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Susanne Klaua - One of the best experts on this subject based on the ideXlab platform.

  • influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects
    Clinical Pharmacology & Therapeutics, 2006
    Co-Authors: Jens Tank, Karsten Heusser, André Diedrich, Stefan Engeli, Susanne Klaua
    Abstract:

    Background Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Methods and Results Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 ± 3 kg/m2; mean age, 42 ± 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. Results The mean blood pressure (systolic/diastolic) was 118 ± 13 mm Hg/70 ± 9 mm Hg with placebo and 120 ± 13 mm Hg/69 ± 8 mm Hg with Sibutramine (P=.29). The mean resting MSNA was 28 ± 14 bursts/min with placebo and 12 ± 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 ± 9 mm Hg/9 ± 9 mm Hg versus 31 ± 12 mm Hg/14 ± 9 mm Hg, P < .01) and MSNA (0.3 ± 0.5 arbitrary units/min versus 1.0 ± 1.1 arbitrary units/min, P=.01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 ± 1.23 bursts/min versus 58 ± 2.99 bursts/min [P < .001]; center point, 65 ± 0.32 mm Hg versus 67 ± 0.81 mm Hg [P < .05]). Conclusions Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism. Clinical Pharmacology & Therapeutics (2006) 79, 500–508; doi: 10.1016/j.clpt.2006.02.002

  • Influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects.
    Clinical pharmacology and therapeutics, 2006
    Co-Authors: Karsten Heusser, Jens Tank, Friedrich C. Luft, André Diedrich, Stefan Engeli, Susanne Klaua, Nadine Krüger, Anke Strauss, Gritt Stoffels, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 +/- 3 kg/m2; mean age, 42 +/- 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. The mean blood pressure (systolic/diastolic) was 118 +/- 13 mm Hg/70 +/- 9 mm Hg with placebo and 120 +/- 13 mm Hg/69 +/- 8 mm Hg with Sibutramine (P = .29). The mean resting MSNA was 28 +/- 14 bursts/min with placebo and 12 +/- 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 +/- 9 mm Hg/9 +/- 9 mm Hg versus 31 +/- 12 mm Hg/14 +/- 9 mm Hg, P < .01) and MSNA (0.3 +/- 0.5 arbitrary units/min versus 1.0 +/- 1.1 arbitrary units/min, P = .01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 +/- 1.23 bursts/min versus 58 +/- 2.99 bursts/min [P < .001]; center point, 65 +/- 0.32 mm Hg versus 67 +/- 0.81 mm Hg [P < .05]). Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.

Jens Tank - One of the best experts on this subject based on the ideXlab platform.

  • influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects
    Clinical Pharmacology & Therapeutics, 2006
    Co-Authors: Jens Tank, Karsten Heusser, André Diedrich, Stefan Engeli, Susanne Klaua
    Abstract:

    Background Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Methods and Results Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 ± 3 kg/m2; mean age, 42 ± 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. Results The mean blood pressure (systolic/diastolic) was 118 ± 13 mm Hg/70 ± 9 mm Hg with placebo and 120 ± 13 mm Hg/69 ± 8 mm Hg with Sibutramine (P=.29). The mean resting MSNA was 28 ± 14 bursts/min with placebo and 12 ± 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 ± 9 mm Hg/9 ± 9 mm Hg versus 31 ± 12 mm Hg/14 ± 9 mm Hg, P < .01) and MSNA (0.3 ± 0.5 arbitrary units/min versus 1.0 ± 1.1 arbitrary units/min, P=.01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 ± 1.23 bursts/min versus 58 ± 2.99 bursts/min [P < .001]; center point, 65 ± 0.32 mm Hg versus 67 ± 0.81 mm Hg [P < .05]). Conclusions Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism. Clinical Pharmacology & Therapeutics (2006) 79, 500–508; doi: 10.1016/j.clpt.2006.02.002

  • Influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects.
    Clinical pharmacology and therapeutics, 2006
    Co-Authors: Karsten Heusser, Jens Tank, Friedrich C. Luft, André Diedrich, Stefan Engeli, Susanne Klaua, Nadine Krüger, Anke Strauss, Gritt Stoffels, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 +/- 3 kg/m2; mean age, 42 +/- 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. The mean blood pressure (systolic/diastolic) was 118 +/- 13 mm Hg/70 +/- 9 mm Hg with placebo and 120 +/- 13 mm Hg/69 +/- 8 mm Hg with Sibutramine (P = .29). The mean resting MSNA was 28 +/- 14 bursts/min with placebo and 12 +/- 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 +/- 9 mm Hg/9 +/- 9 mm Hg versus 31 +/- 12 mm Hg/14 +/- 9 mm Hg, P < .01) and MSNA (0.3 +/- 0.5 arbitrary units/min versus 1.0 +/- 1.1 arbitrary units/min, P = .01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 +/- 1.23 bursts/min versus 58 +/- 2.99 bursts/min [P < .001]; center point, 65 +/- 0.32 mm Hg versus 67 +/- 0.81 mm Hg [P < .05]). Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.

  • Paradoxical Effect of Sibutramine on Autonomic Cardiovascular Regulation
    Circulation, 2002
    Co-Authors: Andreas L. Birkenfeld, Christoph Schroeder, Michael Boschmann, Jens Tank, G Franke, Friedrich C. Luft, Italo Biaggioni, Arya M. Sharma, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is widely used as an adjunctive obesity treatment. Norepinephrine reuptake inhibition with Sibutramine conceivably could exacerbate arterial hypertension and promote cardiovascular disease. In 11 healthy subjects (7 men, age 27+/-2 years, body mass index 23.1+/-0.7 kg/m2), we compared the effect of Sibutramine or matching placebo (ingested 26, 14, and 2 hours before testing) on cardiovascular responses to autonomic reflex tests and to a graded head-up tilt test. In addition, we tested Sibutramine in combination with metoprolol. Testing was conducted in a double-blind and crossover fashion. Supine systolic blood pressure was 113+/-3 mm Hg with placebo, 121+/-3 mm Hg with Sibutramine (P<0.001 versus placebo), and 111+/-2 mm Hg with the combination of Sibutramine and metoprolol. Similarly, Sibutramine increased upright blood pressure. Sibutramine substantially increased upright heart rate. This effect was abolished with metoprolol. The blood pressure response to cold pressor and handgrip testing was attenuated with Sibutramine compared with placebo. Furthermore, Sibutramine decreased low-frequency oscillations of blood pressure and plasma norepinephrine concentrations in the supine position. The cardiovascular effect of the antiobesity drug Sibutramine results from a complex interaction of peripheral and central nervous system effects. The inhibitory clonidine-like action of Sibutramine on the central nervous system attenuates the peripheral stimulatory effect. Our findings strongly suggest that current concepts regarding the action of Sibutramine on the sympathetic nervous system should be reconsidered.

  • paradoxical effect of Sibutramine on autonomic cardiovascular regulation
    Circulation, 2002
    Co-Authors: Andreas L. Birkenfeld, Christoph Schroeder, Michael Boschmann, Jens Tank, G Franke, Friedrich C. Luft, Italo Biaggioni, Arya M. Sharma, Jens Jordan
    Abstract:

    Background—Sibutramine, a serotonin and norepinephrine transporter blocker, is widely used as an adjunctive obesity treatment. Norepinephrine reuptake inhibition with Sibutramine conceivably could exacerbate arterial hypertension and promote cardiovascular disease. Methods and Results—In 11 healthy subjects (7 men, age 272 years, body mass index 23.10.7 kg/m 2 ), we compared the effect of Sibutramine or matching placebo (ingested 26, 14, and 2 hours before testing) on cardiovascular responses to autonomic reflex tests and to a graded head-up tilt test. In addition, we tested Sibutramine in combination with metoprolol. Testing was conducted in a double-blind and crossover fashion. Supine systolic blood pressure was 1133 mm Hg with placebo, 1213 mm Hg with Sibutramine (P0.001 versus placebo), and 1112 mm Hg with the combination of Sibutramine and metoprolol. Similarly, Sibutramine increased upright blood pressure. Sibutramine substantially increased upright heart rate. This effect was abolished with metoprolol. The blood pressure response to cold pressor and handgrip testing was attenuated with Sibutramine compared with placebo. Furthermore, Sibutramine decreased low-frequency oscillations of blood pressure and plasma norepinephrine concentrations in the supine position. Conclusions—The cardiovascular effect of the antiobesity drug Sibutramine results from a complex interaction of peripheral and central nervous system effects. The inhibitory clonidine-like action of Sibutramine on the central nervous system attenuates the peripheral stimulatory effect. Our findings strongly suggest that current concepts regarding the action of Sibutramine on the sympathetic nervous system should be reconsidered. (Circulation. 2002;106:2459-2465.)

