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  • 1
    Electronic Resource
    Electronic Resource
    Impaired renal kallikrein activity and elevated blood pressure normalized by orally applied kallikrein in essential hypertension (1980)
    Springer
    Inflammation research 10 (1980), S. 349-352 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary kallikrein excretion was significantly lower in patients with essential hypertension (0.48±0.05 EU/24 h) than in normotesive controls (1.26±0.14 EU/24 h).Oral administration of hog pancreatic kallikrein normalized decreased urinary kallikrein and reduced arterial pressure.The treatment-induced rise in uriary kallikrei was due to an enhanced release of endogenous enzyme, as was determined by radioimmunoassay. It is proposed that in the hypertensive patients the low urinary kallikrein excretion reflects a defect in renal kallikrein formation which is normalized by oral kallikrein. The hypotensive action of oral kallikrei, as well as its stimulating effects on renal kallikrein release, suggest that the kallikrein-kinin system is involved in blood pressure regulation and that imparied renal kallikrein activity may be a factor in the maintenance of essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01971438
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  • 2
    Electronic Resource
    Electronic Resource
    Hemodynamic, renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: Long-term antihypertensive effect of potassium supplementation in essential hypertension (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 352-360 
    Details
    ISSN: 1432-1440
    Keywords: Potassium intake ; Sodium intake ; Natriuresis ; Essential hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KCl/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2±3.5/99.6±1.9 mm Hg to 137.4±2.9/89.1±1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01731654
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  • 3
    Electronic Resource
    Electronic Resource
    Vorgetäuschte Hyponatriämie bei malignen Paraproteinämien (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 875-880 
    Details
    ISSN: 1432-1440
    Keywords: Multiple myeloma ; Viscosity ; Water of serum ; Hyponatremia ; Maligne Paraproteinämie ; Viskosität ; Serumwassergehalt ; Hyponatriämie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In der vorliegenden Arbeit wurden Häufigkeit und Ursachen von Elektrolytstörungen bei malignen Paraproteinämien untersucht. 7 von 15 Patienten wiesen z.T. extreme (bis 93 mmol/l), jedoch immer symptomlose Hyponatriämien auf. Gegenüber einer Kontrollgruppe war die Serumviskosität signifikant erhöht. Zwischen der Serumnatriumkonzentration und der Viskosität bestand eine hochsignifikante negative Korrelation. Die Kontrolle der Serumnatriumwerte durch viskositätsunabhängige Meßsysteme erwies, daß die beobachteten Hyponatriämien durch Verdünnungsfehler in dem von uns routinemäßig verwandten viskositätsabhängigen Analyseverfahren bedingt waren. Die Erniedrigung des Serumwasseranteils trug in geringem Maße ebenfalls zur Entstehung einer Hyponatriämie bei. Bei der durch Paraproteine hervorgerufenen Serumnatriumverminderung handelt es sich nach unseren Befunden um eine vorgetäuschte und nicht behandlungsbedürftige Hyponatriämie.
