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 expression of vgf gene, first isolated as a gene induced by nerve growth factor in PC12 cells, was investigated in neurons of the suprachiasmatic nucleus (SCN) by in situ hybridization. In the rat forebrain, the vgf mRNA was found most densely in the SCN. Neurons which express vgf mRNA were found both in the dorsomedial and ventrolateral subdivisions. Double-labeling of vgf in situ hybridization and peptide immunocytochemistry demonstrated that vgf mRNA was expressed in most vasopressin- and neurophysin-immunoreactive neurons in the dorsomedial part and in vasoactive intestinal peptide (VIP)- and peptide histidine isoleucine amide (PHI)-immunoreactive neurons in the ventrolateral part. These findings suggest that vgf is a highly expressed gene in both vasopressin/neurophysin neurons and VIP/PHI neurons which were speculated to be involved in the generation and entrainment of circadian rhythm.
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PMID:In situ hybridization histochemistry of vghm1f mRNA in the rat suprachiasmatic nucleus: co-localization with vasopressin/neurophysin and VIP/PHI. 760 15

The relative roles of hypothalamic corticotropin-releasing-hormone (CRH) and vasopressin (AVP) as mediators of the stimulant effect of vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) on ACTH and corticosterone (CORT) secretion, were examined using receptor blockade of endogenous CRH and AVP. ACTH and CORT secretion were stimulated 6- and 7-fold, respectively, by PVN infusion of VIP (3.0 nmol) and 6- and 9-fold, respectively, by PHI (3.0 nmol). ACTH and CORT stimulation by VIP were inhibited 78 and 72%, respectively, by pretreatment with the CRF antagonist, 59 and 57%, respectively, by pretreatment with the AVP antagonist and about 78% by combined pretreatment with the CRF and AVP antagonists. PHI-induced stimulation of ACTH and CORT was inhibited 89 and 81%, 73 and 59% and 93% by pretreatment with the CRF- or AVP-antagonist or combined administration, respectively. These results support the hypothesis that the activation of the hypothalamic-pituitary-adrenal (HPA) axis by VIP and PHI is mediated through the release of endogenous CRH. AVP also plays a role in this response, possibly by enhancing the activity of CRH in a synergistic manner.
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PMID:Involvement of vasopressin and corticotropin-releasing hormone in VIP- and PHI-induced secretion of ACTH and corticosterone. 779 60

The effects of pituitary adenylate cyclase activating polypeptide (PACAP) on regional blood flow in the eye and other tissues were investigated in albino rabbits. Direct determination of the flow from a cannulated vortex vein, in animals pretreated with a vasopressin receptor antagonist, showed that i.v. infusion of either PACAP-27 or PACAP-38 caused a dose-dependent (0.08-0.64 pmol/kg per min) decrease in the uveal vascular resistance. Regional blood flow was determined, with radioactive microspheres, during i.v. infusion of PACAP-27 or PACAP-38 (0.64 pmol/kg per min) in rabbits pretreated with hexamethonium and a vasopressin receptor antagonist. In these experiments, both PACAP-27 and PACAP-38 increased choroidal blood flow by about 50%, whereas there was no effect in the anterior uvea. Nor was there any major effect on blood flow in the anterior uvea after intracameral injection of PACAP-27 or PACAP-38 (3 pmol). The largest blood flow increases, caused by i.v. infusion of PACAP-27 or PACAP-38, were observed in the parotid gland, submandibular gland, eyelids and nictitating membrane. Local blood flow in the choroid plexus, pineal gland, posterior pituitary gland, stomach, kidney and adrenal gland was also significantly increased during the i.v. infusion of PACAP-27. The results of the present investigation indicate that PACAP-27 and PACAP-38 are about 100 times more potent than vasoactive intestinal polypeptide and peptide histidine isoleucine as vasodilators in the rabbit choroid and, possibly, also in many other tissues of the rabbit.
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PMID:PACAP-27 and PACAP-38: vascular effects in the eye and some other tissues in the rabbit. 791 97

For optimal performance of exercising muscle, the charge state of proteins must be maintained; the pH environment of protein histidine imidazole groups must be coordinated with their pK. During exercise, increasing temperature and osmolality as well as changes in strong ions affect the pK of imidazole groups. Production of strong organic anions also decreases the concentration difference between strong cations and anions (strong ion difference, or [SID]), causing a metabolic acidosis in peripheral tissues. Central chemoreceptors regulate PCO2 in relation to the [SID] of brain fluids to maintain a "constant" brain [H+]. In addition, increased osmolality, angiotensin II, and vasopressin during exercise may stimulate circumventricular organs of the brain and interact with chemical control of ventilation. Changes in [SID] of brain fluids during exercise are negligible compared to systemic decreases in [SID]; thus, regulation of PCO2 to maintain brain [H+] homeostasis cannot simultaneously compensate for greater changes in [SID] in peripheral tissues.
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PMID:Respiratory control during exercise: hormones, osmolality, strong ions, and PaCO2. 800 Mar 57