Jens Jordan - One of the best experts on this subject based on the ideXlab platform.

  • Influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects.
    Clinical pharmacology and therapeutics, 2006
    Co-Authors: Karsten Heusser, Jens Tank, Friedrich C. Luft, André Diedrich, Stefan Engeli, Susanne Klaua, Nadine Krüger, Anke Strauss, Gritt Stoffels, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 +/- 3 kg/m2; mean age, 42 +/- 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. The mean blood pressure (systolic/diastolic) was 118 +/- 13 mm Hg/70 +/- 9 mm Hg with placebo and 120 +/- 13 mm Hg/69 +/- 8 mm Hg with Sibutramine (P = .29). The mean resting MSNA was 28 +/- 14 bursts/min with placebo and 12 +/- 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 +/- 9 mm Hg/9 +/- 9 mm Hg versus 31 +/- 12 mm Hg/14 +/- 9 mm Hg, P < .01) and MSNA (0.3 +/- 0.5 arbitrary units/min versus 1.0 +/- 1.1 arbitrary units/min, P = .01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 +/- 1.23 bursts/min versus 58 +/- 2.99 bursts/min [P < .001]; center point, 65 +/- 0.32 mm Hg versus 67 +/- 0.81 mm Hg [P < .05]). Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.

  • influence of Sibutramine on blood pressure evidence from placebo controlled trials
    International Journal of Obesity, 2005
    Co-Authors: Jens Jordan, J Scholze, B Matiba, A Wirth, Hans Hauner, Arya M. Sharma
    Abstract:

    OBJECTIVE: Sibutramine, a serotonin and norepinephrine transporter inhibitor, is widely used as an adjunctive obesity treatment. There have been concerns that norepinephrine reuptake inhibition with Sibutramine could exacerbate arterial hypertension. DESIGN: Combined analysis of two placebo-controlled trials. SUBJECTS: The combined data set consisted of 1336 patients. Of these patients, 966 were randomized to Sibutramine and 370 were randomized to placebo. MEASUREMENTS: Body weight, blood pressure, heart rate (HR). RESULTS: Sibutramine reduced body weight regardless of basal blood pressure. In the complete set of patients, systolic blood pressure did not change with either intervention over the 48-week period (-0.1+/-15.5 mmHg with Sibutramine, -0.2+/-15.2 mmHg with placebo, P=0.9). The change in diastolic blood pressure over the 48 week period was 0.3+/-9.5 mmHg with Sibutramine and -0.8+/-9.2 mmHg with placebo (P=0.049). The blood pressure response was not exacerbated in patients with grade 1 or 2 hypertension or in patients with isolated systolic hypertension. Sibutramine treatment caused a slight increase in supine HR that was sustained throughout the studies. CONCLUSIONS: Sibutramine treatment is unlikely to elicit a critical increase in blood pressure even in hypertensive patients. However, blood pressure and HR should be monitored closely. In patients who experience a clinically significant and sustained increase in blood pressure, the drug should probably be discontinued.

