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)

ACTH and lipotropins (beta- and gamma-LPH) are synthesized from a common precursor by the pituitary corticotropic cell. We have measured LPH plasma levels under physiological and pathological conditions and we have compared them with ACTH plasma levels in the same circumstances. Spontaneous variations (nycthemeral rhythm) in LPH, ACTH and cortisol plasma levels were parallel, while responses to Dexamethasone freination test and stress (Insulin induced hypoglycemia) or more specific stimulation (Metopirone, lysine-vasopressin) were parallel and superimposable. LPH levels were always higher than ACTH levels in two pathological circumstances: chronic renal failure and Cushing's syndromes with ectopic ACTH producing tumors. The determination of both ACTH and LPH levels assists the diagnosis of corticotropic insufficiency and etiologic investigation of Cushing's syndrome, after hypercorticolism had been established. Although unable to confirm the presence of corticotropic adenoma in patients with Cushing's disease, or the predict effectiveness of pituitary surgery, these determination bring good arguments for treated Cushing's diseases follow up.
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PMID:[ACTH, beta-endorphin and lipotropins: physiopathological studies in man (author's transl)]. 628 91

The Brattleboro strain of Long-Evans hooded rats has hereditary hypothalamic diabetes insipidus due to the inability to produce antidiuretic hormone. Animals homozygous for this autosomal recessive trait have extreme polyuria and polydipsia, whereas heterozygotes are less severely affected. Light and electron microscopy were used to study the interstitial tissue of the renal papilla of Brattleboro rats and normal Long-Evans rats. Staining with alcian blue or colloidal iron revealed that homozygous Brattleboro rats (DI) have greatly reduced quantities of glycosaminoglycans in the papillary interstitium. Heterozygotes showed staining similar but not identical to that of normal rats. The papillary interstitial cells of DI rats lacked the cytoplasmic processes seen in normal rats, and the normal relationship of these cells to the tubular elements of the papilla was absent. Electron microscopy revealed that the papillary interstitial cells of DI rats appeared less active than those of heterozygous or normal rats. In DI rats these cells displayed reduced numbers of lipid droplets and mitochondria, and the Golgi apparatus and rough endoplasmic reticulum were poorly developed. The altered ultrastructure of the papillary interstitial cells may be responsible for the reduction of interstitial glycosaminoglycans in DI rats. Glycosaminoglycans possess properties which may contribute to urinary concentration, It is suggested that the interstitial tissue of the renal papilla is influenced by antidiuretic hormone.
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PMID:Histochemistry and ultrastructure of the interstitium of the renal papilla in rats with hereditary diabetes insipidus (Brattleboro strain). 740 59

1. An inositol trisphosphate (InsP3) distinct from Ins(1,4,5)P3 and Ins(1,3,4)P3, which we previously observed in myeloid and lymphoid cells [French, Bunce, Stephens, Lord, McConnell, Brown, Creba and Michell (1991) Proc R. Soc. London B 245, 193-201; Bunce, French, Allen, Mountford, Moore, Greaves, Michell and Brown (1993) Biochem. J. 289, 667-673], is present in WRK1 rat mammary tumour cells and pancreatic endocrine beta-cells. 2. It has been identified as Ins(1,2,3)P3 by a combination of oxidation to ribitol, a structurally diagnostic polyol, and ammoniacal hydrolysis to identified inositol monophosphates. 3. Ins(1,2,3)P3 concentration in HL60 cells changed little during stimulation by ATP or fMetLeuPhe or during neutrophilic or monocytic differentiation, and Ins(1,2,3)P3 was unresponsive to vasopressin in WRK1 cells. 4. Ins(1,2,3)P3 was usually more abundant than Ins(1,4,5)P3, often being present at concentrations between approximately 1 microM and approximately 10 microM. 5. HL60, WRK-1 and lymphoid cells also contain Ins(1,2)P2 or Ins(2,3)P2, or a mixture of these two enantiomers, as a major InsP2 species. 6. Ins(1,2,3)P3 and Ins(1,2)P2/Ins(2,3)P2 are readily detected in cells labelled for long periods, but not in acutely labelled cells. This behaviour resembles that of InsP6, the most abundant cellular inositol polyphosphate that includes the 1,2,3-trisphosphate motif, which also achieves isotopic equilibrium with inositol only slowly. 7. Ins(1,2,3)P3 is the major InsP3 that accumulates during metabolism of InsP6 by WRK-1 cell homogenates. 8. Possible metabolic relationships between Ins(1,2,3)P3, Ins(1,2)P2/Ins(2,3)P2 and other inositol polyphosphates in cells, and a possible role for Ins(1,2,3)P3 in cellular iron handling, are considered.
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PMID:Inositol 1,2,3-trisphosphate and inositol 1,2- and/or 2,3-bisphosphate are normal constituents of mammalian cells. 788 11

