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  • 1
    ISSN: 1432-1440
    Keywords: Aldosteron-Exkretion bei essentieller Hypertonie ; “Low-renin”-Hypertonie ; Spironolacton-Therapie ; Salzbelastung ; Aldosterone excretion in essential hypertension ; Low-renin essential hypertension ; Spironolactone response in essential hypertension ; Sodium loading in essential hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary In patients with grade I and II essential hypertension studied during sodium loading (Na+ excretion above 175 meq·d−1) we found a bimodal behaviour of aldosterone excretion and could distinguish two groups of patients: In the major part of essential hypertensives sodium loading led to a suppression of aldosterone excretion below 6 µg·d−1, which is the highest control value during sodium loading, with an average of 2.7±1.4 (SD) µg·d−1. Aldosterone excretion in a second group of patients was not suppressible below 6 µg·d−1 despite forced sodium loading; it resulted in an average value of 10.0±3.0 (SD) µg·d−1. During sodium deprivation or free sodium intake, aldosterone excretion in the first group of patients followed exactly the behaviour of normotensive controls, while in the second group of essential hypertensives the correlation of aldosterone excretion and log. Na excretion or log. Na+/K+ ratio in 24 h urine (r=−0.59) was far below the control value ofr=−0.87. Serum potassium concentration during sodium loading was significantly (p〈0.001) lower (3.81±0.44 meq·l−1) in the essential hypertensives with non-suppressible aldosterone excretion compared to those with suppressible aldosterone excretion (4.26±0.37 meq·l−1). The blood pressure response to treatment with 200 mg spironolactone·d−1 was better (p〈0.05) in patients with non-suppressible aldosterone excretion compared to the essential hypertensives with normal aldosterone regulation. The plasma renin activity of both groups of patients was not significantly different, however, a tendency prevailed towards lower PRA-values in the patient group with non-suppressible aldosterone excretion during sodium loading.
    Notes: Zusammenfassung Bei Patienten mit essentieller Hypertonie Grad I und II fand sich unter Salzbelastungsbedingungen (Natrium-Exkretion über 175 mval·d−1) eine bimodale Verteilung der Aldosteron-Exkretion, aufgrund welcher zwei Patientengruppen unterschieden wurden: Beim größeren Teil der Patienten mit essentieller Hypertonie führte die Salzbelastung zu einer Suppression der Aldosteron-Exkretion unter 6 µ·d−1, dem höchsten Kontrollwert unter Salzbelastung, im Durchschnitt zu 2,7±1,4 (SD) µg·d−1. Trotz ausgeprägter Salzbelastung über 6 Tage war die Aldosteron-Exkretion bei einer zweiten Gruppe nicht unter 6 µg·d−1 supprimierbar mit einer durchschnittlichen Aldosteron-Exkretion von 10,0±3,0 (SD) µg·d−1. Unter Salzentzug, freier Salzzufuhr oder Salzbelastung war die Aldosteron-Exkretion der ersten Gruppe der der Kontrollpersonen vergleichbar, während bei der zweiten Gruppe der essentiellen Hypertoniker die Korrelation zwischen Aldosteron-Exkretion und Log Natrium-Exkretion oder Log Natrium/Kalium-Quotient im 24 h-Urin (r=−0,59) deutlich unter der der Kontrollpersonen (r=−0.87) lag. Die Serum-Kalium-Konzentration unter Salzbelastung der zweiten Hypertonikergruppe mit nicht supprimierbarer Aldosteron-Exkretion war signifikant (p〈0,001) niedriger (3,81±0,44 mval·l−1) als bei den übrigen Hypertonikern mit supprimierbarer Aldosteron-Exkretion (4,26±0,37 mval·l−1). Die Blutdrucksenkung unter 200 mg Spironolacton täglich war bei den Patienten mit nicht supprimierbarer Aldosteron-Exkretion signifikant (p〈0,05) besser als beim Rest der Patienten. Die Plasmareninaktivität beider Gruppen war noch nicht signifikant unterschiedlich, zeigt jedoch eine Tendenz zu niedrigeren Werten in der Gruppe mit nicht supprimierbarer Aldosteron-Exkretion.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 313 (1980), S. 155-157 
    ISSN: 1432-1912
    Keywords: Spontaneosly hypertensive rats ; Urinary kallikrein ; Sympathetic activity ; 6-Hydroxydopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). “Chemical sympathectomy”, induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.
