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)

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by serum hypoosmolality and hyponatremia, resulting from the aberrant or sustained secretion of antidiuretic hormone (ADH). Its most frequent cause is malignancy, of which small cell or oat cell bronchogenic carcinoma is most common. Because it mimics the clinical manifestations of various disorders, SIADH often is difficult to diagnose. However, with early detection and prompt management, it can be reversed. The oncology nurse frequently is in a position to assist in the early recognition of this condition. The ability to maintain a high index of suspicion for patients at risk is critical to prompt recognition. Familiarity with the conditions that lead to this crisis and its early signs are essential to establishing a diagnosis and administering prompt treatment.
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PMID:Syndrome of inappropriate antidiuretic hormone: assessment and nursing implications. 266 Jan 20

Sixty-eight patients with massive lower gastrointestinal (G.I.) hemorrhage underwent emergency arteriography. Patients were transfused an average of six units of packed red blood cells within 24 hours of admission. The bleeding source was localized arteriographically in 27 (40%), with a sensitivity of 65% among patients requiring emergency resection. However, twelve of the 41 patients with a negative arteriogram still required emergency intestinal resection for continued hemorrhage. Radionuclide bleeding scans had a sensitivity of 86%. The right colon was the most common site of bleeding (35%). Diverticulosis and arteriovenous malformation were the most common etiologies. Selective intra-arterial infusion of vasopressin and embolization were successful in 36% of cases in which they were employed and contributed to fatality in two patients. Twenty-three patients underwent segmental resection, whereas seven patients required subtotal colectomy for multiple bleeding sites or negative studies in the face continued hemorrhage. Intraoperative infusion of methylene blue via angiographic catheters allowed successful localization and resection of bleeding small bowel segments in three patients. Overall mortality was 21%. The mortality for patients without a malignancy, with a positive preoperative arteriogram, and emergency segmental resection was 13%.
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PMID:Evaluation and management of massive lower gastrointestinal hemorrhage. 278 42

A patient with glioblastoma multiforme developed hyponatremia. This was accompanied by decreased mental awareness and seizures following cis-dichlorodiammine platinum II (DDP) chemotherapy. Treatment with hypertonic saline, furosemide diuresis, and fluid restriction promptly restored the serum sodium and neurologic status to normal. Hyponatremia did not recur despite subsequent tumor progression and increased intracranial pressure. The clinical picture suggested a drug-induced syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia should be considered when seizures or mental changes occur in patients treated with DDP.
Cancer 1988 Feb 01
PMID:Cis-dichlorodiammineplatinum II-induced syndrome of inappropriate secretion of antidiuretic hormone. 282 77

Plasma human neurophysins (HNPs) were evaluated as tumor markers for patients with small cell carcinoma of the lung (SCCL) who were entered on limited disease and extensive disease treatment trials conducted by Cancer and Acute Leukemia Group B (CALGB). HNP values obtained before treatment showed 44% of tumors secreting vasopressin-associated HNP (VP-HNP), 14% secreting oxytocin-associated HNP (OT-HNP), and 11% producing both HNPs. There was a significantly higher incidence of HNP-secreting tumors for patients with extensive disease and two or more metastatic lesions than for patients with limited disease. There were no clear differences in response to treatment or in survival between patients with HNP-secreting tumors and those with nonsecreting tumors. Response to treatment evaluated by the change in plasma HNP, gave a 91% agreement with independently derived clinical impressions. Our data indicates that HNP evaluations provide sufficient sensitivity to forecast clinical response when it cannot be clearly assessed by conventional methods.
Cancer 1988 Oct 01
PMID:Neurophysins as tumor markers for small cell carcinoma of the lung. A cancer and Leukemia Group B evaluation. 284 78

Calf serum induced the phospholipase C-mediated hydrolysis of phosphoinositides in normal rat kidney (NRK) cells transformed by a temperature-sensitive Kirsten murine sarcoma virus (tsK-NRK cells). Various growth factors known to induce the phospholipase C reactions in other cell types, such as platelet-derived growth factor, fibroblast growth factor, epidermal growth factor, thrombin, vasopressin, bombesin, cholecystokinin, and prostaglandin F2 alpha, did not induce phospholipase C reactions in the transformed NRK cells. Furthermore, noradrenaline, histamine, dopamine, angiotensin II, carbachol, and tumor growth factor-beta did not induce phospholipase C reactions. However, serotonin did induce phospholipase C reactions. The amount of serotonin contained in the calf serum was sufficient to support 50% of the activity promoted by the serum itself, and calf serum-induced phospholipase C reactions were inhibited to 10-20% of the original level by ketanserin and methysergide, known to be antagonists for the serotonin receptors. Dialysis almost completely removed serotonin from calf serum and reduced the serum-induced phospholipase C reactions. Moreover, the phospholipase C reactions induced by calf serum and serotonin were inhibited by pretreatment of the cells with pertussis toxin or 12-O-tetradecanoylphorbol-13-acetate. These results indicate that serotonin is one of the major serum factors inducing phospholipase C-mediated hydrolysis of phosphoinositides in transformed NRK cells. Serotonin induced phospholipase C reactions not only in tsK-NRK cells but also in nontransformed NRK cells. However, serotonin did not induce these reactions in Swiss 3T3 cells or NIH 3T3 cells.
Cancer Res 1988 Dec 01
PMID:Serotonin as a major serum factor inducing the phospholipase C-mediated hydrolysis of phosphoinositides in normal rat kidney cells. 284 56

