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Dive into the research topics where Walter H. Ziegler is active.

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Featured researches published by Walter H. Ziegler.


Clinical Pharmacology & Therapeutics | 1987

Cardiovascular effects of verapamil in essential hypertension.

Städler P; Luca Leonardi; Walter Riesen; Walter H. Ziegler; Claudio Marone; Carlo Beretta-Piccoli

Calcium antagonists may affect the regulation of body sodium and adrenergic‐dependent mechanisms. Exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, pressor responsiveness to norepinephrine, heart rate responses to isoproterenol, and lipid metabolism were studied in 15 patients with essential hypertension after 8 weeks of treatment with verapamil (348 ± 68 (SD) mg/day). Supine blood pressure decreased from 153/103 ± 19/12 mm Hg to 140/95 ± 14/12 mm Hg (P < 0.01). Exchangeable sodium, blood volume, plasma norepinephrine, renin and aldosterone, serum total cholesterol, the lipoprotein fractions, and apoprotein levels were unchanged. The norepinephrine pressor and the isoproterenol chronotropic doses tended to increase, whereas the dose‐response curve of blood pressure related to plasma norepinephrine was significantly displaced to the right (F = 5.34; P < 0.05). The antihypertensive effect of verapamil is associated with a decreased cardiovascular pressor responsiveness to norepinephrine without changes in endogenous noradrenergic activity. Moreover, verapamil does not modify the sodium/fluid volume state, the activity of the renin‐angiotensin aldosterone axis, or lipid metabolism.


Journal of Molecular Medicine | 1981

Relationship between plasma catecholamines and urinary catecholamine excretion rates in normal subjects and certain diseased states

Helmut Schiffl; Peter Weidmann; Andreas Meier; Walter H. Ziegler

SummaryRelationships between plasma norepinephrine (PNE) or epinephrine (PE) and urinary norepinephrine (UNE) or epinephrine (UE) excretion rates were studied in 37 normal subjects, 39 patients with benign essential hypertension, 23 with unilateral renal hypertension, and 20 with bilateral renal disease (serum creatinine 2.3±2.6 mg/100 ml). Measurements were also performed after 6 weeks of diuretic treatment in 27 normal subjects and all patients with essential hypertension. In the untreated state, PNE and UNE values were generally normal in essential or unilateral renal hypertension; PNE tended to be decreased in diabetics and increased in bilateral renal disease. Diuretic treatment caused a tendency for slightly increased PNE and UNE. UNE correlated significantly with supine PNE or upright PNE or their mean value, and this relationship appeared to be comparable between untreated normal subjects and the various patient groups, except for a tendency for slightly higher PNE at given UNE values in bilateral renal disease. No significant correlations between UE and PE were apparent in the normal subjects or patient groups.These data demonstrate a dissociation of UE from PE levels. In contrast, UNE is an approximative index of PNE, and this relationship appeared to be generally unaltered in essential or unilateral renal hypertension. In patients with bilateral renal disease the slight shift of this relationship indicates that consideration of renal function is necessary for interpretation of NE levels.ZusammenfassungBei 37 Normalpersonen, 39 Patienten mit benigner essentieller Hypertonie, 23 Patienten mit unilateraler renaler Hypertonie und 20 Patienten mit beidseitiger Nierenerkrankung (Serumkreatinin 2,3±2,6 mg/100 ml) wurde die Beziehung zwischen Plasma-Noradrenalin (PNA) oder -Adrenalin (PA) und 24-h-Urin-Noradrenalin (UNA) oder-Adrenalin (UA) untersucht. Bei 27 Normalpersonen und bei allen Patienten mit essentieller Hypertonie wurden die Bestimmungen nach sechs Wochen Diuretika-Behandlung wiederholt. Im unbehandelten Zustand waren bei essentieller oder einseitiger renaler Hypertonie sowohl PNA wie auch UNA im Normbereich; Diabetiker zeigten eine Tendenz zu leicht erniedrigtem, Patienten mit Niereninsuffizienz zu leicht erhöhtem PNA. Diuretika bewirkten nur eine geringfügige Zunahme von PNA und UNA. UNA korrelierte signifikant mit PNA Konzentrationen. Diese Beziehung war bei Normalpersonen und den verschiedenen Patientengruppen vergleichbar, mit Ausnahme der Niereninsuffizienten. Letztere zeigten für ein gegebenes UNA ein leicht erhöhtes PNA. Zwischen PA und UA fand sich weder bei Normalpersonen noch bei den Patientengruppen eine signifikante Beziehung.Diese Befunde weisen auf eine Dissoziation von PA und UA hin. Im Gegensatz dazu scheint UNA ein approximatives Maß für PNA darzustellen. Während diese Beziehung bei essentieller und einseitiger renaler Hypertonie unverändert ist, weist eine Abweichung bei Patienten mit leichter Niereninsuffizienz darauf hin, daß für eine Beurteilung von Plasma-Noradrenalin-Spiegeln auch die Nierenfunktion in Betracht gezogen werden sollte.