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  • 3
    ISSN: 1432-1440
    Keywords: Saralasin ; Angiotensin II ; Renin ; Rezeptoren ; Blutdruck ; Saralasin ; Angiotensin II ; Renin ; Receptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 µg/kg × min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 µg/kg × min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 µg/kg × min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypoor hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.
    Notes: Zusammenfassung Ein verbesserter Test zur Diagnose Renin-abhängiger Bluthochdruckformen mit dem Angiotensin II Rezeptor Antagonisten Saralasin wurde in hypertensiven Ratten, sowie in normotensiven und hypertensiven Patienten geprüft. Kumulative intravenöse Dosen, beginnend mit 0,01 µg/kg × min Saralasin wurde alle 15 Minuten um das zehnfache gesteigert. Ein signifikanter Blutdruckabfall bei der Dosis von 0,1 µg/kg × min wurde bei Ratten mit renaler Hypertonie, bei Patienten mit renaler Hypertonie und bei Patienten nach Diuretika-Vorbehandlung gefunden. Plasmaspiegel von Angiotensin I, Angiotensin II, Plasma Renin Aktivität und Saralasin wurden gemessen. Bei der niedrigsten Infusionsrate von 0,01 µg/kg × min waren die Saralasin-Konzentrationen im Plasma 40fach höher als die Plasma Angiotensin II-Konzentrationen. Der Blutdruckabfall erfolgte bei niedrigeren Dosen von Saralasin als der Anstieg von Plasma-Renin als Folge einer Hemmung des feedbacks der Reninsekretion. Die Ergebnisse zeigen, daß Komplikationen wie schwerwiegende Blutdruckanstiege und -abfälle bei schrittweiser Erhöhung der Saralasin-Infusionsrate vermieden werden können; gleichzeitig wird die diagnostische Zuverlässigkeit des Tests erhöht. Der geringe Angiotensin-ähnliche, blutdrucksteigernde Effekt von Saralasin bei Patienten mit niedrigem Renin wird als Vorteil ausgenutzt und erhöht den Unterschied der Blutdruckantwort bei Patienten mit hohem Plasma-Renin und Blutdruckabfall nach Saralasin-Infusion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: Adenosine Triphosphatase ; Erythrocytes ; Hypertension ; Adenosintriphosphatase ; Erythrozyten ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Erhöhte intraerythrozytäre Natriumkonzentration sowie ein beschleunigter Einstrom von Na22 in die Erythrozyten von Patienten mit essentieller Hypertonie hatten zu der Vermutung geführt, daß dieser Erkrankung eine Transportstörung für Natrium an der Zellmembran zugrunde liegen könnte. Wir fanden bei 27 Patienten mit essentieller Hypertonie eine signifikante Erhöhung der durch Strophantin hemmbaren Na-K-ATP'ase an Erythrozytenghosts im Vergleich zu 32 gesunden Kontrollpersonen. Die Na-K-insensible Mg-APT'ase was dagegen bei beiden Gruppen gleich. Dieser Befund ist mit einer Aktivierung des membrangebundenen Natriumtransportes an Erythrozyten von essentiellen Hypertonikern vereinbar.
