supports the assumption that the increase in renin secretion is probably induced by changes in (renal) hemodynamics.

Aldosterone↗
PubMed1977

[Raised plasma-prolactin levels in essential hypertension: index of reduced hypothalamic dopaminergic activity (author's transl)].

Serial measurements of plasma-prolactin concentration (HPr) and plasma-renin activity (PRA) at 30-min intervals were made in 19 male patients with essential hypertension and in 8 normotensive subjects. HPr was markedly higher in the hypertensive patients than in the normotensive controls. Patients with reduced plasma-renin activity and only slightly elevated HPr-levels showed lower urinary sodium excretion, but a more pronouced 24-h natriuretic response to i.v. furosemide than patients with normal renin and very high HPr-levels. Six patients were treated with the dopaminergic agonist bromocriptine. The drug induced a significant blood pressure reduction in five patients and normalised pressure in two patients. The data do not indicate a role for prolactin in sustaining hypertension via renal salt retaining mechanisms. It is suggested that the raised HPr-levels represent an index of altered central nervous function, characterized by reduced hypothalamic activity. The blood pressure-lowering effect of the dopaminergic agonist bromocriptine fits with the hypothesis that reduced hypothalamic dopaminergic activity might be a factor in the pathogenesis of essential hypertension.

Adult↗
PubMed1977

Hyperprolactinaemia and antihypertensive effect of bromocriptine in essential hypertension. Identification of abnormal central dopamine control.

Plasma-prolactin concentration was up to four times higher in male patients with essential hypertension than in normotensive controls. Oral administration of bromocriptine, a dopaminergic agonist, suppressed plasma-prolactin and lowered arterial pressure. It is proposed that in the hypertensive patients the raised prolactin levels reflect a defect in central dopamine control which is normalised by bromocriptine. The antihypertensive effect of bromocriptine suggests that the dopaminergic system is involved in blood-pressure regulation and that reduced central dopaminergic activity may be a factor in the maintenance of essential hypertension.

Adult↗
PubMed1977

Effect of a spirolactone on plasma and urinary aldosterone in primary aldosteronism.

In primary aldosteronism due to an adrenal adenoma (n=2), treatment with a spirolactone (160 mg Canrenone/day for 7 days) decreased plasma aldosterone and urinary aldosterone-18-glucuronide. However, in the presence of a normalization in urinary aldosterone 18-glucuronide plasma aldosterone remained elevated above normal. Continued therapy with higher doses (320 mg/day for 7 days and 480 mg/day for 28 days) did not significantly alter plasma aldosterone, while urinary aldosterone-18-glucuronide returned to values comparable to those obtained before therapy. Cessation of the drug resulted in a marked increase in plasma aldosterone and urinary aldosterone-18-glucuronide. The results indicate that in primary aldosteronism due to an adrenal adenoma, the spirolactone (Canrenone) inhibits aldosterone biosynthesis and seems to influence aldosterone degradation.

Adenoma↗
PubMed1976

[Paul-Bunnell negative glandular fever (author's transl)].

Cytomegalovirus infections may occur either as congenital and neonatal diseases respectively or postnatally in adults in connection with conditions of antibody or immunologic deficiencies. Reports of postnatally acquired cytomegalovirus infections in apparently healthy adults are scarce. A case of an acquired cytomegalo-virus infection in a 23-year old male patient who never was ill before is reported. Clinical and laboratory features showed a typical course of a Paul-Bunnell negative glandular fever. Diagnosis could be established by detection of cytomegalovirus IgM serum levels by means of immunofluorescence technique.

Adult↗
PubMed1976

[Plasma renin activity and plasma aldosterone in essential hypertension: effect of age and diastolic blood pressure].

In patients with essential hypertension a gradual decrease in basal and stimulated renin secretion was found with increasing age. Stimulated plasma aldosterone decreased similarly; however, the observed changes were less pronounced. Young patients (less than 35 years) with high renin hypertension had lower diastolic blood pressure than patients with low renin hypertension in the same age group. Contrary to these findings, a markedly higher diastolic blood pressure was observed in patients over 35 years of age with high renin hypertension than in the group of patients with low renin hypertension. These results indicate that neither high nor low renin essential hypertension patients represent homogeneous groups. Furthermore, the dissociation between changes in renin activity and plasma aldosterone points to a disturbed relationship between the renin angiotensin system and aldosterone secretion in essential hypertension.

Adolescent↗
PubMed1976

Renin, aldosterone and arterial pressure responses to acute beta-adrenergic receptor blockage in hypertensive patients.

The effect of acute (intravenous) beta-adrenergic blockade with propranolol or pindolol on arterial pressure (BP), plasma renin activity (PRA), and plasma concentration of aldosterone (PA) was evaluated in 20 essential hypertensive men. BP, PRA and PA were determined during continuous recumbency over-night (8 p.m. to 6 a.m.) every 30 min. Two groups of patients were observed. Patients of group 1 exhibited a characteristic day-night rhythm of PRA with low values before midnight and large increases early in the morning. Conversely, no rhythm and very low PRA values were observed in patients of group II. BP was higher in group II than in group I. In group I following intravenous propranolol or pindolol, BP fell within minutes and levels as well as rhythms of PRA were converted to those of group II without treatment. In group II day-night profiles of PRA and BP remained unchanged. Rhythm and concentration of PA in the two groups were not influenced by either drug. In 4 patients of group I infusion of angiotensin II inhibitor did not lower BP. The observations suggest that in the two groups dissimilarities in rhythms of PRA as well as in BP responses to beta-blockade may reflect differences in neuro-adrenergic tone.