    Notes: Summary In the present study frequency and mechanisms of alterations in serum electrolytes in multiple myeloma were investigated. Asymptomatic hyponatremia (up to 93 mmol/l) was present in 7 of 15 patients. Water of serum was significantly lower, viscosity of serum significantly raised as compared to healthy controls. A highly significant negative correlation between sodium concentration and viscosity was found. By measuring serum sodium concentration with viscosity independent dilution systems it could be proved that in each case the observed hyponatremia was caused by flaws in our routinely used viscosity dependent dilution method. The decrease in water of serum contributed only little to the development of hyponatremia. It is concluded that the decrease in serum sodium concentration in multiple myeloma is nothing else than a feigned hyponatremia which needs no therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476999
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  • 4
    Electronic Resource
    Electronic Resource
    Converting enzyme activity and essential hypertension (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 377-378 
    Details
    ISSN: 1432-1440
    Keywords: Angiotensin converting enzyme ; Essential hypertension ; Plasma renin activity ; Angiotensin II ; Captopril
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serum ACE-activity was studied in 27 young patients with uncomplicated essential hypertension. The possible importance of an increase in ACE for the pathogenesis of essential hypertension was evaluated by comparing the ACE levels to PRA, the plasma concentrations of angiotensin II and to the blood pressure lowering effect of captopril. Mean ACE-activity was slightly but significantly elevated in the hypertensive patients when compared to 28 normotensive control subjects. ACE-activity was not correlated to PRA, angiotensin II or the decrease in blood pressure following captopril. It is concluded that the increase in ACE-activity in essential hypertension is not of pathophysiological or clinical significance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01485031
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence for participation of kinins in the antihypertensive effect of converting enzyme inhibition (1981)
    Springer
    Journal of molecular medicine 59 (1981), S. 69-74 
    Details
    ISSN: 1432-1440
    Keywords: Angiotensin-converting-enzyme-inhibition ; Kallikrein-blockade ; Kinins ; Essential hypertension ; Angiotensin-Converting-Enzym-Hemmung ; Kallikrein-Blockade ; Kinine ; Essentielle Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei essentiellen Hypertonikern mit niedriger und normaler Plasmareninaktivität, nicht dagegen bei Patienten mit hohen Reninwerten, konnte der akute antihypertensive Effekt einer Angiotensin-Converting-Enzym-(ACE) Blockade mit Captopril durch eine Aprotinin-induzierte Kallikreinblockade vollständig verhindert werden. Nach chronischer ACE-Hemmung ließ sich die Blutdrucksenkung nur zum Teil durch Aprotinin aufheben. Die Ergebnisse weisen darauf hin, daß bei essentieller Hypertension mit normaler und niedriger Reninaktivität der blutdrucksenkende Effekt einer akuten ACE-Hemmung im wesentlichen Folge einer Kinin-Akkumulation ist. Dagegen scheint bei Patienten mit hoher Reninaktivität eine Abnahme der Angiotensin II-Konzentration für die antihypertensive Wirkung von Captopril verantwortlich zu sein. Der pressorische Effekt von Aprotinin bei Patienten unter Langzeittherapie mit Captopril weist darauf hin, daß Kinine auch für die unter chronischer ACE-Hemmung auftretende Blutdrucksenkung mitverantwortlich sind. Die Beobachtung, daß ACE-Inhibition und Kallikrein-Blockade voraussagbare und gegensinnige Effekte auf den Blutdruck hervorrufen, läßt eine Beteiligung des Kallikrein-Kinin-Systems an der Kontrolle des Gefäßtonus bei essentieller Hypertension vermuten.
    Notes: Summary In low- and normal- renin hypertensive patients, but not in high-renin patients, the acute antihypertensive response to the angiotensin-converting enzyme (ACE) inhibitor captopril was completely blocked by aprotinin-induced kallikrein inhibition. Blood pressure reduction with long-term ACE inhibition could be overcome only in part by aprotinin. It is proposed that in low- and normal-renin hypertension the vasodepressor effect of acute ACE inhibition is mainly due to kinin accumulation. Conversely, in high-renin patients a fall in angiotensin II concentration accounts for the hypotensive response to captopril. From the pressor effect of aprotinin in chronically captopril treated patients it appears that kinins are also involved in the blood pressure reduction with long-term ACE inhibition. The finding that ACE inhibition and kallikrein blockade produced predictable and opposite effects on blood pressure suggests broad participation of changes in depressor kinin production in the control of vascular tone in essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477285
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  • 6
    Electronic Resource
    Electronic Resource
    Interactions of diuretics with the renal kallikrein-kinin and prostaglandin systems (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 1223-1228 
    Details
    ISSN: 1432-1440
    Keywords: Renal kallikrein-kinin system ; Renal prostaglandins ; Action of diuretics ; Renin release ; Essential hypertension ; Renales Kallikrein-Kinin System ; Renale Prostaglandine ; Diuretikawirkung ; Reninfreisetzung ; Essentielle Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das renale Kallikrein-Kinin System ist möglicherweise am diuretischen, natriuretischen und antihypertensiven Effekt von Diuretika beteiligt. In der vorliegenden Studie wurde deshalb an Patienten mit essentieller Hypertension der Einfluß von Hydrochlorothiazid auf das Blutdruckverhalten und die renale Kallikreinaktivität untersucht. Zusätzlich wurde bei Normalpersonen die Beeinflußbarkeit der renalen Furosemidwirkung durch Kallikreinblockade und Hemmung der Prostaglandinsynthese gemessen. Hydrochlorothiazidbehandlung normalisierte die erniedrigte Kallikreinausscheidung hypertensiver Patienten. Der Abfall des mittleren arteriellen Drucks korrelierte mit dem Anstieg der Kallikreinausscheidung. Bei den normotensiven Probanden wurden die akuten Furosemid-induzierten Änderungen von Diurese, Natriurese, glomerulärer Filtration und renalem Plasmafluß durch Kallikreinhemmung mit Aprotinin nicht beeinflußt. Indomethacin hingegen verminderte den diuretischen und natriuretischen Effekt von Furosemid. Die Plasmareninaktivität wurde durch die Kombination von Indomethacin und Aprotinin deutlicher supprimiert als durch Indomethacin allein. Dies könnte auf eine Beteiligung von Kallikrein an der Reninfreisetzung hinweisen. Eine Aktivitätszunahme des renalen Kallikrein-Kinin Systems könnte zum antihypertensiven Effekt der Thiaziddiuretika beitragen. Andererseits scheint dieses System an den akuten renalen Wirkungen von Furosemid nicht beteiligt zu sein.