Responsiveness of cyclic adenosine 3':5'-monophosphate (cAMP) to parathyroid hormone, calcitonin, and vasopressin was studied in six human renal adenocarcinoma cell lines. Four of six renal adenocarcinoma cell lines showed increased cAMP content in response to calcitonin while the other two did not. Neither parathyroid hormone nor vasopressin increased the concentration of cAMP in each of these cell lines. The growth rate of KU-2 cells, which responded to calcitonin with an increase of cAMP content, was inhibited by calcitonin. On the other hand the growth rate of calcitonin-nonsensitive KH-39 cells was unaltered. The growth inhibitory effect of the hormone on KU-2 cells could be considered to be mediated by the increased cAMP levels from the following results: (a) there was positive correlation between the cellular cAMP content and growth inhibition after various amounts of calcitonin addition; (b) KU-2 growth was also suppressed by N6,O2'-dibutyryl cAMP; and (c) a group of KU-2 cells which had become resistant to calcitonin-induced growth inhibition showed a diminished cAMP increase in response to calcitonin.
Cancer Res 1985 Oct
PMID:Calcitonin stimulation of cyclic adenosine 3':5'-monophosphate production with growth inhibition in human renal adenocarcinoma cell lines. 299 68

Biological and immunological relationships between molt-inhibiting hormone (MIH) activity in eyestalk ganglia extracts of the crab, Cancer antennarius Stimpson, and peptides of the vasopressin-oxytocin family were assessed. Lysine vasopressin (LVP), arginine vasopressin (AVP), vasotocin (VT), and oxytocin (OT) mimicked MIH action by inhibiting ecdysteroid production of Y-organ segments in vitro with the relative potencies LVP greater than AVP greater than VT much much greater than OT. The inhibitory effect was reversible and specific (6 other peptides did not alter Y-organ activity). MIH and LVP increased Y-organ cyclic adenosine 3',5' monophosphate (cAMP) levels dose-dependently and with identical time course in which the rise in cAMP preceded inhibition of ecdysteroid production. The synthetic vasopressin antidiuretic agonist 1-deamino-8-D-AVP (dDAVP) inhibited Y-organ steroidogenesis dose-dependently; the vasopressin analog ([1(B-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine[AVP) (d(CH2)5Tyr(Me)AVP), a vasopressor antagonist, had no effect on basal or MIH-suppressed steroidogenesis. AVP antiserum abolished the inhibitory action of MIH, LVP, and AVP. Competitive binding curves for MIH, LVP, AVP, VT, and OT with the AVP antiserum suggested that MIH is most closely related to LVP. MIH may be structurally related to the vasopressins and act on Y-organ cells via type V2 (cAMP-linked) receptors.
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PMID:Functional relations of crab molt-inhibiting hormone and neurohypophysial peptides. 299 30

