PURPOSE: This study aimed to examine the effects of cyclooxgenase-2 inhibitors on patients with nocturia, whose symptoms persisted after the use of first-line drug therapy, such as alpha blockers and/or anticholinergics. MATERIALS AND METHODS: Thirty-three patients whose symptoms persisted after more than three months of first-line drug therapy were chosen to receive additional COX-2 inhibitors or antidiuretic hormones orally. Seven patients (group 1) were given 80mg of zaltoprofen at night, while 15 (group 2) were given 100mg of nimesulide at night. Desmopressin acetate (0.2mg) was administered at night to 11 patients (group 3) as a control group. Median follow up was 35 days (range, 28~90 days). RESULTS: In 25 patients (75.8%), the severity of nocturia was reduced. The median decline of nocturia in the COX-2 inhibitor groups (groups 1 and 2) was once, and it was statistically significant (p<0.001), while the median decline in each of these groups was twice (p=0.026) and once (p=0.002), respectively. The reduction of nocturia in the control group was once (p=0.011). The differences in reduction between the COX-2 inhibitor group and the control group were not statistically significant (p=0.418). CONCLUSIONS: The effects of the COX-2 inhibitors were not significantly different from those of desmopressin. Combination therapy with COX-2 inhibitors can effectively reduce nocturia in patients with refractory nocturia, following first-line drug therapy.
Cholinergic Antagonists ; Cyclooxygenase 2 Inhibitors ; Deamino Arginine Vasopressin ; Drug Therapy ; Follow-Up Studies ; Humans ; Nocturia* ; Vasopressins

Ubiquitination is known to be important for endocytosis and lysosomal degradation of aquaporin-2 (AQP2). Ubiquitin (Ub) is covalently attached to the lysine residue of the substrate proteins and activation and attachment of Ub to a target protein is mediated by the action of three enzymes (i.e., E1, E2, and E3). In particular, E3 Ub-protein ligases are known to have substrate specificity. This minireview will discuss the ubiquitination of AQP2 and identification of potential E3 Ub-protein ligases for 1-deamino-8-D-arginine vasopressin (dDAVP)-dependent AQP2 regulation.
Aquaporin 2 ; Deamino Arginine Vasopressin ; Endocytosis ; Kidney ; Kidney Tubules, Collecting ; Ligases ; Lysine ; Proteins ; Substrate Specificity ; Ubiquitin ; Ubiquitination ; Vasopressins

BACKGROUND: Bilateral ureteral obstuction (BUO) has been known to decrease the expression of renal aquaporin-2 (AQP2) and Na-K-2Cl cotransporter (NKCC2). The polyuria and urinary concentration defect in postobstructive diuresis (POD) may be explained by these molecular changes. By contrast, chronic infusion of antidiuretic hormone (ADH) has been known to increase the expression of renal AQP2 and NKCC2, but there have been no studies regarding the chronic effect of ADH in molecular level when introducing to POD. We tried to identify the changes of renal expression of AQP2 and NKCC2 in 24 hour BUO rat at POD-7 day and the chronic effect of ADH to the expression of AQP2 and NKCC2 in sham operation rat and in 24 hour BUO rat, at sham operation 7 day and at POD-7 day, respectively. METHODS: Twenty four Spraugue-Dawley rats were divided into four groups. Group I (Control group): sham operation rats(n=6). Group II (BUO group): 24 hour BUO and release of it (n=6). Group III (dDAVP group): dDAVP (1-deamino-8d-arginine vasopressin: V2-receptor-selective agonist) infusion at rate of 20 ng/hour by osmotic minipump subcutaneously for 7 days in sham operation rats (n=6). Group IV (BUO+dDAVP group): dDAVP infusion at rate of 20 ng/hour by osmotic minipump by same method as Group III in 24 hour BUO rats (n=6). All rats were sacrificed at POD-7 day (Group II, Group IV) or sham operation-7 day (Group I, Group III) and renal expression of AQP2 and NKCC2 were analyzed by immunohistochemistry and by Western blot method. Blood and urinary chemistry examinations were done concurrently. RESULTS: BUO group showed increased urine output and decreased urine osmolality (p<0.05) and decreased expressions of AQP2 and NKCC2 compared with Control group {29.1 +/- 4.2% vs. 100 +/- 10.0% (p< 0.05); 40.2 +/- 5.4% vs. 100 +/- 7.9% (p<0.05) respectively}. dDAVP group had decreased urine output from POD-1 day to POD-5 day and increased urine osmolality (p<0.05) POD-1 day to POD-7 day during and increased expressions of AQP2 and NKCC2 compared with Control group {206.5 +/- 19.0% vs. 100 +/- 10.0% (p<0.05); 180.6 +/- 13.3% vs. 100 +/- 7.9% (p<0.05) respectively}. But BUO group showed no difference in urine output and urine osmolality and expressions of AQP2 and NKCC2 compared with BUO+dDAVP group {29.1 +/- 4.2% vs. 42.2 +/- 2.3% (p<0.84); 40.2 +/- 5.4 % vs. 47.9 +/- 4.3% (p<0.91) respectively}. CONCLUSION: BUO and POD show decreased expressions of AQP2 and NKCC2 and the unresponsiveness to chronic ADH infusion may be the pathophysiologic basis of POD such as increased urine output, decreased urine osmolality.
Animals ; Aquaporin 2* ; Blotting, Western ; Chemistry ; Deamino Arginine Vasopressin ; Diuresis ; Immunohistochemistry ; Osmolar Concentration ; Polyuria ; Rats* ; Ureter* ; Ureteral Obstruction* ; Vasopressins

