Search

Your search keyword '"Nussberger, Jurg"' showing total 45 results
Start Over Author "Nussberger, Jurg"
45 results on '"Nussberger, Jurg"'

1. Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

Author

Zanchi, Anne, Schaad, Nicolas C., Osterheld, Maria-C., Grouzmann, Eric, Nussberger, Jurg, Brunner, Hans R., and Waeber, Bernard

Subjects
Hypertension -- Causes of, Biological sciences
Abstract

Hypertension caused by the inhibition of the activity of nitric oxide synthase (NOS) increases in the presence of N(super G)-nitro-L-arginine methyl ester (L-NAME) and involves the stimulation of the sympathetic nervous system and the renin-angiotensin system. L-NAME increases the mean intra-arterial blood pressure to the same extent in rats kept on a low sodium and normal sodium diet. The amount of norepinephrine and epinephrine in the plasma increases but the amount of neuropeptide Y is unaffected. The angiotensin II antagonist, losartan, decreases the blood pressure increase caused by inhibition of NOS.

Published
1995

2. Angiotensin II overflow from canine skeletal muscle in vivo: importance of plasma angiotensin I

Author

Schwieler, Jonas H., Nussberger, Jurg, Kahan, Thomas, and Hjemdahl, Paul

Subjects
Epinephrine -- Receptors, Angiotensin -- Physiological aspects, Blood vessels -- Dilatation, Biological sciences
Abstract

Propranolol induced beta-adrenoreceptor blockade, which has a negligible influence on both angiotensin I (ANG I) and angiotensin II (ANG II) overflow from canine skeletal muscle, enhances ANG II overflow and reduces ANG I overflow. Isoprenaline permits vasodilation. Beta-adrenoreceptor induces a major portion of the endothelial surface exhibiting angiotensin converting enzyme activity.

Published
1994

3. Converting enzyme inhibition modulates sympathetic neurotransmission in vivo via multiple mechanisms

Author

Schwieler, Jonas H., Kahan, Thomas, Nussberger, Jurg, and Hjemdahl, Paul

Subjects
Angiotensin converting enzyme -- Physiological aspects, Angiotensin -- Physiological aspects, Neural transmission -- Physiological aspects, Biological sciences
Abstract

The effects of angiotensin-converting enzyme (ACE) inhibition on peripheral neurotransmission were studied by comparing the effects of lozartan, an angiotensin II (ANG II) receptor antagonist, and benazeprilat, and ACE inhibitor. Findings reveal that reduction in ANG II formation and enhancement of bradykinin and prostaglandin production are involved in ACE inhibition of neurotransmission through multiple mechanisms.

Published
1993

5. Increase of bradykinin in plasma of patients undergoing cardiopulmonary bypass *: the importance of lung exclusion. (clinical investigations)

Author

Cugno, Massimo, Nussberger, Jurg, Biglioli, Paolo, Alamanni, Francesco, Coppola, Raffaella, and Agostoni, Angelo

Subjects
Bradykinin -- Measurement -- Physiological aspects, Cardiopulmonary bypass -- Physiological aspects -- Measurement, Health, Physiological aspects, Measurement
Abstract

Study objectives: Hemodynamic complications including hypotensive episodes are frequently associated with cardiopulmonary bypass (CPB) and can be attributed to a generalized inflammatory response in which bradykinin may be a mediator. [...]

Published
2001

9. Plasma Angiotensins, Renin, and Blood Pressure During Acute Renin Inhibition by CGP 38 560A in Hypertensive Patients

Author

Jeunemaître, Xavier, Ménard, Joël, Nussberger, Jurg, Guyene, Tam T., Brunner, Hans R., Corvol, Pierre, Jeunemaître, Xavier, Ménard, Joël, Nussberger, Jurg, Guyene, Tam T., Brunner, Hans R., and Corvol, Pierre

Abstract

The new renin inhibitor CGP 38560A has been shown to block angiotensin (ANG) production in healthy volunteers. In order to determine its potential antihypertensive effect, the compound was administered in a 30-min infusion, in 12 hypertensive patients (mean blood pressure (BP): 112.8 ± 3.5 mm Hg). These patients were selected for their sensitivity to Captopril: a single oral dose of 50 mg Captopril lowered their mean BP by 8.8 ± 2.2 mm Hg after 30 min and by 15.3 ± 1.5 mm Hg after 90 min. At the end of the renin inhibitor infusion, mean blood pressure decreased by 5.7 ± 2.2 mm Hg in the six patients infused with the dose of 0.125 mg/kg and by 6.0 ± 1.8 mm Hg in the six patients infused with 0.250 mg/kg. The fall in blood pressure was correlated to the initial plasma renin activity (PRA) (r = 0.61, P < .05). A dose-dependent effect was observed on plasma ANG I which fell by 74% with 0.125 mg/kg and by 94% with 0.250 mg/kg. Identical falls were found for plasma ANG II (72% and 94%, respectively) and ANG I and ANG II were well correlated (r = 0.91, P < .001). The fall in BP was correlated to the fall in plasma ANG I (r = 0.77, P < .01). The time-course of the BP changes was parallel to the changes in plasma angiotensins, as were the slightly delayed rise and fall in active renin measured by a direct immunoradiometric assay. When measured by the conventional ANG I radioimmunoassay, PRA values indicated a long-lasting inhibition. The arte- factual nature of the latter result is demonstrated by the different results obtained with an ANG I antibody-trapping radioimmunoassay, which followed more closely plasma ANG I levels. Am J Hypertens 1989; 2:819-827

