An interventional study of V2R (Vasopressin 2 receptor) in Electrolyte Imbalance, Hyponatremia and Hypernatremia, sponsored by Oakland University. Completed at 1 site in United States. Open to participants aged 18 Years to 60 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2016-05-12.
Sponsored by Oakland University · Not applicable and Interventional
Among 40 studies in Hyponatremia with a site in United States — none open to participants now, none under way, none of them phase 3. Hyponatremia · United States.
Among the 40 studies in Hyponatremia with a site in United States, this one is the 28th largest by enrollment of the 36 interventional ones, is one of 3 that started in 2011, is one of 9 with no phase, and was the 31st registered.
164 studies on the registry are indexed under Hyponatremia; 16 are open to participants now.
This study's enrollment of 10 is below the median of 60 across 98 interventional studies indexed under Hyponatremia.
Browse Hyponatremia studies →None of the 40 studies in Hyponatremia with a site in United States is open now.
Of the 14 Hyponatremia studies recruiting now, 13 (93%) set no upper age limit and 0 (0%) stop at 75 or younger; 1 take children under 18; 0 take healthy volunteers.
This study: 18 Years to 60 Years · all sexes · healthy volunteers too.
The full table on the hub →40 studies; the count open now beside each. This study's row is marked.
First in 2000; this study’s year is marked. 3 started in 2011.
Median enrollment 51 across the 36 interventional studies, 313 across the 4 observational. Of the 36 that completed or were terminated, 11 (31%) have results posted.
21 of 40 have an industry lead sponsor. The 10 most frequent:
Oakland University is the lead sponsor of 10 studies on the registry; 1 is open to participants now.
Oakland University has 1 study filed under Hyponatremia — fewer than ten, so there is no comparison to draw.
None of the studies under way reaches primary completion within a year.
Among the 40 studies in Hyponatremia with a site in United States, from their registry updates:
Nothing recorded among them since 2026-09-25.
This primary aim of this study was to critically assess whether or not sweat water content and sodium concentration were acutely regulated by dynamic changes in antidiuretic hormone (arginine vasopressin or AVP) acting on the Vasopressin 2 receptor (V2R) during exercise. Secondary aims were to evaluate running performance and core temperature to further characterize the role of AVP in the coordinated balance of fluid and temperature homeostasis during exercise. The primary hypothesis was that activation of the V2R in sweat glands would result in water reabsorption and fluid conservation during endurance exercise.
Ten healthy habitual runners (> 50km running per week) between 18-60 years of age participated in this double blind randomized control trial. Each subject presented to the exercise lab on four separate occasions. Trial 1 was a familiarization trial to determine each subject's maximal aerobic capacity and peak treadmill running speak (VO2 Peak test). Trials 2, 3 and 4 utilized the same exact protocol, differing only in pharmacological intervention. In a randomized, double-blind order (both participant and investigator blinded to the intervention), either a placebo pill, the V2 receptor antagonist tolvaptan (Samsca™, 30mg tablet), or the V2 receptor agonist desmopressin (DDAVP™, 0.2mg tablet) was ingested along with the CorTemp™ Core Temperature Sensor two hours before commencement of the Exercise Trial with 240mL of bottled water. The exercise protocol consisted of 60 minutes of treadmill running at 60% of peak speed (steady-state) followed by a performance test (the VO2 Peak test). Blood, saliva and urine, were collected before the exercise trial (baseline) and again after both the steady-state run and performance runs. Sweat was obtained from sweat patches after both the steady-state and performance runs. Core temperature, fluid intake, performance time, body weight, thirst and sodium palatability ratings were also assessed. Free access to water was allowed during the trial and all urine produced during the trial was measured and collected. The main outcome measure was sweat sodium concentration.
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Exclusion Criteria:
All study participants received all interventions. V2R Antagonist: 30mg Tolvaptan tablet ingested 2 hours before exercise. V2R agonist: 0.2mg DDAVP tablet ingested 2 hours before exercise Placebo
Drug: V2R (Vasopressin 2 receptor)
All ten subjects were used as their own controls in this double-blind, randomized controlled trial assessing the effect of the V2R on sweat sodium concentration via use of a V2R blocker (antagonist), stimulator (agonist), against a placebo (drug naive state).
Also known as: V2R antagonist: tolvaptan (30mg tablet), V2R agonist: desmopressin (0.2mg tablet)
Sweat Sodium Concentration Obtained After the Steady-state Portion of the Trial
Changes in sweat sodium concentration will parallel changes in urine sodium concentration with use of the V2R antagonist, agonist and placebo if the primary hypothesis is true (sweat sodium is regulated by the V2R, similar to how urine sodium is regulated by principle cells located within in the kidney collecting duct)
Time frame: 4 study trials (4 weeks)
Urine Sodium Concentration After the Steady-state Portion of the Trial
Changes in urine sodium concentration after use of the V2R antagonist, agonist and placebo interventions will verify whether or not pharmacologic activation or inhibition was successfully induced.
Time frame: 4 study trials (4 weeks)
Blood Sodium Concentration
Measurement of blood sodium concentration will determine if normonatremia (blood sodium concentrations within the normal physiological range of 135-145mmol/L) were maintained throughout the trial with appropriate fluid intake during the V2R antagonist, agonist and placebo intervention trials.
