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 effects of endogenous or exogenous vasopressin in models of gastric mucosal injury with a different pathophysiology (ethanol, indomethacin, reserpine, cold-restraint stress and haemorrhagic shock-induced lesions) were investigated in rats. [Mca1,TyrMe2,Arg8]vasopressin, a vasopressin pressor (V1) receptor antagonist, was found to reduce dose dependently the extent of the lesions in all models, and to protect the deeper layer of the mucosa (assessed by histology). Endogenous vasopressin deficiency, as in Brattleboro homozygous rats, had a similar effect. [Lys8]Vasopressin injected exogenously aggravated all types of lesions in normal rats. Circulating vasopressin levels were increased by ethanol, reserpine, cold-restraint stress and haemorrhagic shock, but not by indomethacin, whereas the intramucosal vasopressin content was found to be elevated in all models. Additionally, specific binding sites for vasopressin were shown on the blood vessels of the gastric mucosa (assessed by autoradiography). It is concluded that vasopressin plays a significant aggressive role in the generation of these types of lesions.
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PMID:Aggressive role of vasopressin in development of different gastric lesions in rats. 792 94

We determined the effect of a centrally administered V1 receptor antagonist of arginine vasopressin on the brain water content in an animal model of vasogenic brain edema. Using adult rats, a cold injury was induced in the left hemisphere of the brain by applying a frozen copper rod. 50 ng of V1 receptor antagonist was administered into the left lateral ventricle 10 minutes prior to and/or 1 hour after injury. Twenty four hours after the cold injury, the brain water and sodium contents and plasma osmolality were measured. The V1 receptor antagonist significantly suppressed the increase of the brain water and sodium contents in the cortical structure adjacent to the lesion without any changes in plasma osmolality. Our results demonstrate the effectiveness of a V1 receptor antagonist of vasopressin on vasogenic brain edema.
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PMID:Treatment of vasogenic brain edema with arginine vasopressin receptor antagonist--an experimental study. 797 30

The extent of nephron injury after long-term preservation is unknown. An experimental protocol was designed to study the effects of 1 and 24 h of cold storage in preservation solution on renal slices of rabbit cortical collecting duct (CCD) isolated and perfused in vitro and evaluated by water hydraulic conductivity. The preservation solutions were Ringer-bicarbonate, Collins, Euro-Collins, and University of Wisconsin (UW). Under these experimental preservation conditions, the following results were observed: after 1 h of preservation, the CCDs obtained from slices incubated in Ringer-bicarbonate, Collins, and Euro-Collins solutions at 4 degrees C presented a high basal hydraulic conductivity compared to the control group and responded well to arginine-vasopressin (AVP) water permeability stimulation. The CCDs derived from renal slices stored for 24 h in Ringer-bicarbonate solution at 4 degrees C showed no function, while those preserved in Collins and Euro-Collins solutions showed a lack of responsiveness to AVP water permeability stimulation. The CCDs preserved in UW solution showed better values than those preserved in the other solutions, although there was a decrease in hydraulic conductivity after 24 h of preservation. These data show that long-term cold preservation with flushed solutions impairs the cortical collecting duct response to AVP.
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PMID:Effect of several electrolyte preservation solutions on the water permeability of isolated cortical collecting ducts perfused in vitro. 805 Feb 72

Peptides are rapidly being developed as potential new therapeutic agents and the nasal route is being evaluated as a means of achieving systemic absorption. Current research in man is being directed at a number of polypeptides, including calcitonin, growth hormone releasing hormones (GHRH), insulin, gonadotropin hormone releasing hormones (GnRH) and vasopressin analogues. The underlying protective functions of the nose provide anatomical, temporal and enzymatic barriers to absorption of peptides. The nasal route is relatively unsuccessful when used for high molecular weight polypeptides. Penetration enhancers improve bioavailability but are poorly tolerated. Reproducibility of effect is highly variable, major contributing factors including the site of deposition and type of delivery system as well as changes in the mucous secretion and mucociliary clearance, compounded by the presence of allergy, hay fever and the common cold in treated subjects. The future potential for this route lies in development of effective and well tolerated formulations in highly accurate delivery systems for the chronic administration of peptides, enabling the replacement of impractical and invasive intravenous injections in patients on lifelong substitution treatment for various deficiency states.
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PMID:Review: clinical opportunities provided by the nasal administration of peptides. 806 48

Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. In acute myocardial disfunction these systems can play a critical role in patient survival, however, they can directly worsen myocardial function and patient prognosis on a long-term basis. Other neurohumoral systems activated in heart failure (atrial natriuretic factor, prostaglandins, dopamine) tend to counterbalance the vasoconstrictive, sodium retentive mechanisms. Though their secretion is increased in heart failure, it is however not sufficient, and peripheral vasoconstriction and sodium retention prevail. Moreover the role of local factors, such as tissue renin-angiotensin system, EDRF and endothelin secretion has been recently pointed out. Neurohumoral activation is directly related to the severity of the clinical and hemodynamic impairment and prognosis of the patient with heart failure. A thorough evaluation of the neurohumoral mechanisms is therefore of paramount importance for the assessment of patients with heart failure. Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. The method most commonly used to assess neurohumoral activity relies on the direct measurement of the plasma concentrations. It must be noted, however, that plasma levels are critically dependent on many factors besides hormone secretion and metabolism. For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Plasma concentrations of neurohormones are related to the factors controlling their secretion: for example, "normal" values of plasma renin activity in presence of fluid retention and edema are to be judged as excessively elevated. Autonomic nervous system activity can also be assessed studying reflexes in which this system is involved (orthostasis, cold pressor test, phenylephrine test...). Another method consists in the study of the spontaneous variability of some parameters controlled by this system, such as heart rate and blood pressure. The most reliable method is based on the power spectral analysis of heart rate variability. With this last method, a low frequency component depending mainly on sympathetic activity and an high frequency component depending on vagal activity can be identified in heart rate variability. Thus, complex phenomena such as sympatho-vagal balance can be easily studied through simple noninvasive tools.
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PMID:[Neurohormonal assessment in heart failure: from the sophisticated laboratory to practical indications]. 809 6

Seasonal variations in the immunoreactivity of vasopressinergic perikarya in the paraventricular (PVN), supraoptic (SON) and suprachiasmatic nuclei (SCN), and in the labelling of vasopressinergic fibres in the internal zone of the median eminence were studied in Taterillus petteri, a rodent that is found in the north Burkina Faso (formerly Upper Volta). In this region, there are four seasonal climatic combinations: the humid and hot, humid and cold, dry and cold, and dry and hot seasons. In the dry hot season, the rodents experience phases of torpor (adaptation to dryness). Immunoreactivity of the PVN and SON is highest during the dry cold season. Labelling is intense during the dry hot and humid hot seasons, and is at its lowest during the humid cold season. In the SCN, labelling of the perikarya is only dense during the dry hot season, whereas for the rest of the year, the immunoreactivity is weak or undetectable. The pattern of immunoreactive variations of vasopressin-positive fibres located in the internal zone of the median eminence is similar to those of vasopressinergic perikarya in the PVN and SON. These results suggest that there is an association between: (1) seasonal modifications in the immunoreactivity of PVN and SON vasopressinergic perikarya and vasopressinergic fibres of the internal median eminence, and (2) climatic conditions, water metabolism, behavioural activity and diet. It is not possible to establish a correlation between seasonal variations in water availability and fluctuations in the labelling of vasopressinergic perikarya in the SCN. However, labelling is intense when the animals are in torpor during the dry hot season.
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PMID:Seasonal changes in the hypothalamic vasopressinergic system of a wild Sahelian rodent, Taterillus petteri. 845 56

The hypothesis that inhibition of vasopressin (VP) secretion initiates cold-induced diuresis was tested in six Brattleboro homozygous (diabetes insipidus, DI) rats exposed to 60 min at 5 degrees C. For 9-14 days before cold exposure (CE) the rats were treated with VP (750 pg.kg-1.min-1) subcutaneously via osmotic minipumps. Eight vehicle-treated Long-Evans (LE) rats characterized the response to acute exposure at 5 degrees C. Additional groups of six to eight LE and six DI rats were infused with VP (30-90 pg.kg-1.min-1 iv) on the day of CE. The DI rats receiving chronic VP replacement and untreated LE rats exhibited cold-induced diuresis, with peak increases in urine flow (V) of 63 +/- 12 (DIs) and 29 +/- 4 (LEs) microliters.min-1 x 100 g body wt-1. LE rats acutely infused with VP exhibited a diuresis at the two lower doses (peak V was 18 +/- 3 at the 30 and 18 +/- 4 microliters.min-1 x 100 g body wt-1 at the 60 pg.kg-1.min-1 dose), but the diuretic response was completely blunted at the uppermost dose of VP. Cold-induced diuresis was absent at the lowest VP dose in the acutely infused DI rats. A pressor response (30-36 mmHg) to CE was noted with all treatment groups, including those that did not exhibit a diuresis. No changes in glomerular filtration rate (GFR) with CE were observed. These data suggest that when plasma VP levels are controlled by prolonged infusion of VP in the DI rats, other mechanisms can operate to initiate cold-induced diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms for the diuresis of acute cold exposure: role for vasopressin? 845 4