Published
2017

10. Clinical Experience With Angiotensin II Receptor Antagonists

Author

Brunner, Hans R., Christen, Yves, Munafo, Alain, Lee, Robert J., Waeber, Bernard, Nussberger, Jurg, Brunner, Hans R., Christen, Yves, Munafo, Alain, Lee, Robert J., Waeber, Bernard, and Nussberger, Jurg

Abstract

This series of studies was designed to assess in normal volunteers the relationships between various doses (5, 10, 20, 40, 80, and 120 mg) of the orally active angiotensin II antagonist losartan (DuP 753, MK-954) and their inhibitory effect on the pressure response to a given bolus of angiotensin I or II. It was found that the maximal inhibitory effect was reached with a dose of 80 mg. The minimal dose necessary for maximal efficacy would therefore be expected to be between 40 and 80 mg. The effect lasted for more than 24 h and was related almost exclusively to the circulating levels of the active metabolite EXP3174. It remains to be demonstrated in hypertensive patients that the same dose relationship holds for the antihypertensive effect, but preliminary data already suggest that this is the case. Am J Hypertens 1992;5:243S-246S

Published
2017

11. Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice

Author

Meneton, Pierre, Bloch-Faure, May, Hagege, Albert A., Ruetten, Hartmut, Huang, Wei, Bergaya, Sonia, Ceiler, Debbie, Gehring, Doris, Martins, Isabelle, Salmon, Georges, Boulanger, Chantal M., Nussberger, Jurg, Crozatier, Bertrand, Gasc, Jean-Marie, Heudes, Didier, Bruneval, Patrick, Doetschman, Tom, Menard, Joel, and Alhenc-Gelas, Francois

Subjects
Kallikrein -- Physiological aspects, Cardiovascular system -- Abnormalities, Kidneys -- Physiological aspects, Blood pressure -- Physiological aspects, Proteases -- Physiological aspects, Kinins -- Physiological aspects, Blood vessels -- Dilatation, Science and technology
Abstract

Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to [Beta]-adrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein-kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein-kinin system could be involved in the development or progression of cardiovascular diseases.

Published
2001

12. Vasopeptidase inhibition and angio-oedema

Author

Messerli, Franz H and Nussberger, Jurg

Subjects
Omapatrilat (Medication) -- Evaluation, Congestive heart failure -- Physiological aspects, Angioneurotic edema -- Risk factors
Published
2000

13. Angiotensin-converting enzyme inhibition versus blockade of the renin-angiotensin system

Author

Brunner, Hans R., Waeber, Bernard, and Nussberger, Jurg

Subjects
Renin -- Physiological aspects, ACE inhibitors, Angiotensin -- Physiological aspects, Health, Health care industry
Abstract

Angiotensin-converting enzyme (ACE) inhibitors have been designed to reduce the generation of angiotensin II, i.e., to block the renin-angiotensin system. Interestingly, there exists a considerable dissociation between the time course of ACE inhibition and that of blockade of the renin-angiotensin system. Due to the greatly improved methodology used to estimate the degree of ACE inhibition in vitro and in vivo, it has become evident that the compensatory increase in renin levels in response to ACE inhibition is the key factor determining the degree and duration of blockade of the renin-angiotensin system resulting from ACE inhibition. A better understanding of these relationships would seem to be useful in determining duration of action and particularly the optimal dose of any ACE inhibitor., The enzyme renin is produced by the kidneys. Renin converts the blood protein angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasopressor, in that it constricts blood vessels, and also increases the production and release of the mineralocorticoid hormone aldosterone from the adrenal glands. Aldosterone controls the metabolism of sodium, chloride, and potassium. Agents which prevent the action of ACE and the formation of angiotensin II have been used to treat hypertension, or abnormally high blood pressure. Studies have shown that there is a delay between the inhibition of angiotensin-converting enzyme by ACE inhibitors and reduction in angiotensin II levels, which reflect suppression of the renin-angiotensin system. In addition, because renin release by the kidneys is activated by low blood pressure, the lowering of blood pressure by ACE inhibitors causes an increase in renin and the subsequent increase in angiotensin I. This compensatory increase in renin in response to ACE inhibition is a major factor influencing the extent and duration of blockade of the renin-angiotensin system by ACE inhibitors. A better understanding of the relation between renin levels and ACE inhibitors may be useful in determining the duration of action and effective dose of ACE inhibitors. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1989