Novel mutations in the V2 vasopressin receptor gene were identified in two Japanese pedigrees with X-linked congenital nephrogenic diabetes insipidus. The V2 receptor belongs to the family of G-protein-coupled receptors that contain seven distinct transmembrane domains, and the V2 receptor gene is encoded by three exons. The coding regions amplified by polymerase chain reaction were directly sequenced. In a pedigree, one of four consecutive guanine sequences (nucleotides 528-531) in the second exon was deleted (528delG). This deletion mutation results in a frame shift beginning at codon 154 in the second intracellular domain and a premature termination at codon 161. In another pedigree, a missense mutation (A-->G) was identified at nucleotide position 310 in the second exon. This point mutation, H80R, changes a histidine at codon 80 in the second transmembrane domain to an arginine that is more positively charged than histidine under the neutral environment. Each mutation cosegregated with the phenotype of diabetes insipidus and supposed to be a cause for resistance to arginine vasopressin.
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PMID:Novel mutations in the V2 vasopressin receptor gene in two pedigrees with congenital nephrogenic diabetes insipidus. 804 48

The tetanus toxin light chain blocks calcium induced vasopressin release from neurohypophysial nerve terminals. Here we show that histidine residue 233 within the putative zinc binding motif of the tetanus toxin light chain is essential for the inhibition of exocytosis, in the rat. The zinc chelating agent dipicolinic acid as well as captopril, an inhibitor of zinc-dependent peptidases, counteract the effect of the neurotoxin. Synthetic peptides, the sequences of which correspond to motifs present in the cytoplasmic domain of the synaptic vesicle membrane protein synaptobrevin 1 and 2, prevent the effect of the tetanus toxin light chain. Our results indicate that zinc bound to the zinc binding motif constitutes the active site of the tetanus toxin light chain. Moreover they suggest that cleavage of synaptobrevin by the neurotoxin causes the inhibition of exocytotic release of vasopressin from secretory granules.
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PMID:Exploring the functional domain and the target of the tetanus toxin light chain in neurohypophysial terminals. 815 48

A 55-year-old male smoker developed polyuria and polydipsia in November 1983. A water deprivation study revealed a defect in the urine concentrating function, which was corrected by vasopressin. Plasma antidiuretic hormone (ADH) was not increased by smoking. His condition was well controlled by deamino-D-arginine vasopressin. However, since February 1992 he has become completely free from the need for medication to control his urine volume. Re-evaluation studies with water deprivation and smoking revealed dramatic improvements in the urine concentrating function and ADH response. A patient with idiopathic diabetes insipidus with spontaneous remission after 8 years is reported.
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PMID:A case of central diabetes insipidus with spontaneous remission after 8 years of the disease. 828 64

The coding region of the human vasopressin type 2 receptor gene bears mutations in the individuals affected with congenital nephrogenic diabetes insipidus, a disease characterized by the inability of the kidney to concentrate urine in response to vasopressin. Although it is assumed that the mutations result in loss of receptor function, proof of this hypothesis is lacking. We introduced one of these naturally occurring point mutations leading to a single amino acid change (Arg137-->His) into wild type cDNA. The mutant protein was expressed, and the functional properties of the receptor were examined. The mutant receptor exhibited an unaltered binding affinity for vasopressin compared to the wild type but failed to stimulate the Gs/adenylyl cyclase system. These data provide biochemical proof that the mutant receptor is the cause of the disease.
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PMID:Nephrogenic diabetes insipidus. A V2 vasopressin receptor unable to stimulate adenylyl cyclase. 851 44

A 50-year-old Japanese man had been suffering from polydipsia and polyuria for 2 months without any other specific symptoms. His daily urinary output reached 5 liters. On admission, no abnormalities of the kidneys, heart, thyroid, adrenals, pituitary or hypothalamus were detected by laboratory tests and MRI of the head. Pure psychogenic polydipsia was ruled out because his urine volume did not decrease sufficiently with 18 h of water deprivation and the subsequent injection of aqueous vasopressin. Plasma arginine vasopressin (AVP) levels against plasma osmolality remained within the normal range during the test. These results indicated that diabetes insipidus in this case was caused by renal insensitivity to AVP. The symptoms disappeared spontaneously, and marked improvement was observed in a second water deprivation test 1 month later, although the maximum urine concentration was still subnormal. The combination of both latent insufficiency of AVP secretion and impairment of the renal countercurrent system induced by psychogenic polydipsia was speculated as a possible mechanism for the transient nephrogenic diabetes insipidus in this case.
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PMID:Transient nephrogenic diabetes insipidus accompanied by possible psychogenic polydipsia. 852 83

Aquaporin-2 (AQP-2) is a vasopressin-regulated water channel in the kidney collecting duct. AQP-2 is selectively permeable to water molecule and is translocated between the apical membrane and subapical endosomes in response to vasopressin. To investigate the localization and structure of the aqueous pathway of the AQP-2 water channel, a series of site-directed mutants was constructed and functionally analyzed. Insertion of N-glycosylation reporter sequence into each hydrophilic loop (HL) indicated that AQP-2 has a six-membrane spanning topology and that insertional mutations in HL-2 or HL-5 do not alter water channel function. Mercury-sensitive site of AQP-2 is located near the second asparagine-proline-alanine (NPA) domain at cysteine 181, but not near the first NPA domain. Replacement of HL-3 or HL-4 with the corresponding part of Escherichia coli glycerol facilitator abolished water channel function without changing plasma membrane expression of the channel protein. Introduction of cysteine residues in His-122, Asn-123, Gly-154, Asp-155, or Asn-156 induced partial mercury sensitivity, and point mutations in asparagine 123 significantly altered water permeability. Our results implicate that the structure of AQP-2 is different from models previously proposed for AQP-1 and that HL-3 and HL-4 are closely located to the aqueous pathway.
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PMID:Structure of aquaporin-2 vasopressin water channel. 861 98


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