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 role of reactive SH groups (presumably in proteins) of the apical plasma membrane in transepithelial Na+ transport was studied in the isolated urinary bladder of the toad. On the basis of assays for TCA-soluble SH compounds (e.g., glutathione, methionine), PCMB, PCMPS, NTCB, and DTNB did not penetrate the intracellular compartment from the luminal media either in control or vasopressin-treated bladders. In contrast, PCMB from the serosal side and NEM from the luminal side titrated significant fractions of the TCA-soluble SH compounds. We conclude, therefore, the PCMB, PCMPS, NTCB, and DTNB are suitable reagents for studies on the physiological properties of apical plasma membrane SH groups. Titration of apical membrane SH groups with PCMPS, NTCB, and DTNB revealed heterogeneity in functional responses: PCMPS and NTCB elicited transient, 25-60% increases in SCC. In substrate-free media, pretreatment with these reagents inhibited the increase in SCC produced by vasopressin or cyclic AMP (+ theophylline). In glucose-enriched media, the responses to combinations of vasopressin and PCMPS or NTCB were additive, implying activation via parallel pathways. Simultaneous addition of vasopressin or cyclic AMP (+ theophylline) and NTCB resulted in marked synergism, presumably as a result of unmasking of SH groups by the the hormone (or the intermediate). These results suggest that basal Na+ transport is regulated in part by SH compounds in the apical membrane that are distinct, although not necessarily different in kind, from those involved in the response to vasopressin.
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PMID:Effects of sulfhydryl reagents on basal and vasopressin-stimulated Na+ transport in the toad bladder. 16 61

To determine if harmala alkaloids affect transport systems other than (Na +K)-ATPase, effects of harmaline on Na and water fluxes were studied in amphibian skins. Net Na flux was evaluated from short-circuit current, and water flux monitored with automatic, volumetric methods. At 2 to 5 mM, harmaline consistently inhibited SCC and prevented the natriferic effects of oxytocin and norepinephrine. However, at 0.1 to 0.5 mM, harmaline produced an increase in SCC inhibitable with amiloride. The stimulatory effects of harmaline and oxytocin were either nonadditive or additive depending on whether the hallucinogen was present in the inner solution or in the outer solution bathing the skin, respectively. Water flow was not modified by harmaline on the outer medium. In contrast, addition of the drug to the inner medium elicited a conspicuous, sustained, vasopressin-like, hydrosmotic effect, comparable to and competive with those of vasopressin and norepinephrine. The ensemble of these results suggests that harmaline may affect three distinct transport systems: (i) the Na pump; (ii) the cyclic nucleotide system; (iii) the Na entry pathway at the outer membrane of the skin that is also activated by agents such as diphenylhydantoin, lanthanides and propranolol.
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PMID:Vasopressin-like effects of a hallucinogenic drug--harmaline--on sodium and water transport. 41 80

The urinary bladder of the toad Bufo marinus has been used to examine the effect on sodium transport, measured by short-circuit current, of natural antidiuretic hormones and several synthetic peptide analogs. In mammals, these synthetic analogs show specificity for different receptors, designated V1 and V2 receptors, whose biological responses are mediated by phosphatidyl inositol breakdown products or adenylate cyclase activity, respectively. All analogs stimulated SCC, with relative potencies AVT greater than AVP greater than Phe2 OVT (V1 agonist) much greater than d(CH2)5Tyr(Me)AVP (V1 antagonist) = d(CH2)5[D-Ile2,Abu4]AVP (V2 antagonist). The V1 and V2 antagonists inhibited the SCC response to AVT and Phe2OVT, with similar inhibitory potencies. We conclude that the stimulation of sodium transport by antidiuretic hormones involves one hormone receptor which does not show the selectivity of mammalian antidiuretic hormone receptors, and may represent a more primitive type of receptor.
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PMID:Response of toad urinary bladder to vasopressin analogs possessing V1 or V2 specificity. 296 74

The physiological and morphological response of toad urinary bladder was examined during mucosal exposure of LiCl both with and without vasopressin (VP). With 20 or 100 mU/ml of VP in the serosal bath there was a decrease in Jv between the first and second VP stimulation in LiCl-treated bladders (VP20, -14 +/- 6%; VP100, -16 +/- 5%) that was not different from that observed without LiCl (VP20, -8 +/- 3%, P = NS). However, with 1 mU/ml of VP, a significant decrease in Jv was evident in LiCl-treated (-30 +/- 10%) versus control sacs (+6 +/- 8%; P less than 0.02). At all VP concentrations tested, a significant decrease in SCC and PD was observed between the first stimulation without LiCl and the second stimulation with LiCl. Both osmotic (Pf) and diffusional water permeability (Pd) were increased significantly with 11 mM LiCl only, while neither basal nor VP-stimulated urea permeability (Pu) was affected. Morphological changes paralleled the physiological alterations induced by LiCl. These data demonstrate that LiCl interferes with the osmotic response of the toad bladder to low concentrations of VP, and increases both Pf and Pd while leaving Pu unaffected. These findings coupled with the cell swelling and intracellular vacuolization suggest the presence of a defect in transepithelial water movement somewhere beyond the apical membrane of the granular cell exposed to LiCl.
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PMID:Structural and functional response of toad urinary bladder to LiCl. 632 97

A 60 -year-old man complained of dysphagia and was admitted to our hospital for adjuvant chemotherapy under a diagnosis of esophageal carcinoma(squamous cell carcinoma[SCC], Stage II ). He was treated with cisplatin(CDDP)and 5- fluorouracil(5-FU). On the fifth day after administration, he experienced mild disorientation, and early morning on the sixth day, he showed impaired consciousness. Laboratory studies revealed a serum sodium level of 111mEq/L and a serum chloride level of 73mEq/L. The findings of computed tomography and magnetic resonance imaging of the head were unremarkable. Other laboratory studies revealed a plasma vasopressin level of 19.2 pg/mL, a plasma osmolality of 219mOsm/kg, a serum creatinine level of 0.61mg/dL, a serum cortisol level of 27.1 mg/dL, a urine osmolality of 665mOsm/kg, and a urine sodium level of 157.1mEq/L. There were no signs of dehydration, and so the patient was diagnosed with syndrome of inappropriate antidiuretic hormone secretion(SIADH). We discontinued chemotherapy and initiated fluid restriction and sodium supplementation. After this treatment, the patient's consciousness progressively improved. On the fifth day of treatment, laboratory studies revealed a serum sodium level of 138mEq/L and a serum chloride level of 98mEq/L, indicating recovery from hyponatremia.
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PMID:[A case of syndrome of inappropriate antidiuretic hormone secretion in a patient with esophageal carcinoma possibly induced by cisplatin in neoadjuvant chemotherapy]. 2513 33