16. Proximal Sodium Reabsorption

Author

Chiolero, Arnaud, primary, Maillard, Marc, additional, Nussberger, Jurg, additional, Brunner, Hans-R., additional, and Burnier, Michel, additional

Published
2000
Full Text
View/download PDF

38. Plasma Angiotensins, Renin, and Blood Pressure During Acute Renin Inhibition by CGP 38 560A in Hypertensive Patients

Author

Jeunemaître, Xavier, Ménard, Joël, Nussberger, Jurg, Guyene, Tam T., Brunner, Hans R., Corvol, Pierre, Jeunemaître, Xavier, Ménard, Joël, Nussberger, Jurg, Guyene, Tam T., Brunner, Hans R., and Corvol, Pierre

Abstract

The new renin inhibitor CGP 38560A has been shown to block angiotensin (ANG) production in healthy volunteers. In order to determine its potential antihypertensive effect, the compound was administered in a 30-min infusion, in 12 hypertensive patients (mean blood pressure (BP): 112.8 ± 3.5 mm Hg). These patients were selected for their sensitivity to Captopril: a single oral dose of 50 mg Captopril lowered their mean BP by 8.8 ± 2.2 mm Hg after 30 min and by 15.3 ± 1.5 mm Hg after 90 min. At the end of the renin inhibitor infusion, mean blood pressure decreased by 5.7 ± 2.2 mm Hg in the six patients infused with the dose of 0.125 mg/kg and by 6.0 ± 1.8 mm Hg in the six patients infused with 0.250 mg/kg. The fall in blood pressure was correlated to the initial plasma renin activity (PRA) (r = 0.61, P < .05). A dose-dependent effect was observed on plasma ANG I which fell by 74% with 0.125 mg/kg and by 94% with 0.250 mg/kg. Identical falls were found for plasma ANG II (72% and 94%, respectively) and ANG I and ANG II were well correlated (r = 0.91, P < .001). The fall in BP was correlated to the fall in plasma ANG I (r = 0.77, P < .01). The time-course of the BP changes was parallel to the changes in plasma angiotensins, as were the slightly delayed rise and fall in active renin measured by a direct immunoradiometric assay. When measured by the conventional ANG I radioimmunoassay, PRA values indicated a long-lasting inhibition. The arte- factual nature of the latter result is demonstrated by the different results obtained with an ANG I antibody-trapping radioimmunoassay, which followed more closely plasma ANG I levels. Am J Hypertens 1989; 2:819-827

39. Clinical Experience With Angiotensin II Receptor Antagonists

Author

Brunner, Hans R., Christen, Yves, Munafo, Alain, Lee, Robert J., Waeber, Bernard, Nussberger, Jurg, Brunner, Hans R., Christen, Yves, Munafo, Alain, Lee, Robert J., Waeber, Bernard, and Nussberger, Jurg

Abstract

This series of studies was designed to assess in normal volunteers the relationships between various doses (5, 10, 20, 40, 80, and 120 mg) of the orally active angiotensin II antagonist losartan (DuP 753, MK-954) and their inhibitory effect on the pressure response to a given bolus of angiotensin I or II. It was found that the maximal inhibitory effect was reached with a dose of 80 mg. The minimal dose necessary for maximal efficacy would therefore be expected to be between 40 and 80 mg. The effect lasted for more than 24 h and was related almost exclusively to the circulating levels of the active metabolite EXP3174. It remains to be demonstrated in hypertensive patients that the same dose relationship holds for the antihypertensive effect, but preliminary data already suggest that this is the case. Am J Hypertens 1992;5:243S-246S

45. Compensatory up-regulation of angiotensin II subtype1 receptors in alphaENaC knockout heterozygous mice.

Author

Qing Wang, Hummler, Edith, Maillard, Marc, Nussberger, Jurg, Rossier, Bernard C., Brunner, Hans R., and Burnier, Michel

Subjects
*SODIUM channels, *MICE, *SCIENTIFIC experimentation
Abstract

Presents a study on the importance of an up-regulation of the number of angiostensin II subtype 1 receptors as a compensatory mechanism in the alpha subunit of epithelial sodium channel (ENaC) heterozygous mice. Role of ENaC; Methodology; Results and discussion.

Published
2001
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results