Treatment of Supine Hypertension in Autonomic Failure
Public ClinicalTrials.gov record NCT00223717. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.
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Official title
The Pathophysiology and Treatment of Supine Hypertension in Patients With Autonomic Failure
Brief summary
Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.
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.
Study identification
- NCT ID
- NCT00223717
- Recruitment status
- Completed
- Study type
- Interventional
- Phase
- Phase 1
- Enrollment
- 152 participants
Conditions and interventions
Conditions
Interventions
- Clonidine Drug
- Nitroglycerin transdermal Drug
- Dipyridamole/ Aspirin (Aggrenox) Drug
- Desmopressin (DDAVP) Drug
- Sildenafil Drug
- Nifedipine Drug
- Hydralazine Drug
- Hydrochlorothiazide Drug
- Placebo Drug
- Bosentan Drug
- Diltiazem Drug
- Eplerenone Drug
- guanfacine Drug
- L-arginine Dietary Supplement
- captopril Drug
- carbidopa Drug
- losartan Drug
- metoprolol tartrate Drug
- nebivolol hydrochloride Drug
- prazosin hydrochloride Drug
- tamsulosin hydrochloride Drug
- Head-up tilt. Other
- aliskiren Drug
- Local heat stress Other
Drug · Dietary Supplement · Other
Eligibility (public fields only)
- Age range
- 18 Years to 80 Years
- Sex
- All
- Healthy volunteers
- Healthy volunteers not accepted
This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.
Study timeline
- Start date
- Dec 31, 2000
- Primary completion
- Dec 31, 2016
- Completion
- Dec 31, 2016
- Last update posted
- Oct 12, 2017
2001 – 2017
United States locations
- U.S. sites
- 1
- U.S. states
- 1
- U.S. cities
- 1
| Facility | City | State | ZIP | Site status |
|---|---|---|---|---|
| Vanderbilt University | Nashville | Tennessee | 37232 | — |
Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.
About this trial record page
- What this page shows
- Public field values for ClinicalTrials.gov record NCT00223717, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
- What this page does not do
- No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
- Where the data comes from
- Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
- Last refresh
- Last update posted Oct 12, 2017 · Synced Sep 5, 2026
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Open the official record
The complete protocol, eligibility criteria, and contact information for NCT00223717 live on ClinicalTrials.gov.