In decapod crustaceans steroidogenic glands (Y-organs) produce the molting hormone, ecdysone. A putative neuropeptide, molt-inhibiting hormone (MIH), released from eyestalk neurosecretory cells, directly regulates Y-organs by suppressing steroidogenesis; the effect is mediated by an increase in cAMP. We explored calcium-cAMP interactions in the regulation of Y-organs in vitro of the crab, Cancer antennarius. Basal ecdysteroid production was enhanced by extracellular calcium (EC). MIH suppression did not require EC but its action was blocked by high EC. The inhibitors of Ca2+ flux, lanthanum and ruthenium red, mimicked and enhanced MIH action. Calcium ionophore A23187 raised basal steroidogenesis dose-dependently (10(-6) to 10(-4) M) and with time course (effect evident after 2 h) similar to that of suppression by MIH. Low EC enhanced the suppressive effects on steroidogenesis of forskolin and dibutyryl cyclic AMP ((Bu)2cAMP) but not of MIH, lysine vasopressin (LVP), or 3-isobutyl-1-methyl-xanthine (IBMX); basal Y-organ cAMP levels were elevated by low EC and reduced by A23187. A23187 reduced the steroidogenic-suppressive effects of MIH, LVP, forskolin and (Bu)2cAMP but not of IBMX; rises in cAMP induced by MIH, LVP, and forskolin but not by IBMX were blunted by A23187. These findings suggested a stimulatory action of calcium on phosphodiesterase (PDE). The calmodulin (CM) inhibitor trifluoperazine (TFP; 10(-5) to 10(-4) M) reduced basal and A23187-stimulated steroidogenesis, enhanced the inhibitory effects of MIH and (Bu)2cAMP on ecdysteroid production, enhanced the stimulatory effects of MIH and forskolin on cAMP, and blocked the inhibition of cAMP by A23187. Y-organ PDE activity was enhanced by increasing free Ca2+ (10(-7) to 10(-5) M) and inhibited by TFP (10(-5) to 10(-4) M). Adenylate cyclase activity of Y-organ cell particulate fraction was unaffected by Ca2+ or TFP. Calcium stimulates steroidogenesis, apparently by activating a calcium-CM-dependent cAMP-PDE: the action is counter to the cAMP-mediated MIH-inhibitory system. Ca2+ fluxes were measured with dispersed Y-organ cells, in the presence and absence of agents that alter cAMP levels. The ionophore A23187, but not MIH or forskolin, increased 45Ca2+ entry by 45% over untreated control cells. Efflux from 45Ca2+-preloaded cells was increased 30% by MIH and forskolin, but not A23187. These data, together with those further above, suggest that MIH suppresses steroidogenesis in part by fostering Ca2+ depletion, and that the effect is mediated by cAMP.
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PMID:Regulation of crab Y-organ steroidogenesis in vitro: evidence that ecdysteroid production increases through activation of cAMP-phosphodiesterase by calcium-calmodulin. 302 69

In most diabetic patients, the presence of hyponatremia is usually ascribed to severe hyperglycemia, hypertriglyceridemia, oral hypoglycemic agents, or other drugs. We describe two insulin-treated type II diabetic patients who were seen with severe rapid weight loss, hyponatremia, and diabetic amyotrophy despite good metabolic control. Laboratory evaluation of the hyponatremia suggested the syndrome of inappropriate antidiuretic hormone secretion. Their clinical presentations led to the suspicion of an underlying malignant neoplasm in each case. One patient required demeclocycline for treatment of his symptomatic hyponatremia, while the other improved with fluid restriction and intermittent furosemide therapy. The hyponatremia resolved spontaneously with improvement in body weight and the amyotrophy resolved after four to six months. After 24 to 36 months of close follow-up, no evidence of malignancy has been documented in either of the patients. We conclude that this clinical entity of amyotrophy is benign and should be included in the differential diagnosis of chronic hyponatremia in diabetic patients.
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PMID:Chronic hyponatremia associated with diabetic amyotrophy. 308 5

The synthetic vasopressin analogue, desmopressin (dDAVP), has been shown to influence membrane transport of melphalan in murine L5178Y lymphoblasts. Accordingly, the effect of dDAVP on the cytocidal activity of melphalan in L5178Y cells was evaluated. dDAVP did not affect the cytocidal activity of melphalan in these cells, but significantly affected the cloning efficiency of stationary phase or slowly dividing L5178Y cells over a range of concentrations. In particular, stationary phase cells showed an increase in cloning efficiency from 4.3 +/- 0.5% in control cells to 7.0 +/- 0.3% in cells treated with 25 nM dDAVP (P less than 0.001), whereas cells doubling every 26 h showed an increase from 10.8 +/- 1.2% in control cells to 21.0 +/- 2.0% in cells treated with 150 nM dDAVP (P less than 0.001). This phenomenon was associated with significant elevations of 1,2[3H] diacylglycerol after incubation with dDAVP for 9 min (P less than 0.01) and of total [3H]diacylglycerols after incubation for both 3 min (P less than 0.05) and 9 min (P less than 0.02). Within 10 s of treatment with 100 nM dDAVP, there was a marked decrease in the levels of inositol 1,4,5-trisphosphate and inositol 1-phosphate, but subsequently no change was observed for up to 9 min after treatment. We postulate that the increase of diacylglycerol content produced by dDAVP might be primarily from a phosphatidylcholine source and that the growth-promoting activity of desmopressin may be a consequence of activation of protein kinase C.
Cancer Res 1988 Dec 15
PMID:Growth-promoting activity of desmopressin in murine leukemia cells treated in vitro. 319 81


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