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)

1. The kinetics of excretion of water, sodium and potassium following a stomach load of water, with and without an initial injection of vasopressin, are described in each of four strains of mice: RAP, CBA/FaCam, Peru and A/Cam.2. In general there was a diuretic lag followed by an increase in the rate of excretion of water to a maximum, after which the rate of excretion fell again to near resting levels. The rate of excretion of sodium rose to an initial maximum which significantly preceded the maximum rate of water excretion. The rate of excretion of sodium then fell to a minimum at a time not significantly different from the time of maximum rate of water excretion.3. The effect of an initial injection of vasopressin was to increase and to prolong the initial rise in rate of sodium excretion. The maximum rate of water excretion and the minimum sodium concentration were delayed, but the levels eventually reached were not significantly altered, by the vasopressin injection.4. The strains of mice differed significantly in diuretic lag, maximum rate of diuresis, and 3 hr excretion of water and electrolytes.5. The strains also differed significantly in the effects of vasopressin, both in increasing diuretic lag and in increasing sodium excretion. There was no correlation between the antidiuretic and natriuretic effects of vasopressin.
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PMID:Diuretic responses to water-load in four strains of mice. 569 76

In the adult, corticotropin-releasing hormone (CRH) is the key mediator for the behavioural and neuroendocrine response to stress. It has also been hypothesized that, during postnatal development of the stress system, CRH controls the activity of the HPA axis and mediates the effects of early disturbances, e.g. 24 h of maternal deprivation. In the current study we investigated the function of specific brain corticotropin-releasing hormone receptor type 1 (CRHR1) subpopulations in the control of the HPA axis during postnatal development under basal conditions as well as after 24 h of maternal deprivation. We used two conditional CRHR1-deficient mouse lines which lack this receptor, either specifically in forebrain and limbic structures (Cam-CRHR1) or in all neurons (Nes-CRHR1). Basal circulating corticosterone was increased in Nes-CRHR1 mice compared to controls. Corticosterone response to maternal deprivation was significantly increased in both CRHR1-deficient lines. In the paraventricular nucleus, Cam-CRHR1 animals displayed enhanced CRH and decreased vasopressin expression levels. In contrast, gene expression in Nes-CRHR1 pups was strikingly similar to that in maternally deprived control pups. Furthermore, maternal deprivation resulted in an enhanced response of Cam-CRHR1 pups in the brain, while expression levels in Nes-CRHR1 mouse pups were mostly unchanged. Our results demonstrate that brainstem and/or hypothalamic CRHR1 contribute to the suppression of basal corticosterone secretion in the neonate, while limbic and/or forebrain CRHR1 dampen the activation of the neonatal HPA axis induced by maternal deprivation.
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PMID:Differential disinhibition of the neonatal hypothalamic- pituitary-adrenal axis in brain-specific CRH receptor 1-knockout mice. 1704 89