References of "Vetter, H."
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See detailIsolated myocardial cells: a new tool for the investigation of hypertensive heart disease.
Neyses, Ludwig UL; Vetter, H.

in Journal of Hypertension. Supplement) (1990), 8(4), 99-102

Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart. For example, delayed relaxation is a prominent feature, impairing ventricular filling and ... [more ▼]

Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart. For example, delayed relaxation is a prominent feature, impairing ventricular filling and coronary flow. In intact heart preparations the relative contribution of fibrosis and of the myocardial cell itself to these abnormalities cannot be correctly assessed. Biochemical studies on the mechanisms of impaired contraction and relaxation and hypertensive heart failure are hampered by the fact that 75% of all heart cells are non-myocytes. We therefore established the model of the isolated calcium-tolerant, adult rat cardiomyocyte as a new approach to the investigation of these problems. Contractility was measured using a videomicroscope system with high time resolution (1 ms). Angiotensin II induced a marked relaxation delay in the cardiomyocyte from normotensive rats and showed a moderate positive inotropic effect, whereas isoproterenol had a strong positive inotropic effect but accelerated relaxation. Therefore, angiotensin II is capable of inducing a relaxation delay even in the absence of coronary ischaemia or hypertension. These first results show that the isolated cardiomyocyte model may be a useful approach to investigating the mechanisms of hypertensive heart disease. [less ▲]

Detailed reference viewed: 68 (1 UL)
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See detail[Disturbed endothelium-dependent blood vessel relaxation in essential hypertension].
Neyses, Ludwig UL; Vetter, H.

in Deutsche medizinische Wochenschrift (1946) (1990), 115(51-52), 1981

Detailed reference viewed: 59 (0 UL)
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See detailAction of atrial natriuretic peptide and angiotensin II on the myocardium: studies in isolated rat ventricular cardiomyocytes.
Neyses, Ludwig UL; Vetter, H.

in Biochemical and biophysical research communications (1989), 163(3), 1435-43

Isolated calcium-tolerant rat ventricular cardiomyocytes were used to characterize the effects of atrial natriuretic peptide (ANP), Angiotensin II (AII) and their interaction on the myocardial contraction ... [more ▼]

Isolated calcium-tolerant rat ventricular cardiomyocytes were used to characterize the effects of atrial natriuretic peptide (ANP), Angiotensin II (AII) and their interaction on the myocardial contraction-/relaxation pattern free of interference from other types of cardiac cells. Binding of 125I-ANP showed a KD of 12 pM and approximately 600 binding sites per cell. At 37 degrees C (rate 140 bpm) ANP decreased the contraction maximum with an EC50 of about 70 pM, maximal decrease was 35%. ANP (10(-7) M) raised cellular cyclic-GMP from 0.76+/-0.12 to 1.32+/-0.13 pmole/10(6) cells (73%, p less than 0.05). Angiotensin II increased contractility by a maximum of 32% at 10(-7) M; the EC50 was 8 x 10(-10) M. AII markedly delayed relaxation (reduction of maximum relaxation velocity from 0.092 to 0.063 mm/s; p less than 0.05). ANP (10(-7) M) increased the effect of AII (10(-8) M) on contractility by 66% without changing relaxation parameters significantly. This unexpected interaction may be relevant in pathological conditions where both AII and ANP are stimulated, such as heart failure or secondary hypertension. [less ▲]

Detailed reference viewed: 105 (0 UL)
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See detailImpaired relaxation of the hypertrophied myocardium is potentiated by angiotensin II.
Neyses, Ludwig UL; Vetter, H.

in Journal of Hypertension. Supplement) (1989), 7(6), 104-5

Relaxation delay is an important feature of hypertensive heart disease which impairs diastolic coronary flow and ventricular filling and therefore contributes to heart failure. We investigated the ... [more ▼]

Relaxation delay is an important feature of hypertensive heart disease which impairs diastolic coronary flow and ventricular filling and therefore contributes to heart failure. We investigated the hypothesis that impaired relaxation is a property of the myocardium, rather than the consequence of ischaemia or interstitial fibrosis. A new videomicroscope system was used to define the contraction-relaxation cycle of isolated cardiac myocytes from spontaneously hypertensive rats (SHR) and normotensive control (Wistar-Kyoto, WKY) rats. The SHR cells showed a marked relaxation delay. Angiotensin II (Ang II) increased the contraction maximum by about 35% in WKY rats and induced a relaxation delay. In SHR Ang II greatly potentiated this relaxation delay. Our results demonstrate that impairment of relaxation is a property of the single cardiomyocyte. Angiotensin II induces a relaxation delay that is independent of blood pressure. The combination of hypertrophy and high levels of Ang II potentiates relaxation impairment and may therefore contribute to hypertensive left ventricular failure. [less ▲]

Detailed reference viewed: 109 (1 UL)
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See detail[Divisible tablets--source of error in therapeutic drug dosages].
Stimpel, M.; Vetter, H.; Kuffer, B. et al

in Schweizerische Rundschau für Medizin Praxis (1985), 74(5), 84-6

Detailed reference viewed: 76 (1 UL)
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See detailCompliance with salt restriction as a limiting factor in the primary prevention of hypertension.
Neyses, Ludwig UL; Dorst, K.; Michaelis, J. et al

in Journal of Hypertension. Supplement) (1985), 3(1), 87-90

It is an important but still unresolved question whether reduction of salt intake in the offspring of hypertensives (a high risk group) prevents the development of the disease. Therefore, 178 offspring ... [more ▼]

It is an important but still unresolved question whether reduction of salt intake in the offspring of hypertensives (a high risk group) prevents the development of the disease. Therefore, 178 offspring (14-26 years old) of hypertensives were enrolled in a 2-year pilot trial aimed mainly at a reduction in salt consumption. For the intervention group (n = 99) a behavioural approach was chosen with extensive counselling by experienced dietitians. The controls (n = 79) received no continuous dietary advice. Both groups showed a small decline in sodium intake over time, but the differences between the two groups were not significant. Division into subgroups with and without sodium reduction revealed no differences in blood pressure. We conclude that the inherent resistance to any change of lifestyle among healthy subjects may require new and more comprehensive motivational approaches. [less ▲]

Detailed reference viewed: 56 (1 UL)
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See detailTrilostane - a new and effective drug for primary aldosteronism
Neyses, Ludwig UL; Groth, H; Vetter, H et al

in The adrenal gland and hypertension (1985)

Detailed reference viewed: 53 (1 UL)
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See detail[Nifedipine in hypertensive emergencies and severe hypertension].
Groth, H.; Foerster, E. C.; Neyses, Ludwig UL et al

in Schweizerische Rundschau für Medizin Praxis (1984), 73(2), 45-9

Detailed reference viewed: 107 (1 UL)