Arginine vasotocin has long been known as an antidiuretic hormone in non-mammalian vertebrates. The peptide has also been found in mammalian tissues. The physiological significance of the peptide, however, has not yet been clarified in mammals. To define the effect of arginine vasotocin on the water and electrolyte balance in mammalian vertebrates, experiments have been done. Intrarenal arterial infusion of arginine vasotocin, 0.01-10ng/kg/min resulted in dose-dependent decreases in urine volume and free water clearance and an increase in urinary osmolarity. Arginine vasotocin, in a dose of 0.03ng/kg/min, induced an increase in water reabsorption without changes in glomerular filtration rate. Intrarenal infusion of arginine vasotocin in doses ranging from 0.1 to 3.0 or 10.0ng/kg/min resulted in decreases in glomerular filtration rate and renal plasma flow. However, no dose dependence were observed. Intrarenal infusion of arginine vasotocin from 0.3 to 10 ng/kg/min induced dose-dependent natriuretic and kaliuretic effects with concomitant suppression of renin secretion. The renal effects of arginine vasotocin were blocked by arginine vasopressin V2-receptor antagonist [d(CH2)5, D-Phe2, Ile4, Ala9-NH2]-vasopressin but were not blocked by[d(CH2)5, D-Ile2, Ile4, Arg8]- vaso pression. These data suggest that the effect of arginine vasotocin on the renal function are similar to that of vasopressin in mammalian vertebrates. The data also suggest that the renal effects of arginine vasotocin may be coupled to the receptor system which is similar, if not identical, to that of arginine vasopressin.
Arginine Vasopressin ; Arginine* ; Glomerular Filtration Rate ; Mammals ; Osmolar Concentration ; Renal Plasma Flow ; Renin ; Vasopressins ; Vasotocin* ; Vertebrates ; Water ; Water-Electrolyte Balance

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

Sheehan's syndrome occurs as a result of ischemic pituitary necrosis due to severe postpartum hemorrhage. The manifestations of this clinical syndrome are most often caused by a deficiency in the hormones produced by the anterior pituitary gland, whereas the neurohypophysis is usually preserved but can be involved in severe cases that manifest as diabetes insipidus. This is a report of Sheehan's syndrome that manifested with diabetes insipidus as presenting symptom 2 month's after delivery. The patient suffered massive bleeding, so received a blood transfusion. A combined pituitary stimulation and water deprivation test revealed deficiencies of not only anterior pituitary hormones, such as growth hormone and prolactin, but also of anti-diuretic hormone. We report this case, with a review of the literature.
Blood Transfusion ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Growth Hormone ; Hemorrhage ; Humans ; Hypopituitarism* ; Necrosis ; Pituitary Gland, Anterior ; Pituitary Gland, Posterior ; Pituitary Hormones, Anterior ; Postpartum Hemorrhage ; Prolactin ; Water Deprivation

Sheehan's syndrome occurs as a result of ischemic pituitary necrosis due to severe postpartum hemorrhage. The manifestations of this clinical syndrome are most often caused by a deficiency in the hormones produced by the anterior pituitary gland, whereas the neurohypophysis is usually preserved but can be involved in severe cases that manifest as diabetes insipidus. This is a report of Sheehan's syndrome that manifested with diabetes insipidus as presenting symptom 2 month's after delivery. The patient suffered massive bleeding, so received a blood transfusion. A combined pituitary stimulation and water deprivation test revealed deficiencies of not only anterior pituitary hormones, such as growth hormone and prolactin, but also of anti-diuretic hormone. We report this case, with a review of the literature.
Blood Transfusion ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Growth Hormone ; Hemorrhage ; Humans ; Hypopituitarism* ; Necrosis ; Pituitary Gland, Anterior ; Pituitary Gland, Posterior ; Pituitary Hormones, Anterior ; Postpartum Hemorrhage ; Prolactin ; Water Deprivation

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: 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

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: 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

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

Gestational diabetes insipidus, which occurs rarely during late pregnancy, may injure the mother and fetus neurologically. It takes place in about 4 of every 100,000 pregnancies. Increased placental-derived vasopressinase in late pregnancy markedly degrades vasopressin. The decreased vasopressin activity causes hypotonic polyuria, polydipsia, and dehydration. We report a woman with gestational diabetes insipidus who had no abnormal laboratory tests before developing symptoms. The diabetes insipidus was controlled well by administering nasal desmopressin (1.desamino.8.D.arginine vasopressin, DDAVP) followed by resolution of the signs and symptoms after delivery. Although gestational diabetes insipidus is rare, a prompt diagnosis and appropriate treatment to reduce the risks of maternal and fetal injury are important.
Cystinyl Aminopeptidase ; Deamino Arginine Vasopressin ; Dehydration ; Diabetes Insipidus ; Diabetes, Gestational ; Female ; Fetus ; Humans ; Hypogonadism ; Mitochondrial Diseases ; Mothers ; Ophthalmoplegia ; Polydipsia ; Polyuria ; Pregnancy ; Pregnancy Trimester, Third ; Vasopressins