We studied the urinary concentrating capacity in experimental hemochromatosis. Sprague-Dawley rats were randomized into iron (Fe)-loaded (injected sc with 1.2 g elemental iron/kg body weight as iron dextran) and pair-fed control groups. The urinary concentrating ability was studied after 10 months of iron loading. At basal condition, urine osmolality (Uosm) was significantly lower (P < 0.05) in the Fe-loaded rats compared with the control animals despite comparable urinary arginine-vasopressin (AVP) excretion in the two groups. Although 48-h water deprivation resulted in comparable rises in plasma concentration and urinary excretion of AVP in the two groups, maximal Uosm in the Fe-loaded animals was significantly lower than that seen in the control group (P < 0.01). Moreover, the observed urinary concentrating defect could not be corrected by pharmacological doses of exogenous AVP. There was no significant difference in renal chloride, sodium, calcium, or magnesium handling at either basal or sodium depleted states. Histologic studies showed marked iron deposition in the cortex and outer medulla accompanied by mild tubular atrophy particularly in the distal convoluted tubules. Thus, chronic experimental iron overload leads to nephrogenic diabetes insipidus marked by AVP-resistant urinary concentrating defect.
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PMID:Urinary concentrating defect in experimental hemochromatosis. 880 19

Since iron has been implicated as a potential nephrotoxin, we examined the effect of iron on several aspects of cultured renal tubular epithelial cell biology. We found that exposure to 10(-4) M of either the ferrous or ferric form of iron impaired healing of denuded areas made within confluent monolayers of LLC-PK1 cells. This impairment required 30 to 80 hours of exposure to iron to occur and was also seen in another renal tubular epithelial cell line (MDCK cells). To delineate the potential mechanism(s) of this impairment, we examined the expression of a key integrin subunit involved in cell-matrix adhesion. Exposure of LLC-PK1 cells to 10(-4) M ferric citrate for 72 hours significantly decreased expression of the beta 1 integrin subunit as determined by flow cytometry. To determine if iron impairs another process that occurs at the basolateral surface, the effects of 72 hours of exposure to iron on adenylate cyclase activity were examined. Both ferric and ferrous citrate significantly enhanced vasopressin- and forskolin-stimulated adenylate cyclase activity. To examine if iron can regulate proliferation, the effect of iron on 3H-thymidine uptake was measured. We found that ferric citrate diminished proliferation and this decrease required the presence of either serum or transferrin. To ascertain if iron affected ultrastructure, we used transmission electron microscopy and found that iron accumulation within cells was much more apparent with ferric than ferrous citrate. Ferric iron induced mild-to-moderate cytopathic changes. These results indicate that iron is capable of inducing multiple changes in renal tubular epithelial function. The effect of iron to impair wound healing may be related to diminished expression of the beta 1 integrin subunit and perhaps to impaired proliferation.
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PMID:Effect of iron on renal tubular epithelial cells. 884 Feb 71