    Notes: Summary Increased sodium concentration and high influx of Na22 are reported in erythrocytes of patients with essential hypertension. It was speculated, that these findings are due to a disturbed transport for sodium across red cell membranes. We found a significantly increased activity of the ouabainsensitive Na-K-ATP'ase in red cell ghosts of 27 patients with essential hypertension compaired with 32 normotensive controls. There existed no difference in Mg-ATP'aseactivity between the two groups. These findings suggest an increased activity of the Na-pump in red cell membranes of patients with essential hypertension.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1440
    Keywords: Human atrial natriuretic peptide ; Sodium ; Primary hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma levels of α-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〈0.05) and with urinary aldosterone during unrestricted diet (r=0.536,P〈0.05). There was an inverse correlation between plasma ANP levels and plasma renin concentration during low and high sodium intake (r=−0.469,r=−0.496,P〈0.05). These studies demonstrate raised circulating plasma ANP levels in patients with essential hypertension. The modulation of ANP by different sodium intake and by upright posture is maintained similar to the changes in plasma ANP in normotensive controls. Raised ANP levels in the hypertensives are correlated with low renin secretion and high aldosterone excretion. High ANP levels, therefore, might indicate sodium retention in essential hypertension.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 67 (1989), S. 1085-1095 
    ISSN: 1432-1440
    Keywords: Bradykinin ; Blood pressure ; Prostaglandins ; Kallikrein-kinin system ; Pulmonary circulation ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In our studies we investigated the vasodepressor effects of bradykinin in vivo in normotensive and hypertensive subjects. Bradykinin was injected intravenously and intraarterially (40–6050 pM/kg) respectively was infused intraarterially (40–6050 pM/kg/min). The investigations were performed in 21 normotensives and 15 hypertensives. Bradykinin injections were performed after the following pharmacological interventions: salt restriction (10 mmol Na/d), salt loading (300 mmol Na/d), captopril (50 mg), ramipril (5 mg), lisinopril (20 mg), ketotifen (2×1 mg), indomethacin (2×50 mg), and propranolol (80 mg). The results show that bradykinin lowers blood pressure dose related by marked reduction in peripheral vascular resistance. The blood pressure reduction was strongly correlated with the increase in kinin concentration. This effect of bradykinin appears to be independent of changes in sodium metabolism, of betaadrenoceptors, of histamin-1 receptors, and of prostaglandins. ACE-inhibitors potentiate the blood pressure lowering effect of bradykinin about 20- to 50-fold. In case of an intraarterial injection of bradykin in only 2–5% of the intravenously used dose of bradykinin are needed to produce an identical fall in blood pressure. From this experiments a pulmonary clearance rate of bradykinin over 95% can be calculated. In the pulmonary arteries bradykinin has no effect on the vascular resistance. In patients suffering from primary or renovascular hypertension the blood pressure response to bradykinin was enhanced. The bradykinin potentiating effect of the ACE-inhibitors was not altered in the hypertensives. In patients suffering from borderline hypertension or primary hyperaldosteronism bradykinin developed the same blood pressure lowering effect as in the normotensives.
