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 effect of vasopressin (VP) on prostaglandin (PG) synthesis in the renal collecting tubule remains equivocal. To further address this issue, the present study determined the effects of chronic absence of VP on renal medullary collecting tubule PG synthesis. Prostaglandin E2 (PGE2) synthesis was measured in both inner and outer medullary slices and collecting tubules microdissected from the inner medulla (PCD) and outer medulla (MCT) of Brattleboro homozygous diabetes insipidus (DI) rats, which are genetically devoid of VP, and from Long Evans (LE) control rats. In vitro PGE2 synthesis was significantly lower in both inner medullary (delta - 56%; p less than 0.001) and outer medullary (delta - 56%; p less than 0.01) slices of DI rats compared to controls. Vasopressin tannate treatment (0.5 U/day for 5 days) increased urinary PG excretion, and increased in vitro PGE2 synthesis in both inner and outer medullary slices of DI rats to levels that did not differ from vehicle-treated LE controls. In contrast, PGE2 synthesis in both PCD and MCT of DI rats did not differ from LE controls when incubated either in an isotonic (300 mOsm) medium, or in an hypertonic (1000 mOsm) medium. These results suggest that PGE2 biosynthetic capacity of medullary collecting tubules in the DI rat is not dependent on VP, while depressed PGE2 synthesis in renal medullary slices of DI rats, suggests that the interstitial cell is the primary medullary site of PG synthesis which is modulated by VP.
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PMID:Renal prostaglandin E2 synthesis in the Brattleboro homozygous diabetes insipidus rat. 345 94

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71

Serotonin (5-HT), 5-HT agonists, the 5-HT precursor 5-hydroxytryptophan, 5-HT-releasers and -reuptake inhibitors stimulate the release of vasopressin and oxytocin. We investigated the involvement of 5-HT receptors in the serotonergic regulation of vasopressin and oxytocin secretion. Vasopressin and oxytocin secretion was stimulated by 5-HT, the 5-HT(1A+1B+5A+7) agonist 5-carboxamidotryptamine (5-CT), the 5-HT(2A+2C) agonist DOI, the 5-HT(2C+2A) agonist mCPP, the 5-HT(2C) agonist MK-212, the 5-HT(3) agonist SR 57277 and the 5-HT(4) agonist RS 67506. The 5-HT(1A) agonist 8-OH-DPAT, which had no effect on vasopressin secretion, stimulated oxytocin secretion. The 5-HT-induced release of vasopressin and oxytocin was inhibited by central infusion of the 5-HT antagonists WAY 100635 (5-HT(1A)), LY 53857 (5-HT(2A+2C)), ICS 205-930 (5-HT(3+4)) and RS 23597 (5-HT(4)). The 5-HT2+6+7 antagonist metergoline in combination with the 5-HT1A+2+7 antagonist methysergide inhibited the stimulatory effect of 5-CT on both hormones, whereas the 5-HT1A+1B antagonist cyanopindolol only inhibited the oxytocin response. The 5-HT(2A) antagonist 4-(4-flourobenzoyl)-1-(4-phenylbutyl)-piperidine oxalate had no effect on DOI-induced hormone response. The 5-HT(2C) antagonist Y 25130 partly inhibited the stimulating effect of MK-212. ICS 205-930 and RS 23597 inhibited vasopressin and oxytocin secretion induced by RS 67506. WAY 100635 inhibited 8-OH-DPAT-induced oxytocin secretion. We conclude that 5-HT-induced vasopressin secretion primarily is mediated via 5-HT(2C), 5-HT(4) and 5-HT(7) receptors, whereas 5-HT(2A), 5-HT(3) and 5-HT(5A) receptors seem to be of minor importance. 5-HT-induced oxytocin secretion involves 5-HT(1A), 5-HT(2C) and 5-HT(4) receptors; in addition an involvement of 5-HT(1B), 5-HT(5A) and 5-HT(7) receptors seems likely, whereas 5-HT(2A) and 5-HT(3) receptors seem to be less important.
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PMID:Serotonin receptors involved in vasopressin and oxytocin secretion. 1258 12