Journal of Hypertension | 1988

Mechanism of action of ketanserin: studies on cardiovascular reactivity in essential and diabetes-associated hypertension.

Marco Waser; Walter H. Ziegler; Carlo Beretta-Piccoli

Ketanserin is a selective serotonin-S2 receptor antagonist with alpha 1-adrenoceptor inhibiting activity. The relative contribution of the latter mechanism to antihypertensive efficacy was studied in a group comprising eight normal subjects, 10 patients with essential hypertension and eight diabetics with arterial hypertension. Ketanserin treatment administered over a period of 8 weeks, decreased arterial pressure in patients with essential hypertension and, to a lesser extent, in diabetics, but not in normal subjects. In all three groups, exchangeable sodium, blood volume, the activity of the adrenergic and renin-angiotensin-aldosterone systems and the pressor responsiveness to norepinephrine (NE) or angiotensin II (Ang II) were unaltered, while the pressor reactivity to phenylephrine showed a significant decrease in normal subjects only. This suggests that the antihypertensive mechanism of ketanserin does not involve a modification of the physiological relationship between endogenous noradrenergic and pressor reactivity to NE. Moreover, ketanserin does not interfere with Ang II-dependent mechanisms.


Journal of Hypertension | 1990

Cardiovascular regulation during angiotensin converting enzyme inhibition with captopril in diabetes-associated hypertension

Carlo Beretta-Piccoli; Walter H. Ziegler; Pietro Antonini; Michaela Bernasconi-Zapf; Helene Kressebuch; Fabio Pianezzi

Diabetes-associated hypertension is accompanied by high levels of body sodium and cardiovascular hyper-reactivity to noradrenaline. Captopril, a promising drug for the treatment of hypertension in diabetics, may influence sodium metabolism and adrenergic pathways. This possibility was investigated in 11 patients with non-azotaemic diabetes mellitus and hypertension, studied after a 3-week placebo phase and after an 8-week phase of captopril treatment (50-100 mg/day). Blood pressure, exchangeable body sodium, blood volume, plasma renin activity, angiotensin II (Ang II), aldosterone, catecholamine levels and the pressor reactivity to infused Ang II or noradrenaline were measured. Compared with placebo, captopril caused a significant decrease in arterial pressure and stimulation of plasma renin activity. Exchangeable sodium, blood volume, plasma Ang II, aldosterone, noradrenaline and adrenaline levels, the pressor and aldosterone responsiveness to infused Ang II and the pressor response to infused noradrenaline (alone or combined with atropine) were not modified. These findings suggest that in hypertensive diabetics angiotensin converting enzyme inhibition causes a marked decrease in blood pressure. The mechanism of action is unrelated to changes in body sodium or noradrenergic-dependent pressor reactivity. In the stable phase of therapy, Ang II-dependent pathways are left unaltered when captopril is administered twice a day.


The Journal of Clinical Endocrinology and Metabolism | 1979

Increased ratio between changes in blood pressure and plasma norepinephrine in essential hypertension.

Peter Weidmann; Gerald W. Keusch; Josef Flammer; Walter H. Ziegler; F. C. Reubi


The Journal of Clinical Endocrinology and Metabolism | 1980

Plasma Prolactin in Normal and Hypertensive Subjects: Relationships with Age, Posture, Blood Pressure, Catecholamines, and Renin

Andreas Meier; Peter Weidmann; Ulrike Hennes; Walter H. Ziegler


The Journal of Clinical Endocrinology and Metabolism | 1980

Effects of Physiological Infusion of Epinephrine in Normal Humans: Relationship between the Metabolic Response and β-Adrenergic Binding

Vijay Soman; Harry Shamoon; Robert S. Sherwin; Walter H. Ziegler


Journal of Molecular Medicine | 1982

Katecholamine und Blutdruck unter Betablockade bei Diuretika-behandelten Patienten mit essentieller Hypertonie

Andreas Meier; Peter Weidmann; Walter H. Ziegler


Journal of Molecular Medicine | 1981

Katecholamine, Renin, Aldosteron und Blutvolumen whrend chronischer Minoxidil-Therapie

Andreas Meier; Peter Weidmann; Walter H. Ziegler


Journal of Molecular Medicine | 1981

Beziehung zwischen Plasma-Katecholaminspiegel und Urin-Katecholaminexkretionsrate bei Normalpersonen und verschiedenen Erkrankungen

Helmut Schiffl; Peter Weidmann; Andreas Meier; Walter H. Ziegler

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Peter Weidmann

Cedars-Sinai Medical Center

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Gerald W. Keusch

University of Southern California

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Walter Riesen

University of St. Gallen

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Peter Weidmann

Cedars-Sinai Medical Center

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