    Notes: Summary The renal kallikrein-kinin system may participate in the diuretic, natriuretic and antihypertensive effect of diuretics. This possibility was investigated by studying the influence of hydrochlorothiazide on blood pressure and urinary kallikrein excretion in patients with essential hypertension. Furthermore, the effect of kallikrein-blockade and prostaglandin-synthesis inhibition on the acute furosemide-induced changes of diuresis, natriuresis, GFR and renal plasma flow were studied in normotensive subjects. Thiazide treatment normalized the reduced kallikrein excretion of the hypertensive patients. The fall in mean arterial blood pressure was significantly correlated with the increase in urinary kallikrein excretion. In the normotensive subjects aprotinin-induced kallikrein inhibition failed to alter the acute response to furosemide, whereas indomethacin attenuated the diuretic and natriuretic effect of furosemide. The combination of indomethacin and aprotinin had a greater suppressive effect on plasma renin activity than indomethacin alone, suggesting a participation of kallikrein in renin release. An increase in the activity of the renal kallikreinkinin system may contribute to the long-term antihypertensive effect of thiazide diuretics but it does not seem to be involved in the acute renal responses to furosemide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01716727
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  • 7
    Electronic Resource
    Electronic Resource
    Decreased urinary kallikrein activity and elevated blood pressure normalized by orally applied kallikrein in essential hypertension (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 37-42 
    Details
    ISSN: 1432-1440
    Keywords: Urin-Kallikrein ; Essentielle Hypertension ; Orale Kallikrein-Therapie ; Urinary kallikrein ; Essential hypertension ; Oral kallikrein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Urinary kallikrein excretion was significantly lower in patients with essential hypertension (0.48±0.05 EU/24 h) than in normotensive controls (1.26±0.14 EU/24 h). Oral administration of hog pancreatic kallikrein normalized decreased urinary kallikrein and reduced arterial pressure. The treatment-induced rise in urinary kallikrein was due to an enhanced release of endogenous enzyme, as was determined by radioimmunoassay. It is proposed that in the hypertensive patients the low urinary kallikrein excretion reflects a defect in renal kallikrein formation which is normalized by oral kallikrein. The hypotensive action of oral kallikrein as well as its stimulating effects on renal kallikrein release suggest that the kallikrein-kinin system is involved in blood pressure regulation and that impaired renal kallikrein activity may be a factor in the maintenance of essential hypertension.
