CLINICAL TRIALS PROFILE FOR LOSARTAN POTASSIUM
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All Clinical Trials for losartan potassium
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00090259 ↗ | Study to Evaluate Potential Decrease in Hospitalization Events, Time Between Events, and Increasing Longevity in Patients With Symptomatic Heart Failure (0954-948) | Completed | Merck Sharp & Dohme Corp. | Phase 3 | 2001-12-19 | This is a multicenter study to evaluate potential decrease in hospitalization events and time between events and increasing longevity in patients with symptomatic congestive heart failure and intolerant of first-line medication for heart failure. This study will evaluate if higher doses of the investigational drug given daily will be superior to the lower dose of the same investigational drug given daily. |
| NCT00140907 ↗ | ALLOGRAFT, A Study to Evaluate the Renal Protective Effects of Losartan (0954-222)(COMPLETED) | Completed | Merck Sharp & Dohme Corp. | Phase 4 | 2000-03-14 | To demonstrate that losartan (+ conventional therapy) compared to placebo (+ conventional therapy) will reduce the number of RT patients who experience histological lesions of chronic allograft nephropathy |
| NCT00140985 ↗ | Antiproteinuric Efficacy of Losartan Potassium in Patients With Non-Diabetic Proteinuric Renal Diseases (0954-213) | Completed | Merck Sharp & Dohme Corp. | Phase 4 | 2000-02-01 | Antiproteinuric Efficacy of Losartan Potassium in Patients with Non-Diabetic Proteinuric Renal Diseases. |
| NCT00157963 ↗ | Hydrochlorothiazide (+) Losartan Potassium vs. Amlodipine Comparative Study (0954A-314) | Completed | Merck Sharp & Dohme Corp. | Phase 4 | 2005-02-05 | An efficacy and safety study of hydrochlorothiazide (+) losartan potassium compared to amlodipine at week 12 in Korean patients with essential hypertension |
| NCT00185094 ↗ | A Comparison of the Effect of Olmesartan Medoxomil, Losartan Potassium, and Atenolol on the Ability of Overweight Patients With High Blood Pressure to Respond to Insulin | Completed | Daiichi Sankyo Inc. | Phase 4 | 2004-02-01 | To examine the effect of three different blood pressure medications on the insulin sensitivity in overweight patients with high blood pressure. |
| NCT00185094 ↗ | A Comparison of the Effect of Olmesartan Medoxomil, Losartan Potassium, and Atenolol on the Ability of Overweight Patients With High Blood Pressure to Respond to Insulin | Completed | Daiichi Sankyo, Inc. | Phase 4 | 2004-02-01 | To examine the effect of three different blood pressure medications on the insulin sensitivity in overweight patients with high blood pressure. |
| NCT00223717 ↗ | Treatment of Supine Hypertension in Autonomic Failure | Completed | Vanderbilt University | Phase 1 | 2001-01-01 | Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general. |
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