Treatment for the paraneoplastic syndrome associated with lung cancer was reviewed. The principle of the treatment of paraneoplastic syndrome is to control cancer as an underlying disease. Therefore, the standard therapy for Cushing's syndrome associated with lung cancer is surgical treatment if the tumor is operable. There is no standard therapy for Cushing's syndrome associated with advanced small-cell lung cancer. Metyrapone is used in combination with systemic chemotherapy. The effects of ketoconazole and octreotide are under investigation. To control hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion, fluid restriction is standard. When hyponatremia cannot be controlled with fluid restriction, demeclocycline can be used. For life-threatening hyponatremia, hypertonic saline with intravenous furosemide is administered under careful monitoring. Followed by hydration with saline, pamidronate is effective for the control of symptomatic hypercalcemia. Combined use of calcitonin facilitates rapid normalization of serum calcium for critically ill cases. Heparin is used for patients with recurrent episodes of thrombosis resulting from chronic disseminated intravascular coagulation, although the efficacy is controversial. Thrombocytes and coagulation factors are combined with heparin for patients with uncontrollable bleeding, although the efficacy is not established.
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PMID:[Paraneoplastic syndrome]. 936 21

Experiments were conducted to gain insight into mechanisms responsible for exaggerated renal vascular reactivity to ANG II and vasopressin (AVP) in spontaneously hypertensive rats (SHR) during the development of hypertension. Cytosolic calcium concentration ([Ca2+]i) was measured by ratiometric fura 2 fluorescence and a microscope-based photometer. Vascular smooth muscle cells (SMC) from preglomerular arterioles were isolated and dispersed using an iron oxide-sieving method plus collagenase treatment. ANG II and AVP produced rapid and sustained increases in [Ca2+]i. ANG II elicited similar dose-dependent increases in [Ca2+]i in SMC from SHR and Wistar-Kyoto rats (WKY). In contrast, AVP caused almost twofold larger responses in afferent arteriolar SMC from SHR. ANG II effects were inhibited by the AT1 receptor antagonist losartan. AVP action was blocked by the V1 receptor antagonist [d(CH2)5,Tyr(NH2)9]AVP. In SMC pretreated with nifedipine, neither ANG II nor AVP elicited [Ca2+]i responses. Poststimulation nifedipine reversed elevated [Ca2+]i to basal levels. Short-term reductions in external [Ca2+]i (EGTA) mimicked the nifedipine effects. Our study shows that AT1 and V1 receptors stimulate [Ca2+]i by a common mechanism characterized by preferential action on voltage-gated L-type channels sensitive to dihydropyridines. Calcium signaling elicited by AT1 receptors does not differ between SHR and WKY; thus the in vivo exaggerated reactivity may be dependent on interactions with other cell types, e. g., endothelium. In contrast, AVP produced larger changes in [Ca2+]i in arteriolar SMC from SHR, and such direct effects can account for the exaggerated renal blood flow responses.
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PMID:Exaggerated Ca2+ signaling in preglomerular arteriolar smooth muscle cells of genetically hypertensive rats. 995 Sep 57

The studies presented here were performed to determine the effect of agonist stimulation on the cytosolic free Ca2+ concentration ([Ca2+]i) in single smooth muscle cells, freshly isolated from afferent arterioles and interlobular arteries averaging between 10 to 40 microns in diameter. Microvessels were obtained from male Sprague-Dawley rats using an iron oxide collection technique followed by collagenase digestion. Freshly isolated microvascular smooth muscle cells (MVSMC) were loaded with fura 2 and studied using fluorescence photometry techniques. The resting [Ca2+]i averaged 67 +/- 3 nM (N = 82 cells). Increasing the extracellular K+ concentration significantly increased [Ca2+]i dose-dependently (P < 0.05). Involvement of extracellular Ca2+ in the response to KCl-induced depolarization was also evaluated. Resting [Ca2+]i increased approximately 132% from 40 +/- 5 nM to 93 +/- 26 nM in response to 90 mM extracellular KCl. This change was abolished in nominally Ca(2+)-free conditions and markedly attenuated by diltiazem. Inhibition of K+ channels with charybdotoxin or tetraethylammonium chloride produced a modest transient increase in [Ca2+]i during the response to 30 mM K+ and had no detectable effect on responses to 90 mM K+. Studies were also performed to establish whether freshly isolated renal MVSMC exhibit appropriate responses to receptor-dependent physiological agonists. Angiotensin II (100 nM) increased cell Ca2+ from 97 +/- 10 nM to 265 +/- 47 nM (N = 12 cells). Similarly, 100 microM ATP increased MVSMC [Ca2+]i from a control level of 71 +/- 14 nM to 251 +/- 47 nM (N = 11 cells). Norepinephrine administration caused [Ca2+]i to increase from 63 +/- 4 nM to 212 +/- 47 nM (N = six cells), and vasopressin increased [Ca2+]i from 86 +/- 10 nM to 352 +/- 79 nM (N = five cells). These data demonstrate that receptor-dependent and -independent vasoconstrictor agonists increase [Ca2+]i in MVSMC, freshly isolated from rat preglomerular vessels. Furthermore, the ability to measure [Ca2+]i in responses to physiological stimuli in these single cells permits investigation of signal transduction mechanisms involved in regulating renal microvascular resistance.
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PMID:Agonist-induced calcium regulation in freshly isolated renal microvascular smooth muscle cells. 1049 86