PURPOSE: This study aimed to investigate the effects of vasopressin and desmopressin on the contractile and relaxative responses of rabbit cavernosal smooth muscle. MATERIALS AND METHODS: Isometric tension studies were conducted to investigate the effects of vasopressin(10(-14)-10(-8)M) and desmopressin(10(-14)- 10(-8)M) on the contraction and relaxation responses of rabbits cavernous muscle strips in an organ bath. The effects of pretreatment with phenylephrine(10(-5)M), L-NAME(10(-5)M) and indomethacin(10(-5)M) on the contraction and relaxation responses of the vasopressin and desmopressin were also investigated. The statistics were analyzed by Student's t-test and ANOVA. RESULTS: Vasopressin contracted the strips in a dose-dependent manner, while desmopressin did not. The phenylephrine-induced contraction was dose-dependently increased by vasopressin, but it was dose-dependently relaxed by desmopressin. L-NAME pre-treatment did not block the relaxation response, but indomethacin pre-treatment did. Vasopressin- induced contraction occurred the via V(1) receptor, while desmopressin- induced relaxation occurred via the V(2) receptor. CONCLUSIONS: Vasopressin, in pathophysiological circumstances, would worsen erectile dysfunction. On the contrary, desmopressin, which may induce an endothelium-dependent relaxation of the cavernous smooth muscles, would be good for erectile function.
Baths ; Caves ; Contracts ; Deamino Arginine Vasopressin ; Erectile Dysfunction ; Indomethacin ; Male ; Muscle, Smooth ; Muscles ; NG-Nitroarginine Methyl Ester ; Rabbits ; Relaxation ; Vasopressins

Diabetes insipidus is an unusual cause of urinary frequency during pregnancy. It occurs in 2 to 6 per 100,000 pregnancies. It is a disorder in which the abnormal secretion, degradation, or activity of vasopressin cause hypotonic polyuria, polydipsia, and dehydration. And this syndrome appears to be associated with multiple gestations, preeclampsia, and abnormal liver function. We report two cases of pregnancies complicated with diabetes insipidus. One patient was diagnosed during pregnancy and DDAVP (L-deamino-8-d-arginine vasopressin) was used to manage diabetes insipidus. The other patient was diagnosed before pregnancy and DDAVP was not used.
Deamino Arginine Vasopressin ; Dehydration ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Humans ; Liver ; Polydipsia ; Polyuria ; Pre-Eclampsia ; Pregnancy* ; Vasopressins

PURPOSE: Cell volume regulation is critical in kidney collecting duct cells which are subjected to large transepithelial osmotic gradients and stimulation of vasopressin. The present study aimed at validating the usefulness of the fluorescence quenching method to measure rapid changes in the cell volume of the kidney collecting duct cells in response to changes of extracellular osmolality and/or dDAVP (V2 receptor agonist) stimulation. METHODS: M-1 cell (a mouse cortical collecting duct cell line) was used and the data presented traces of cellular fluorescence in M-1 cells loaded with calcein collected over time as extracellular osmolality was repeatedly changed or dDAVP was treated. And the "initial relative rate of cell volume changes" was calculated. RESULTS: M-1 cells loaded with calcein revealed that fluorescence was increased when exposed to low extracellular osmolality (250 mOsm/KgH2O), whereas it was decreased by high extracellular osmolality (350 mOsm/KgH2O). This could reflect volume-dependent changes in fluorescence intensity in the range of quenching concentrations. The calculated "initial relative rate of cell volume changes" in M-1 cells during 1 sec was increased-7-fold by dDAVP treatment (10(-8)M, 2 min), compared with vehicle treatment when extracellular osmolality was changed from 350 to 250 mOsm/KgH2O. CONCLUSION: This study suggests that a fluorescence quenching method could be exploited for investigating an effect of dDAVP or other drugs/chemicals on the relative rate of cell volume changes in the kidney collecting duct cells.
Animals ; Aquaporins ; Cell Size ; Deamino Arginine Vasopressin ; Fluoresceins ; Fluorescence ; Kidney ; Kidney Tubules ; Kidney Tubules, Collecting ; Mice ; Osmolar Concentration ; Vasopressins