Neuroendocrine activation belongs to the main characteristics of the stress response. This response is not uniform but depends on the stress stimulus involved and on many other factors including the gender of the individual. In rats, corticosterone and ACTH levels as well as functional activity of the hypothalamo-pituitary-adrenocortical axis are higher in females compared to males under both basal and stress conditions. Marked sex differences were observed in stress-induced changes posterior pituitary hormone release. In male rats, release of vasopressin is not stimulated during stress conditions without an osmotic component while in female rats a rise in plasma vasopressin levels was observed even after short immobilization. Oxytocin release is enhanced in response to the majority of stress stimuli and it was found to be greater in females than in males. Mentioned gender differences are attributed to the effect of sex steroids, particularly those of estrogens. Not enough information is available on gender differences in the neuroendocrine response during stress in humans. We observed a greater neuroendocrine activation in women than in men in response to heat exposure in sauna with pronounced differences in ACTH and prolactin release and partly also after a cold-pressor test. Understanding of gender differences in neuroendocrine response during stress might contribute to the explanation of the development of some emotional and other disorders with higher incidence in women.
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PMID:Neuroendocrine response during stress with relation to gender differences. 891 6

The ability to respond to adverse environmental cues is present in the neonatal and infant rat, although in an immature form: A number of laboratories have demonstrated stress-induced elevations of plasma glucocorticoids during the first two postnatal weeks. The limbic and hypothalamic mechanisms controlling the hormonal stress-response during this period are not fully understood and are, therefore, the focus of this report. Both hypothalamic corticotropin-releasing hormone (CRH) and vasopressin contribute to the release of ACTH from the pituitary in the adult. The relative roles of these two peptides during the neonatal (first week) and infant (second week) developmental period, are controversial. Evidence is presented that argues strongly for a major role for CRH. Up-regulation of hypothalamic CRH synthesis is a major component in the mature stress response. CRH-mRNA levels in the hypothalamic PVN are increased with cold stress by ninth postnatal day, but not during the first postnatal week. Further, down-regulation of CRH gene expression by glucocorticoids (GC) constitutes a critical "shut-down" mechanism for the hormonal stress response. In vivo and in vitro experiments supporting the "immaturity" of GC feedback on CRH synthesis during the first postnatal week are described. CRH-mediated neurotransmission, in both the endocrine and neuronal effector arms of the response to stress may be modulated via alteration of receptor number. The first member of the CRH receptor family, CRF1, probably mediates the neuroendocrine effects of CRH. The developmental profile of CRF1-mRNA reveals several distinctive spatial and temporal patterns. In the hippocampal CA1, CA2, and CA3a peak (300-600% adult values) CRF1-mRNA is found on postnatal day 6. In the amygdala, CRH receptor mRNA levels are maximal on the ninth postnatal day (at 180% of adult values). In cortex, a steady decline from high postnatal day 2 levels results in adult levels by 12. These findings demonstrate distinct, regional, age-specific control of the synthesis of CRF1. Receptor expression profile may provide important information regarding modulation of the age-specific roles of CRH in different regions. For example, a high ratio of hippocampus/amygdala receptors may preferentially activate negative hippocampal input to the hypothalamus during the neonatal period. Additionally, increased CRH receptor mRNA in the infant compared with the adult provides a mechanism for enhanced excitatory effect of the peptide at this age. In conclusion, increasing evidence exists for multiple control points of the early postnatal response and adaptation to stress. CRH synthesis in hypothalamus and amygdala, its sensitivity to GC feedback, and the abundance and distribution of at least two distinct CRH receptors in the limbic central nervous system and the pituitary are developmentally regulated. All serve as control points permitting an effective endocrine, autonomic, and behavioral response to stressful environmental cues.
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PMID:Development neurobiology of the stress response: multilevel regulation of corticotropin-releasing hormone function. 916 Sep 75

The hormonal responsiveness of freshly isolated rat hepatocytes was compared to that of a) cold-preserved isolated hepatocytes and b) hepatocytes isolated from cold-preserved whole liver. Cold-preserved hepatocytes and cells isolated from cold-preserved whole liver increased phosphorylase alpha activity in response to norepinephrine (plus propranolol), vasopressin, angiotensin II and glucagon. However, the maximal response to these agents was smaller than that of freshly isolated hepatocytes. Basal phosphorylase alpha activity was increased in cold-preserved hepatocytes. Similarly, cold preservation decreased the accumulation of cyclic AMP induced by glucagon and the effects of norepinephrine (plus propranolol), vasopressin and angiotensin II on the production of inositol phosphates. Basal levels of cyclic AMP were similar in the three conditions studied but basal production of [3H]IP2 plus [3H]IP3 was increased in cold-preserved hepatocytes. There was a very small effect of beta-adrenergic activation on phosphorylase activity and a small accumulation of cyclic AMP in response to isoproterenol in the conditions studied.
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PMID:Hormonal responsiveness of hepatocytes after hypothermic preservation in University of Wisconsin solution. 921 28


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