Time frame: 4 study trials (4 weeks)
Saliva Sodium Concentration
Measurement of salivary sodium concentration will allow us to determine if the V2R antagonist, agonist and placebo interventions activate aquaporin-5 (AQP5) water channels that are also located in sweat glands. If the V2R acts on the sweat glands through AQP5, there should be parallel changes in sweat, urine and saliva sodium concentrations with each pharmaceutical intervention.
Time frame: 4 trials (4 weeks)
Body Weight
Changes in body weight during the V2R antagonist, agonist and placebo conditions will provide researchers with an additional measure of overall fluid balance (fluid in versus fluid out) as well as an estimate of overall sweat water losses.
Time frame: 4 trials (4 weeks)
Core Temperature
Measurement of core temperature using an ingestible CorTemp sensor during the V2R antagonist, agonist and placebo trials will allow researchers to assess if fluid homeostasis and thermoregulation were intertwined in response to each pharmacological intervention.
Time frame: 4 trials (4 weeks)
Thirst Rating
To determine if fluid intake behaviors were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Time frame: 4 trials (4 weeks)
Sodium Palatability Ratings
To determine if sodium preference ratings were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Time frame: 4 weeks (4 trials)
Performance
To determine if exercise performance, as determined by overall exercise time, was affected in response to the V2R antagonist, agonist and placebo conditions.
Time frame: 4 trials (4 weeks)
Fluid Intake
To determine if fluid intake behaviors were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Time frame: 4 weeks (4 trials)
| Milestone | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Started | 10 |
| Completed | 10 |
| Not completed | 0 |
Changes in sweat sodium concentration will parallel changes in urine sodium concentration with use of the V2R antagonist, agonist and placebo if the primary hypothesis is true (sweat sodium is regulated by the V2R, similar to how urine sodium is regulated by principle cells located within in the kidney collecting duct)
| mEq/L | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Placebo | 80.1 ± 21.6 |
| V2R Agonist | 76.8 ± 24.5 |
| V2R Antagonist | 84.7 ± 25.7 |
Changes in urine sodium concentration after use of the V2R antagonist, agonist and placebo interventions will verify whether or not pharmacologic activation or inhibition was successfully induced.
| mEq/L | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Placebo | 82.0 ± 48.5 |
| V2R Agonist | 89.3 ± 21.5 |
| V2R Antagonist | 16.4 ± 5.0 |
Measurement of blood sodium concentration will determine if normonatremia (blood sodium concentrations within the normal physiological range of 135-145mmol/L) were maintained throughout the trial with appropriate fluid intake during the V2R antagonist, agonist and placebo intervention trials.
| mEq/L | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Placebo | 143.6 ± 1.5 |
| V2R Agonist | 144.3 ± 2.3 |
| V2R Antagonist | 145.9 ± 2.0 |
Measurement of salivary sodium concentration will allow us to determine if the V2R antagonist, agonist and placebo interventions activate aquaporin-5 (AQP5) water channels that are also located in sweat glands. If the V2R acts on the sweat glands through AQP5, there should be parallel changes in sweat, urine and saliva sodium concentrations with each pharmaceutical intervention.
| mEq/L | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Placebo | 20.5 ± 11.0 |
| V2R Agonist | 28.1 ± 9.5 |
| V2R Antagonist | 31.0 ± 13.3 |
Changes in body weight during the V2R antagonist, agonist and placebo conditions will provide researchers with an additional measure of overall fluid balance (fluid in versus fluid out) as well as an estimate of overall sweat water losses.
Results for this outcome have not been posted.
Measurement of core temperature using an ingestible CorTemp sensor during the V2R antagonist, agonist and placebo trials will allow researchers to assess if fluid homeostasis and thermoregulation were intertwined in response to each pharmacological intervention.
Results for this outcome have not been posted.
To determine if fluid intake behaviors were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Results for this outcome have not been posted.
To determine if sodium preference ratings were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Results for this outcome have not been posted.
To determine if exercise performance, as determined by overall exercise time, was affected in response to the V2R antagonist, agonist and placebo conditions.
Results for this outcome have not been posted.
To determine if fluid intake behaviors were appropriately regulated in response to the V2R antagonist, agonist and placebo conditions during exercise.
Results for this outcome have not been posted.
Non-serious events are listed at a 0% frequency threshold.
| Group | Deaths | Serious | Other |
|---|---|---|---|
| 1/Placebo, V2R Agonist, V2R Antagonist | — | 0/10 (0%) | 0/10 (0%) |
| Age, Continuous(years) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Mean | 35.5 ± 13.1 |
| Sex: Female, Male(Participants) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Female | 2 |
| Male | 8 |
| Region of Enrollment(participants) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| United States | 10 |
| years of running experience(years) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Mean | 8.8 ± 8.7 |
| BMI(kg/m2) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Mean | 22.5 ± 3.3 |
| VO2 Peak(ml/kg/minute) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Mean | 58.7 ± 6.2 |
| Peak treadmill running speed(mph) | 1/Placebo, V2R Agonist, V2R Antagonist |
|---|---|
| Mean | 11.0 ± 1.4 |
The record gives a start of Jun 2011, a primary completion of Oct 2011 and a completion of Oct 2012. It does not say whether these dates are actual or estimated.
Results were first posted in May 2016, 4 years 7 months after primary completion.
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This study is completed, as verified in Apr 2016. You cannot join it, but the record below documents what was studied.
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Oakland University