Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken in order to establish the possible involvement of serotonergic receptors in the control of physical exercise-stimulated vasopressin secretion. Twenty-one healthy men (divided in three groups of seven) underwent bicycle-ergometer tests until exhaustion: exercise control test (n=21), exercise plus ondansetron, selective 5-HT3 antagonist (n=7), exercise plus buspirone, selective 5-HT1A receptor agonist (n=7), exercise plus sumatriptan, selective 5-HT1D receptor agonist (n=7). AVP levels, physiological and biochemical variables were measured and compared during tests. Results showed that exercise-induced AVP rise did not change after the administration of buspirone and sumatriptan. In contrast, the administration of ondansetron significantly reduced physical exercise-induced AVP rise. Mean peak levels during physical exercise were 4.9 times higher than basal values in the control test and 2.6 times higher than basal values in the ondansetron plus exercise test. These data demonstrate that 5-HT3 serotonergic receptors at least partially mediate the AVP response to physical exercise. On the other hand, 5-HT1A and 5-HT1D serotonergic receptors do not appear to be involved in the control of AVP secretion during exercise.
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PMID:Effect of serotonergic system on AVP secretion induced by physical exercise. 1991 13

This study was performed in order to establish whether endogenous opioids play a role in the inhibitory effect of melatonin on arginine-vasopressin (AVP) response to physical exercise. Seven healthy men underwent four bicycle ergometer tests until exhaustion [exercise control test, exercise plus naloxone (2mg injected plus 5mg infused intravenously), exercise plus melatonin (6mg), exercise plus melatonin plus naloxone]. Plasma AVP concentrations, non endocrine physiological parameters (NEPP) and biochemical parameters were evaluated during all tests. NEPP and biochemical values had a similar pattern during all tests. Physical exercise significantly increased the AVP levels. The pre-treatment with melatonin inhibited the AVP response to physical exercise. In contrast, naloxone had no effect on AVP rise during exercise, when given alone, whereas it abolished the negative effect of melatonin on AVP response to physical exercise. Our data indicate that naloxone-sensitive endogenous opiates mediate the inhibitory modulation exerted by melatonin on the AVP response to physical exercise.
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PMID:Effect of naloxone on the inhibitory effect of melatonin on the release of arginine-vasopressin induced by physical exercise in man. 2034 89

To establish whether glucocorticoids inhibit the arginine-vasopressin (AVP) response to physical exercise, 10 healthy men underwent bicycle ergometer tests until exhaustion (exercise control test, exercise plus dexamethasone [2 or 4 mg in an intravenous bolus]). Physiological and biochemical variables were similar in all tests. Pretreatment with dexamethasone (2 or 4 mg) partially but significantly decreased the AVP response induced by physical exercise. Our results demonstrate a partial inhibition induced by glucocorticoids of AVP neurosecretion during cycle ergometer tests.
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PMID:Inhibitory effect of dexamethasone on arginine-vasopressin release induced by physical exercise in man. 2122 38

A regulatory effect of arginine vasopressin (AVP) on sweat water conservation has been hypothesized but not definitively evaluated. AVP-mediated insertion of sweat and salivary gland aquaporin-5 (AQP5) water channels through activation of the vasopressin type 2 receptor (V2R) remains an attractive, yet unexplored, mechanism that could result in a more concentrated sweat with resultant decreased water loss. Ten runners participated in a double-blind randomized control treadmill trial under three separate pharmacological conditions: a placebo, V2R agonist (0.2 mg desmopressin), or V2R antagonist (30 mg tolvaptan). After a familiarization trial, runners ran for 60 min at 60% of peak speed followed by a performance trial to volitional exhaustion. Outcome variables were collected at three exercise time points: baseline, after the steady-state run, and after the performance run. Body weight losses were <2% across all three trials. Significant pharmacological condition effects were noted for urine osmolality [F = 84.98; P < 0.0001] and urine sodium concentration ([Na(+)]) [F = 38.9; P < 0.0001], which verified both pharmacological activation and inhibition of the V2R at the kidney collecting duct. Plasma osmolality and [Na(+)] demonstrated significant exercise (F = 26.0 and F = 11.1; P < 0.0001) and condition (F = 5.1 and F = 3.8; P < 0.05) effects (osmolality and [Na(+)], respectively). No significant exercise or condition effects were noted for either sweat or salivary [Na(+)]. Significant exercise effects were noted for plasma [AVP] (F = 22.3; P < 0.0001), peak core temperature (F = 103.3; P < 0.0001), percent body weight change (F = 6.3; P = 0.02), plasma volume change (F = 21.8; P < 0.0001), and thirst rating (F = 78.2; P < 0.0001). Performance time was not altered between conditions (P = 0.80). In summary, AVP acting at V2R does not appear to regulate water losses from body fluids other than renal excretion during exercise.
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PMID:Characterization of the effects of the vasopressin V2 receptor on sweating, fluid balance, and performance during exercise. 2494 42


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