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  • 7
    ISSN: 1432-1440
    Keywords: Furosemide ; Hydrochlorothiazide ; Diuresis ; Kallikrein ; Kinins ; ACE-inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In healthy volunteers the acute effect of furosemide (40 mg i.v.) and hydrochlorothiazide (100 mg p.o.) on diuresis, natriuresis and renal kallikrein and kinin excretion was investigated. 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 probably due to a diminished (about 50%) proximal-tubular secretion of furosemide. Captopril did not alter significantly the furosemide induced changes in urinary kallikrein and kinin excretion. After captopril there was a clear 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. Other ACE-inhibitors like ramipril (5 mg) or enalapril (20 mg) did not influence the stimulatory effects of furosemide on diuresis or kallikrein-kinin excretion. Ramipril at a dose of 10 mg, however, enhanced the initial diuretic effect of furosemide by increased furosemide secretion and increased relative sodium excretion. Hydrochlorothiazide induced a prolonged diuresis which was not changed by either captopril or ramipril. Urinary kallikrein excretion was not stimulated by hydrochlorothiazide. Our results show an important drug interference between captopril and furosemide, which is independent of ACE-inhibition and probably only due to an interference in proximal-tubular secretion of both drugs. Between captopril and hydrochlorothiazide no such interaction could be observed.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1440
    Keywords: Renovascular hypertension ; Saralasin-infusion-Test ; Renal venous renin-determination ; 131J-Hippuric-acid-clearance-Test ; Renovaskuläre Hypertonie ; Saralasin-Infusions-Test ; Nierenvenenrenin ; 131Jod-Hippuran-Clearance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei Patienten mit einseitiger Nierenerkrankung und Hypertonie, vorwiegend einseitigen renovaskulären Erkrankungen, wurden der Nierenvenenreninquotient, die seitendifferente131Jod-Hippuran-Clearance und der Saralasin-Test untersucht und in ihrer Aussagefähigkeit verglichen: Dabei zeigte sich bei allen Patienten eine statistisch signifikante Zunahme des Nierenvenenreninquotienten mit zunehmendem Seitenunterschied des mittels131Jod-Hippuran-Clearance gemessenen renalen Plasmastroms. Der Nierenvenenreninquotient ist also nicht nur Ausdruck einer seitenunterschiedlichen Reninsekretion, sondern auch modifiziert durch die seitenunterschiedliche Durchblutung. Auch bei Angiotensin-unabhängigen Hypertonien bei einseitiger Nierenerkrankung ergaben sich bei starker Durchblutungsdifferenz beider Nieren Nierenvenenreninquotienten bis 2,0, ohne daß diese auf Hochdruckwirksamkeit hinwiesen. Bei geringerer Durchblutungsdifferenz beider Nieren zeigten dagegen schon niedrigere Nierenvenenreninquotienten eine einseitige Reninsekretion mit Hochdruckwirkung an. Nierenvenenreninquotienten im Grenzbereich zwischen 1,5 und 2,5 sollten deshalb nur unter gleichzeitiger Berücksichtigung der seitenunterschiedlichen Nierendurchblutung interpretiert werden. Patienten, bei denen auch unter Berücksichtigung der seitendifferenten Nierendurchblutung im Vergleich zur Angiotensin-unabhängigen Hypertonikergruppe erhöhte Nierenvenenreninquotienten gemessen wurden, zeigten im Saralasin-Infusions-Test ohne Ausnahme einen signifikanten Blutdruckabfall.
    Notes: Summary In patients with unilateral vascular kidney disease and hypertension, ratio of renal-vein-renin was compared with131I-Hippuric-acid clearance and change in blood pressure during Saralasininfusion. The ratio of renal-vein-renin was positively correlated with the ratio in renal plasma flow between the kidneys in all patients studied. The ratio of renins therefore is a result of two factors: The difference in renin secretion and the difference in blood flow in the two kidneys. In patients with angiotensin independent hypertension renin-ratios up to 2.0 were found without relevance to elevated blood pressure. When the difference in renal blood flow between both kidneys was small, even a slight difference in renal vein renin indicated hypertension related to increased renin secretion. Renin-ratios in the critical range between 1.5 and 2.5 should only be interpreted in respect to a similar ratio in renal blood flow.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 36 (1980), S. 865-866 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Rat urine, even at a 1∶10 final dilution in Tyrode's solution, stimulates contraction of the ureteral musculature in vitro. This effect can be ascribed to the presence of kallikrein or a kallikrein-like enzyme in urine. Isometric contractions of ureters were prevented by previous addition of aprotinin to the organ bath. Urine also lost its activity after inactivation of enzymes by heat or acid treatment.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 38 (1982), S. 941-943 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Adrenalectomy reduces, and sodium depletion increases, both the daily urinary excretion of kallikrein and the kallikrein activity in the renal cortex. These 2 variables were found to correlate significantly in normal, sodium depleted and adrenalectomized rats, thus supporting the view that kallikrein excretion reflects the activity of the enzyme in the kidney.
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