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Biomedical subjects

F Krück

Publications and source records attributed to F Krück.

At least 19 recordsLinked to original sources
PubMed1979

Low urinary kallikrein excretion and elevated blood pressure normalized by orally kallikrein in essential hypertension.

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein-kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.

Administration, Oral↗
PubMed1978

[Effect of a chronic alpha adrenergic receptor blockade on basal secretion of renin in essential hypertension].

To investigate the effect of chronic alpha-adrenergic receptor blockade on renin release, plasma renin activity (PRA) was determined overnight at short intervals in 9 patients with essential hypertension before and after 7 days medication with phenoxybenzamine (20 mg orally/day). Inhibition of basal (supine) renin secretion in response to alpha-adrenergic receptor blockade was more apparent in patients with elevated PRA (n = 3) than in those with normal PRA. On the other hand, patients with low PRA (n = 2) even showed an increase in renin release. In addition, night-day variations with secretory episodes in PRA were blunted during drug administration. It is suggested that alpha-adrenergic receptor blockade inhibits renin secretion distal to its blockade of specific adrenergic receptors. However, the increase in renin release during phenoxybenzamine observed in patients with low PRA indicates that the responsiveness of renin secretion to stimulatory effects (most probably induced by the lowered blood pressure in our patients) remained intact during alpha-adrenergic receptor blockade.

Adrenergic alpha-Antagonists↗
PubMed1978

Clinical and pharmacological investigations of the new saluretic azosemid.

Ple 1053 (Azosemid) is a diuretic which resembles furosemide chemically and in its mode of action. When administered intravenously, Ple 1053 was approximately 5 times more potent on a weight basis than furosemide, its dose-response relationship was closer and the slope was steeper. After oral administration Ple 1053 and furosemide were approximately equal in potency. However, the effect of Azosemid in healthy subjects was relatively prolonged and abrupt peaks did not occur.

Administration, Oral↗
PubMed1978

Third factor and edema formation.

Urine extracts as well as plasma and urine fractions from normal persons during extracellular volume expansion and from patients with edema of different origin were tested for natriuretic (rat bioassay) and antinatriferetic (frog skin) activity. Whereas the extracts and fractions from normal persons with extracellular volume expansion proved to have a distinct natriuretic and antinatriferetic effect, no such effect was observed with urine and plasma preparations from patients with sodium retention and edema. Whether or not edema formation is mediated by a loss of natriuretic activity remains still to be clarified.

Adult↗
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↗