    Notes: Zusammenfassung Patienten mit essentieller Hypertension schieden signifikant weniger Kallikrein im Urin (0,48±0,05 EU/24 h) aus als normotensive Kontrollpersonen (1,26±0,14 EU/24 h). Eine 8wöchige Therapie mit oralem Schweinepankreas-Kallikrein normalisierte die verminderte Kallikreinausscheidung und führte zu einer signifikanten Blutdrucksenkung. Der durch die Behandlung induzierte Anstieg der renalen Kallikreinexkretion war Folge einer vermehrten endogenen Freisetzung des Enzyms, wie mit Hilfe eines spezifischen Radioimmunoassays festgestellt werden konnte. Es ist denkbar, daß die bei den hypertensiven Patienten nachgewiesene verminderte Kallikreinausscheidung einen Defekt in der Bildung von endogenem renalen Kallikrein reflektiert, der durch die orale Kallikrein-Therapie behoben wurde. Die blutdrucksenkende Wirkung von oralem Kallikrein sowie der stimulierende Effekt des Enzyms auf die renale Kallikreinfreisetzung lassen vermuten, daß das Kallikrein-Kinin System an der Blutdruckregulation beteiligt ist, und daß eine verminderte renale Kallikrein-Aktivität ein Faktor bei der Aufrechterhaltung der essentiellen Hypertension darstellen könnte.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477142
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of the new angiotensin-converting enzyme inhibitor, ramipril, in patients with essential hypertension (1986)
    Springer
    Journal of molecular medicine 64 (1986), S. 558-562 
    Details
    ISSN: 1432-1440
    Keywords: Angiotensin-converting enzyme inhibition ; Ramipril ; Essential hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The antihypertensive and hormonal effects of the new angiotensin-converting enzyme (ACE) inhibitor, ramipril, were assessed by means of a single-blind trial in ten unselected patients with mild-to-moderate essential hypertension. After a 2-week period on placebo, 5 mg ramipril was administered once daily for 2 weeks. Blood pressure returned to normal in five patients and decreased in the remaining patients, without significant changes in heart rate or orthostatic hypotension. A fall in blood pressure was apparent within 1–2 h of the first dose; the maximum decrease was reached at 4–6 h and a fall in pressure was still detectable after 24 h. At 24 h post dose angiotensin-converting enzyme activity was suppressed to 40% of the baseline. Blood pressures for the 10 h interval post dosing showed smooth through-the-day control with minimal peak/trough difference in lowering effect. The magnitude of the blood pressure decrement achieved with the inhibitor did not correlate with baseline renin levels or the rise in renin following treatment. No side-effects were noted during the 2-week observation period. The study demonstrates that ramipril, given in a once-daily regimen over a period of 2 weeks, is well tolerated and provides smooth and effective blood pressure control throughout the 24-h interval between doses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01735319
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  • 9
    Electronic Resource
    Electronic Resource
    Computed tomographic high-attenuation mediastinal lymph nodes after aluminum exposition (2000)
    Springer
    European radiology 10 (2000), S. 1945-1946 
    Details
    ISSN: 1432-1084
    Keywords: Key words: Mediastinal lymph nodes – CT density – Aluminosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. A case with increased computed tomographic densities of mediastinal lymph nodes with histologically proven aluminum storage is presented. We suggest consideration of aluminosis as differential diagnosis in patients with increased native CT densities beyond 50 HU.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003300000534
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  • 10
    Electronic Resource
    Electronic Resource
    Decreasing diffusion limitation on exercise in lower-graded interstitial lung disease (1998)
    Springer
    Pflügers Archiv 435 (1998), S. 762-766 
    Details
    ISSN: 1432-2013
    Keywords: Key words Isotopic analysis ; Overall fractionation factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In this study we investigated the contribution of diffusion limitation to the exercise-induced hypoxaemia in interstitial lung disease (ILD). We applied isotopic analysis to the composition of the stable isotopic oxygen molecules 16O2 and 16O18O in expiratory gas mixtures obtained from six ILD patients and six healthy subjects at rest and during ergometer work (60 W). The changes in the 16O18O/16O2 ratios were interpreted by using the overall fractionation factor of respiration (α O) which would be increased towards 1.03 on increasing diffusion limitation. In addition, the O2 partial pressures of alveolar gas and arterial blood (P AO2, P aO2) were determined. In the patients, α O was significantly reduced from 1.0066 ± 0.0004 (mean ± SD) at rest to 1.0035 ± 0.0004 during exercise and in the healthy subjects from 1.0072 ± 0.0008 to 1.0044 ± 0.0004. Furthermore, the exercise-induced reduction of P aO2 (from 77 to 69 mmHg) was due to a drop of alveolar PO2 found in each patient, whereas in each healthy subject P aO2 was increased on exercise. On the basis of a resistance model we conclude that the patients’ data were inconsistent with increasing diffusion limitation but showed an increasing impairment of O2 transport by ventilation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050581
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