Adult↗
PubMed1976

Acute and long-term studies of the mechanisms of action of beta-blocking drugs in lowering blood pressure.

The antihypertensive effect of intravenous (acute) and oral (long-term) beta-adrenergic blockade with propranolol or pindolol was evaluated in 46 male patients with either borderline (group I; 23 patients) or sustained (group II; 23 patients) essential hypertension. Arterial pressure, plasma renin activity and plasma concentration of aldosterone were determined during continuous recumbency overnight every 30 minutes before and after treatment. Patients of group I exhibited a marked variation of their recumbent plasma renin activity with relatively low values before midnight and large increases early in the morning. In contrast, low plasma renin activity values and only minimal fluctuations in renin were observed in patients of group II. Plasma renin activity had a consistent relationship with blood pressure both after acute (r = 0.79) and long-term (r = 0.4) beta-blockade. In four patients of group I, who had high plasma renin activity and had responded to intravenous propranolol, infusion of angiotensin II inhibitor did not lower pressure. In group I following beta-blockade, day-night profiles of renin were similar to those observed in group II before treatment. Thus in this latter subgroup, low renin profiles might reflect reduced beta-adrenergic activity. Acute as well as long-term beta-blockade consistently eliminated the day-night rhythm of plasma renin activity, but it did not change rhythm of plasma concentration of aldosterone. Plasma concentration of aldosterone was lower in group II but appeared to be inappropriately high relative to renin levels. These observations suggest that in hypertensive patients classified according to blood pressure and recumbent plasma renin activity profiles a significant relationship exists between changes in plasma renin activity and arterial pressure responses. Thus, patients with high renin levels respond better to treatment than patients with low renin levels. We conclude that in the patients studied, sympathetic nervous system activity mainly determined renin levels as well as antihypertensive effectiveness of the beta-blocking drugs.

Administration, Oral↗
PubMed1976

Renin and aldosterone secretion in pheochromocytoma. Effect of chronic alpha-adrenergic receptor blockade.

Patients suffering from pheochromocytoma characterized by an exclusive or almost exclusive excess of norepinephrine showed no (one patient) or only a moderate increase (two patients) in renin and aldosterone secretion. In those three patients with concomitant distinct hypersecretion of epinephrine, renin release (and aldosterone secretion except in one patient) was markedly enhanced. Similar results were obtained in a patient with excess norepinephrine and dopamine secretion. Renin release was markedly reduced in all patients during preoperative long-term alpha-adrenergic receptor blockade. With the exception of one patient, increased renin and aldosterone secretion was abolished. The results indicate that augmentation in renin release depends on the ratio of the different catecholamines secreted by the pheochromocytoma and their different effe-tiveness in stimulating beta-adrenergic receptors. Even in the presence of excess catecholamine secretion, there is evidence that renin secretion is predominantly mediated by beta receptors rather than by renal vascular alpha-adrenergic receptors. Normalization of catecholamine-induced enhanced renin release in patients with pheochromocytoma during chronic alpha-adrenergic receptor blockade supports the assumption that (alpha-) adrenergic blocking agents inhibit renin secretion distal to their blockade of specific adrenergic receptors. However, contrary to beta-adrenergic blockade, circadian rhythm of renin release seems to remain intact during alpha-adrenergic blockade.

Adolescent↗
PubMed1976

Differential effects of acute and chronic beta-adrenoreceptor blockade on blood pressure and the renin-angiotensin-aldosterone system in essential hypertension.

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0-79) or chronic (r = 0.4) beta-receptor blockade. 4. In group 1, after beta-receptor blockade the day-night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced beta-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the beta-blocking drugs.

Adult↗
PubMed1976

Functional and metabolic studies on red blood cell sodium transport in chronic uremia.

Red blood cells from 7 out of 13 patients with chronic uremia were found to have increased intracellular concentrations of sodium associated with a reversible inhibition of ouabain-sensitive Na efflux when incubated in control plasma. Although mean Na-K-ATPase activity of RBC hemolysates was only moderately decreased (21.8 +/- 1.5 vs. 26.5 +/- 1.8 nmol Pi/mg protein/h), enzyme kinetics revealed a significant increase in KmATP values for this enzyme in uremic RBCs (1.01 +/- 0.1 vs. 0.58 +/- 0.03; p less than 0.001) which was closely correlated to serum creatinine concentration (r = 0.9034). While aerobic glycolysis was unaltered, an increase in glucose-6-phosphate dehydrogenase activity was observed, i.e. the enzyme initiating the pentose-phosphate cycle. In addition, intracellular ATP concentrations of uremic RBCs were significantly higher than ATP concentrations of control RBCs (2.13 +/- 0.22 vs. 1.32 +/- 0.06 mmol/l RBC; p less than 0.01). These data suggest that high intracellular concentrations of Na and ATP in uremic RBCs partially result from a competitive reversible inhibition of the transport ATPase by uremic toxins.

Adenosine Triphosphatases↗