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 combined administration of CRH and vasopressin to man now offers a powerful means to directly assess the pituitary corticotroph reserve. A double blind, randomized, placebo-controlled, cross-over trial offered the opportunity to perform the combined CRH/lysine vasopressin (LVP) test (100 micrograms ovine CRH, followed by 1 IU LVP over 15 min) on 3 different occasions without treatment in 10 normal male subjects. We showed that peak ACTH plasma levels after stimulation had wide intersubject variation, whereas they were remarkably stable in a given individual, with a mean intraclass correlation coefficient of 0.90 (95% confidence limits, 0.74-0.96). Peak ACTH plasma levels after CRH/LVP administration were not significantly correlated with basal plasma cortisol levels (r = -0.14; P > 0.45), but were strongly and inversely correlated with peak cortisol plasma levels after Cortrosyn stimulation (0.25 mg, im; r = -0.78; P < 0.0001). These data provide the first evidence that the overall hypothalamic-pituitary-adrenocortical axis has an intrinsic activity that is constitutively fixed for a given individual. The power of the combined CRH/LVP test offers a unique means to measure a genuine corticotroph phenotype in each individual.
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PMID:The combined corticotropin-releasing hormone/lysine vasopressin test discloses a corticotroph phenotype. 804 53

Prolonged use of glucocorticoids (GCs) can cause prolonged suppression of the hypothalamus-pituitary-adrenal (HPA) axis. This study examined the possibility that corticotropin or its secretagogues such as vasopressin, corticotropin-releasing hormone (CRH), or insulin accelerate recovery of the HPA axis after prolonged treatment with dexamethasone (DEX). Suppression of the HPA axis was induced in rats by DEX at a dosage of 250 micrograms/100 g body weight (BW)/d for 14 days, after which rats were administered saline, corticotropin (Cortrosyn 0.1 mg), ovine CRH (oCRH 6 micrograms), vasopressin (2 U), or insulin (2 U) each morning. Adrenal weight (AW), BW, plasma corticosterone, and corticotropin, as well as pituitary corticotropin content, decreased significantly after DEX treatment. The plasma corticotropin level was significantly elevated 7 days after discontinuation of DEX treatment (day 8) and remained so until day 11, whereas the pituitary corticotropin content had returned to normal on day 8. Plasma corticosterone was suppressed until day 8, but was not significantly different from normal on day 11. The AW was also decreased until day 4, but was not different from normal on day 8 or day 11. The BW of experimental rats remained subnormal during the study period. Treatment of DEX-suppressed rats with exogenous corticotropin induced adrenal hyperplasia, but suppressed the plasma corticotropin level and delayed the normalization of plasma corticosterone until day 11. The insulin-treated group differed in no respect from the saline-treated group. Treatment with oCRH or vasopressin for 8 days normalized plasma and pituitary corticotropin, as well as plasma corticosterone. Hypothalamic immunoreactive CRH (iCRH) did not differ among any treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin secretagogues facilitate recovery of the hypothalamus-pituitary-adrenal axis suppressed by prolonged treatment with dexamethasone. 817 41