Oxytocin receptors (OTR) and vasopressin V1a receptors (V1aR) in the ventral forebrain play critical roles in the formation of pair bonds in the monogamous prairie vole. Previous reports have been inconsistent in the identification of the specific brain regions in the ventral forebrain that express these receptors. To delineate more clearly the neuroanatomical boundaries of the OTR and V1aR fields in this species, we compared OTR and V1aR binding in adjacent brain sections and also with markers that delineate neuroanatomical boundaries in the ventral forebrain. OTR binding displayed an overlapping distribution with substance P mRNA and preproenkephalin mRNA, both markers for the shell and core of the nucleus accumbens. V1aR binding was nonoverlapping with each of these markers but colocalized with iron accumulation as shown by Perls' iron stain as well as leucine-enkephalin immunoreactivity, both markers for the ventral pallidum. OTR and V1aR mRNA were also restricted within the nucleus accumbens and ventral pallidum, respectively. Furthermore, destruction of ventral striatal dopaminergic terminals with 6-hydroxydopamine infusions into the nucleus accumbens did not alter OTR binding. Immunocytochemical analysis of oxytocin and vasopressin in the ventral forebrain demonstrated the presence of oxytocin-immunoreactive fibers in the nucleus accumbens and vasopressin-immunoreactive fibers in the ventral pallidum, with males showing a greater density of vasopressin fibers than females, but there was no such sex difference in the oxytocin system. Based on these results, we discuss potential neural mechanisms by which receptors in these brain regions mediate pair bond formation in this monogamous species. J. Comp. Neurol. 468:555-570, 2004.
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PMID:Ventral striatopallidal oxytocin and vasopressin V1a receptors in the monogamous prairie vole (Microtus ochrogaster). 1468 86

Mucosal tissues such as the gastrointestinal tract are typically exposed to a tremendous number of microorganisms and many of them are potentially dangerous to the host. In contrast, the urogenital tract is rather infrequently colonized with bacterial organisms and also devoid of physical barriers as a multi-layered mucus or ciliated epithelia, thereby necessitating separate host defence mechanisms. Recurrent urinary tract infection (UTI) represents the successful case of microbial host evasion and poses a major medical and economic health problem. During recent years considerable advances have been made in our understanding of the mechanisms underlying the immune homeostasis of the urogenital tract. Hence, the system of pathogen-recognition receptors including the Toll-like receptors (TLRs) is able to sense danger signalling and thus activate the host immune system of the genitourinary tract. Additionally, various soluble antimicrobial molecules including iron-sequestering proteins, defensins, cathelicidin and Tamm-Horsfall protein (THP), as well as their role for the prevention of UTI by modulating innate and adaptive immunity, have been more clearly defined. Furthermore, signalling mediators like cyclic adenosine monophosphate (cAMP) or the circulatory hormone vasopressin were shown to be involved in the defence of uropathogenic microbes and maintenance of mucosal integrity. Beyond this, specific receptors e.g. CD46 or beta1/beta 3-integrins, have been elucidated that are hijacked by uropathogenic E. coli to enable invasion and survival within the urogenital system paving the way for chronic forms of urinary tract infection. Collectively, the majority of these findings offer novel avenues for basic and translational research implying effective therapies against the diverse forms of acute and chronic UTI.
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PMID:Current concepts of molecular defence mechanisms operative during urinary tract infection. 1882 79


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