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Life sciences · Phase 1 Trial
ClinicalTrials.gov · September 25, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Phase 1 Trial.
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Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
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Registry record from ClinicalTrials.gov (NCT02966665). This is a study registration, not published results. Lead sponsor: D. Walter Wray. Recruitment status: RECRUITING. Phase: PHASE1. Study type: INTERVENTIONAL. Enrollment: 420 participants (ESTIMATED). Conditions: Chronic Obstructive Pulmonary Disease, Pulmonary Artery Hypertension, Heart Failure, Hypertension. Interventions: OTHER: Maximum Exercise Tests; DRUG: BH4, L-NMMA, Vitamin C, Vitamin E, α-Lipoic Acid and L-Ascorbate; DRUG: BQ-123; DRUG: Fexofenadine, Ranitidine; OTHER: Angiotensin-II, Valsartan; DRUG: Acetylcholine, Sodium Nitroprusside, Angiotensin-II, Norepinephrine, Phentolamine; DRUG: BQ-123, MitoQ, BH4. Primary outcome measures: Change in Limb Blood Flow , Baseline and 1 hour. Brief summary: Many control mechanisms exist which successfully match the supply of blood with the metabolic demand of various tissues under wide-ranging conditions. One primary regulator of vasomotion and thus perfusion to the muscle tissue is the host of chemical factors originating from the vascular endothelium and the muscle tissue, which collectively sets the level of vascular tone. With advancing age and in many disease states, deleterious adaptations in the production and sensitivity of these vasodilator and vasoconstrictor substances may be observed, leading to a reduction in skeletal muscle blood flow and compromised perfusion to the muscle tissue. Adequate perfusion is particularly important during exercise to meet the increased metabolic demand of the exercising tissue, and thus any condition that reduces tissue perfusion may limit the capacity for physical activity. As it is now well established that regular physical activity is a key component in maintaining cardiovascular health with advancing age, there is a clear need for further studies in populations where vascular dysfunction is compromised, with the goal of identifying the mechanisms responsible for the dysfunction and exploring whether these maladaptations may be remediable. Thus, to better understand the etiology of these vascular adaptations in health and disease, the current proposal is designed to study changes in vascular function with advancing age, and also examine peripheral vascular changes in patients suffering from chronic obstructive pulmonary disease (COPD), Sepsis, Pulmonary Hypertension, and cardiovascular disease. While there are clearly a host of vasoactive substances which collectively act to govern vasoconstriction both at rest and during exercise, four specific pathways that may be implicated have been identified in these populations: Angiotensin-II (ANG-II), Endothelin-1 (ET-1), Nitric Oxide (NO), and oxidative stress.