  • Paradoxical Effect of Sibutramine on Autonomic Cardiovascular Regulation
    Circulation, 2002
    Co-Authors: Andreas L. Birkenfeld, Christoph Schroeder, Michael Boschmann, Jens Tank, G Franke, Friedrich C. Luft, Italo Biaggioni, Arya M. Sharma, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is widely used as an adjunctive obesity treatment. Norepinephrine reuptake inhibition with Sibutramine conceivably could exacerbate arterial hypertension and promote cardiovascular disease. In 11 healthy subjects (7 men, age 27+/-2 years, body mass index 23.1+/-0.7 kg/m2), we compared the effect of Sibutramine or matching placebo (ingested 26, 14, and 2 hours before testing) on cardiovascular responses to autonomic reflex tests and to a graded head-up tilt test. In addition, we tested Sibutramine in combination with metoprolol. Testing was conducted in a double-blind and crossover fashion. Supine systolic blood pressure was 113+/-3 mm Hg with placebo, 121+/-3 mm Hg with Sibutramine (P<0.001 versus placebo), and 111+/-2 mm Hg with the combination of Sibutramine and metoprolol. Similarly, Sibutramine increased upright blood pressure. Sibutramine substantially increased upright heart rate. This effect was abolished with metoprolol. The blood pressure response to cold pressor and handgrip testing was attenuated with Sibutramine compared with placebo. Furthermore, Sibutramine decreased low-frequency oscillations of blood pressure and plasma norepinephrine concentrations in the supine position. The cardiovascular effect of the antiobesity drug Sibutramine results from a complex interaction of peripheral and central nervous system effects. The inhibitory clonidine-like action of Sibutramine on the central nervous system attenuates the peripheral stimulatory effect. Our findings strongly suggest that current concepts regarding the action of Sibutramine on the sympathetic nervous system should be reconsidered.

  • paradoxical effect of Sibutramine on autonomic cardiovascular regulation
    Circulation, 2002
    Co-Authors: Andreas L. Birkenfeld, Christoph Schroeder, Michael Boschmann, Jens Tank, G Franke, Friedrich C. Luft, Italo Biaggioni, Arya M. Sharma, Jens Jordan
    Abstract:

    Background—Sibutramine, a serotonin and norepinephrine transporter blocker, is widely used as an adjunctive obesity treatment. Norepinephrine reuptake inhibition with Sibutramine conceivably could exacerbate arterial hypertension and promote cardiovascular disease. Methods and Results—In 11 healthy subjects (7 men, age 272 years, body mass index 23.10.7 kg/m 2 ), we compared the effect of Sibutramine or matching placebo (ingested 26, 14, and 2 hours before testing) on cardiovascular responses to autonomic reflex tests and to a graded head-up tilt test. In addition, we tested Sibutramine in combination with metoprolol. Testing was conducted in a double-blind and crossover fashion. Supine systolic blood pressure was 1133 mm Hg with placebo, 1213 mm Hg with Sibutramine (P0.001 versus placebo), and 1112 mm Hg with the combination of Sibutramine and metoprolol. Similarly, Sibutramine increased upright blood pressure. Sibutramine substantially increased upright heart rate. This effect was abolished with metoprolol. The blood pressure response to cold pressor and handgrip testing was attenuated with Sibutramine compared with placebo. Furthermore, Sibutramine decreased low-frequency oscillations of blood pressure and plasma norepinephrine concentrations in the supine position. Conclusions—The cardiovascular effect of the antiobesity drug Sibutramine results from a complex interaction of peripheral and central nervous system effects. The inhibitory clonidine-like action of Sibutramine on the central nervous system attenuates the peripheral stimulatory effect. Our findings strongly suggest that current concepts regarding the action of Sibutramine on the sympathetic nervous system should be reconsidered. (Circulation. 2002;106:2459-2465.)

Karsten Heusser - One of the best experts on this subject based on the ideXlab platform.

  • influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects
    Clinical Pharmacology & Therapeutics, 2006
    Co-Authors: Jens Tank, Karsten Heusser, André Diedrich, Stefan Engeli, Susanne Klaua
    Abstract:

    Background Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Methods and Results Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 ± 3 kg/m2; mean age, 42 ± 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. Results The mean blood pressure (systolic/diastolic) was 118 ± 13 mm Hg/70 ± 9 mm Hg with placebo and 120 ± 13 mm Hg/69 ± 8 mm Hg with Sibutramine (P=.29). The mean resting MSNA was 28 ± 14 bursts/min with placebo and 12 ± 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 ± 9 mm Hg/9 ± 9 mm Hg versus 31 ± 12 mm Hg/14 ± 9 mm Hg, P < .01) and MSNA (0.3 ± 0.5 arbitrary units/min versus 1.0 ± 1.1 arbitrary units/min, P=.01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 ± 1.23 bursts/min versus 58 ± 2.99 bursts/min [P < .001]; center point, 65 ± 0.32 mm Hg versus 67 ± 0.81 mm Hg [P < .05]). Conclusions Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism. Clinical Pharmacology & Therapeutics (2006) 79, 500–508; doi: 10.1016/j.clpt.2006.02.002

  • Influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects.
    Clinical pharmacology and therapeutics, 2006
    Co-Authors: Karsten Heusser, Jens Tank, Friedrich C. Luft, André Diedrich, Stefan Engeli, Susanne Klaua, Nadine Krüger, Anke Strauss, Gritt Stoffels, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 +/- 3 kg/m2; mean age, 42 +/- 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. The mean blood pressure (systolic/diastolic) was 118 +/- 13 mm Hg/70 +/- 9 mm Hg with placebo and 120 +/- 13 mm Hg/69 +/- 8 mm Hg with Sibutramine (P = .29). The mean resting MSNA was 28 +/- 14 bursts/min with placebo and 12 +/- 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 +/- 9 mm Hg/9 +/- 9 mm Hg versus 31 +/- 12 mm Hg/14 +/- 9 mm Hg, P < .01) and MSNA (0.3 +/- 0.5 arbitrary units/min versus 1.0 +/- 1.1 arbitrary units/min, P = .01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 +/- 1.23 bursts/min versus 58 +/- 2.99 bursts/min [P < .001]; center point, 65 +/- 0.32 mm Hg versus 67 +/- 0.81 mm Hg [P < .05]). Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.

André Diedrich - One of the best experts on this subject based on the ideXlab platform.

  • influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects
    Clinical Pharmacology & Therapeutics, 2006
    Co-Authors: Jens Tank, Karsten Heusser, André Diedrich, Stefan Engeli, Susanne Klaua
    Abstract:

    Background Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Methods and Results Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 ± 3 kg/m2; mean age, 42 ± 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. Results The mean blood pressure (systolic/diastolic) was 118 ± 13 mm Hg/70 ± 9 mm Hg with placebo and 120 ± 13 mm Hg/69 ± 8 mm Hg with Sibutramine (P=.29). The mean resting MSNA was 28 ± 14 bursts/min with placebo and 12 ± 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 ± 9 mm Hg/9 ± 9 mm Hg versus 31 ± 12 mm Hg/14 ± 9 mm Hg, P < .01) and MSNA (0.3 ± 0.5 arbitrary units/min versus 1.0 ± 1.1 arbitrary units/min, P=.01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 ± 1.23 bursts/min versus 58 ± 2.99 bursts/min [P < .001]; center point, 65 ± 0.32 mm Hg versus 67 ± 0.81 mm Hg [P < .05]). Conclusions Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism. Clinical Pharmacology & Therapeutics (2006) 79, 500–508; doi: 10.1016/j.clpt.2006.02.002

  • Influence of Sibutramine treatment on sympathetic vasomotor tone in obese subjects.
    Clinical pharmacology and therapeutics, 2006
    Co-Authors: Karsten Heusser, Jens Tank, Friedrich C. Luft, André Diedrich, Stefan Engeli, Susanne Klaua, Nadine Krüger, Anke Strauss, Gritt Stoffels, Jens Jordan
    Abstract:

    Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that Sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in Sibutramine-treated patients have not been conducted. Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 +/- 3 kg/m2; mean age, 42 +/- 8 years). They were treated for 5 days with 15 mg Sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions. The mean blood pressure (systolic/diastolic) was 118 +/- 13 mm Hg/70 +/- 9 mm Hg with placebo and 120 +/- 13 mm Hg/69 +/- 8 mm Hg with Sibutramine (P = .29). The mean resting MSNA was 28 +/- 14 bursts/min with placebo and 12 +/- 10 bursts/min with Sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 +/- 9 mm Hg/9 +/- 9 mm Hg versus 31 +/- 12 mm Hg/14 +/- 9 mm Hg, P < .01) and MSNA (0.3 +/- 0.5 arbitrary units/min versus 1.0 +/- 1.1 arbitrary units/min, P = .01) in response to cold pressor testing. Baroreflex heart rate control was similar with Sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 +/- 1.23 bursts/min versus 58 +/- 2.99 bursts/min [P < .001]; center point, 65 +/- 0.32 mm Hg versus 67 +/- 0.81 mm Hg [P < .05]). Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that Sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.