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)

A sensitive and specific radioimmunoassay has been developed capable of measuring thyrotropin releasing hormone (TRH) in extracted human plasma and urine. All of three TRH analogues tested had little cross-reactivity to antibody. Luteinizing hormone releasing hormone, lysine vasopressin, rat growth hormone and bovine albumin were without effect, but rat hypothalamic extract produced a displacement curve which was parallel to that obtained with the synthetic TRH. Sensitivity of the radioimmunoassay was 4 pg per tube with intraassay coefficient of variation of 6.2-9.7%. Synthetic TRH could be quantitatively extracted by methanol when added to human plasma in concentration of 25, 50 and 100 pg/ml. TRH immunoreactivity was rapidly reduced in plasma at 20 degrees C than at 0 degrees C, but addition of peptidase inhibitors, FOY-007 and BAL, prevented the inactivation of TRH for 3 hr at 0 degrees C. The TRH in urine was more stable at 0 degrees C than 20 degrees C, and recovered 75 +/- 4.6% hr after being added. The plasma levels of TRH were 19 pg/ml or less in normal adults and no sex difference was observed. The rate of disappearance of TRH administered i.v. from the blood could be represented as half-times of 4-12 min. Between 5.3-12.3% of the injected dose was excreted into urine within 1 hr as an immunoreactive TRH. These results indicate the usefulness of TRH radioimmunoassay for clinical investigation.
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PMID:Radioimmunoassay of thyrotropin releasing hormone in plasma and urine. 81 57

Visceral hypersensitivity and stress have been implicated in the pathophysiology of functional gastrointestinal disorders. We used a selective vasopressin 3 (V(3)) receptor antagonist SSR149415 to investigate the involvement of the vasopressin (AVP)/V(3) signaling system in the development of stress-induced visceral hyperalgesia in rats. Rats were exposed to a daily 1-h session of water avoidance stress (WAS) or sham WAS for 10 consecutive days. The visceromotor response to phasic colorectal distension (CRD, 10-60 mmHg) was assessed before and after stress. Animals were treated daily with SSR149415 (0.3, 1, or 3 mg/kg ip 30 min before each WAS or sham WAS session), with a single dose of SSR149415 (1 mg/kg ip), or the selective corticotropin-releasing factor 1 (CRF(1)) antagonist DMP-696 (30 mg/kg po) before CRD at day 11. Effects of a single dose of SSR149415 (10 mg/kg iv) on acute mechanical sensitization during repetitive CRD (12 distensions at 80 mmHg) were also assessed. In vehicle-treated rats, repeated WAS increased the response to CRD, indicating visceral hypersensitivity. Repeated administration of SSR149415 at 1 or 3 mg/kg completely prevented stress-induced visceral hyperalgesia. Similarly, a single dose of DMP-696 or SSR149415 completely blocked hyperalgesic responses during CRD. In contrast, a single dose of SSR149415 did not affect the acute hyperalgesic responses induced by repeated, noxious distension. These data support a major role for V(3) receptors in repeated psychological stress-induced visceral hyperalgesia and suggest that pharmacological manipulation of the AVP/V(3) pathway might represent an attractive alternative to the CRF/CRF(1) pathway for the treatment of chronic stress-related gastrointestinal disorders.
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PMID:Involvement of vasopressin 3 receptors in chronic psychological stress-induced visceral hyperalgesia in rats. 1903 33

Many trauma patients are acutely intoxicated with alcohol. Animal studies have demonstrated that acute alcohol intoxication inhibits the normal release of epinephrine, norepinephrine, and vasopressin in response to acute hemorrhage. Ethanol also increases nitric oxide release and inhibits antidiuretic hormone secretion. This article studies the effects of alcohol intoxication (measured by blood alcohol level, BAL) on the presentation and resuscitation of trauma patients with blunt hepatic injuries. A retrospective registry and chart review was conducted of all patients who presented with blunt liver injuries at an ACS-verified, level I trauma center. Data collected included admission BAL, systolic blood pressure, hematocrit, International Normalized Ratio (INR), liver injury grade, Injury Severity Score (ISS), intravenous fluid and blood product requirements, base deficit, and mortality. From September 2002 to May 2008, 723 patients were admitted with blunt hepatic injuries. Admission BAL was obtained in 569 patients, with 149 having levels >0.08%. Intoxicated patients were more likely to be hypotensive on admission (p = 0.01) despite a lower liver injury grade and no significant difference in ISS. There was no significant difference in the percent of intoxicated patients requiring blood transfusion. However, when blood was given, intoxicated patients required significantly more units of packed red blood cells (PRBC) than their nonintoxicated counterparts (p = 0.01). Intoxicated patients also required more intravenous fluid during their resuscitation (p = 0.002). Alcohol intoxication may impair the ability of blunt trauma patients to compensate for acute blood loss, making them more likely to be hypotensive on admission and increasing their PRBC and intravenous fluid requirements. All trauma patients should have BAL drawn upon admission and their resuscitation should be performed with an understanding of the physiologic alterations associated with acute alcohol intoxication.
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PMID:Acute ethanol intoxication and the trauma patient: hemodynamic pitfalls. 2174 16