No abstract available.
Nifedipine* ; Vasopressins*

A 17-year-old girl presented with polyuria (7 L/day) and polydipsia for one year. Initial urine osmolality was 113mOsm/kg H₂O. Following 6 h of fluid restriction, serum plasma osmolality reached 300mOsm/kg H₂O, whereas urine osmolality was 108mOsm/kg H₂O. Urine osmolality was increased by 427% from 108 to 557mOsm/kg after vasopressin challenge. The patient was diagnosed with central diabetes insipidus, possibly derived from the atypical occupation of a Rathke's cleft cyst at the pituitary stalk following magnetic resonance imaging with enhancement. She was discharged with desmopressin nasal spray (10 µg); urine output was maintained at 2-3 L/day, and urine osmolality was >300 mOsm/kg. Additional pituitary image studies and evaluation of hypopituitarism should be included in the differential diagnosis of patients with central diabetes insipidus.
Adolescent* ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Neurogenic* ; Diagnosis, Differential ; Female* ; Humans ; Hypopituitarism ; Magnetic Resonance Imaging ; Occupations ; Osmolar Concentration ; Pituitary Gland ; Plasma ; Polydipsia ; Polyuria* ; Vasopressins

We report on a case of limited form of granulomatosis with polyangiitis (GPA) with pituitary involvement which presented with central diabetes insipidus. This rare form of GPA has not been reported in Korea. The patient presented with fever, headache, productive cough, nasal symptoms, and polyuria. Laboratory data and imaging studies demonstrated inflammatory lesions in nasal sinus and lungs. Pituitary stalk thickening and enhancement were observed on brain magnetic resonance imaging. The histopathology of the lung lesions showed chronic active granulomatous inflammation. Polyuria, hyperosmolar hypernatremia, and decreased urine osmolality which responded to synthetic vasopressin analog were consistent with central diabetes insipidus. Based on the clinical findings and histopathological results, a diagnosis of GPA with pituitary involvement was established. Treatment with desmopressin as well as concurrent glucocorticoids and immunosuppressant resulted in clinical improvement.
Brain ; Cough ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Neurogenic* ; Diagnosis ; Fever ; Glucocorticoids ; Headache ; Humans ; Hypernatremia ; Inflammation ; Korea ; Lung ; Magnetic Resonance Imaging ; Osmolar Concentration ; Pituitary Gland ; Polyuria ; Vasopressins

Ingestion of puffer fish can result in severe and potentially lethal intoxication, referred to as tetrodotoxin intoxication. Tetrodotoxin is a potent neurotoxin well known for its ability to ability neuromuscular function. Tetrodotoxin is a specific and potent blocker of axonal sodium channel; it may block sodium channels in the axon of the neurons of the neurohypophysis, thereby inhibiting the release of vasopressin and causing diabetes insipidus neurotoxin. To our knowledge, previous report on diabetes insipidus causing tetrodotoxin is the only one case in Singapore. A married couple (69-year-old man and 57-year-old woman) ingested two green rough-backed puffer fish (Lagocephalus lunaris). They complained of paresthesia on perioral area and extremity and developed not only grade IV intoxication but also an increased urine output (4455 ml/day and 5035 ml/day), elevated serum sodium (157.4 mEq/L and 166.7 mEq/L) and elevated serum osmolality (324 mosmol/kg and 339 mosmol/kg), which suggested the development of diabetes insipidus. The administration of desmopressin nasal spray was successful in normalizing urine volume. Both were discharged on 20th and 18th hospital day, respectively, without any complications.
Axons ; Deamino Arginine Vasopressin ; Diabetes Insipidus ; Eating ; Extremities ; Neurons ; Osmolar Concentration ; Paresthesia ; Pituitary Gland, Posterior ; Sodium ; Sodium Channels ; Tetraodontiformes ; Tetrodotoxin ; Vasopressins