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)

To determine whether the renal sympatho-inhibition and bradycardia in responses to acute increases in arterial pressure are altered in the diabetic state, the renal nerve discharge and heart rate were measured in streptozotocin (STZ) induced diabetic (DIA) rats. Integrated renal sympathetic nerve activity and heart rate were measured before and during an acute increase in blood pressure in anesthetized (Inactin 0.1 g/kg, i.p.) control (vehicle) and DIA rats (Sprague Dawley rats injected with STZ 65 mg/kg i.p.). Blood glucose levels were significantly elevated in the DIA group compared with the control group. Baroreflex changes in renal nerve activity and heart rate were not significantly different in the DIA rats compared with control rats at a time when the renal sympatho-inhibition in response to acute volume expansion was blunted in the diabetic rats. In addition, blocking the effect of elevated angiotensin II in diabetic rats with the converting enzyme inhibitor enalapril did not change the baroreflex function in DIA rats compared with control rats. However, administration of vasopressin failed to potentiate the baroreflex in diabetic rats as it did in normal control rats. This study demonstrates that (1) the baroreflex function is normal in STZ induced diabetic rats unlike the volume reflex during the early phase of the disease, (2) blockade of the AII system does not alter baroreflex function in diabetic rats and (3) vasopressin fails to potentiate the baroreflex in diabetic rats as it does in the euglycemic normal rats.
Diabetes Res Clin Pract 1995 Jan
PMID:Baroreflex function in streptozotocin (STZ) induced diabetic rats. 778 88

Hypothalamic mechanisms of neurohormone regulation of endocrine pancreas in diabetes mellitus, adaptation to hypoxia and their combination were studied on Wistar rats. To evaluate the condition of supraoptic nucleus (SON) secretory function, paraventricular subnuclei (PVH) of hypothalamus and endocrine pancreas, we used radioimmunoassay, immunocytochemical, morphometrical and histochemical methods. Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process.
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PMID:[The vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in rats with diabetes mellitus under hypoxic exposures]. 790 84

Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process.
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PMID:[Hypothalamic mechanisms of neurohormone regulation of the endocrine part of the pancreas]. 790 82

Progressive dehydration due to water deprivation and streptozotocin diabetes both produce increased activity of the hypothalamoneurohypophysial system and enhanced vasopressin secretion. To determine whether enhanced metabolic activity affects glucose transporter protein expression, this study examined the effect of these conditions on 45-kDa GLUT-1 and the neuronal glucose transporter, GLUT-3, which mediate glucose transport in the rat neurohypophysis. Progressive water deprivation increased hematocrit, plasma electrolytes Na+ and Cl-, and vasopressin over 3 days, relative to the severity of dehydration. Plasma vasopressin increased threefold by 24 h, reaching 4.5-fold by 72 h. These changes were reflected in a 56 and 75% decrease in neurohypophysial vasopressin content by 48 and 72 h, respectively. Significant changes in glucose transporters were also observed at 48 and 72 h, with GLUT-1 increasing by 18 and 44% and GLUT-3 increasing by 42 and 55%, respectively. Streptozotocin-induced diabetes produced increases in hematocrit, plasma Cl-, and vasopressin, although the magnitude of these changes was less than with dehydration. There was a twofold increase in plasma vasopressin by 3 days, commensurate with the onset of overt diabetes, and a threefold increase by 2 wk. These changes were reflected in a 30 and 40% decline in neural lobe vasopressin content, respectively. Despite the difference in the magnitude of hormone response, GLUT-3 increased by the same amount (53%) as in dehydration. GLUT-1, however, was decreased 16% by 3 days and 25% by 1 and 2 wk of diabetes. Although the opposite effects on GLUT-1 may relate to differences in circulating insulin or glucose, this study is the first demonstration of increased expression of GLUT-3 in response to a common hypothalamic signal in these two conditions.
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PMID:Altered expression of GLUT-1 and GLUT-3 glucose transporters in neurohypophysis of water-deprived or diabetic rats. 794 11

The immunolocalization of cathepsin L in the hypothalamus of normal rats was compared with the distribution of the enzyme in streptozotocin-treated animals and in vasopressin-deficient rats (Brattleboro strain). In rats with a normal metabolic status the neurons of magnocellular nucl. supraopticus and paraventricularis stood out by intense immunostaining for cathepsin L. In rats suffering from an experimentally induced diabetes mellitus and in homozygous Brattleboro rats we observed a strong reduction in enzyme immunoreactivity in these nuclei. Since cathepsin L is capable of splitting certain hypothalamic neuropeptides that are changed in diabetic animals, a role of the enzyme in the metabolism of these peptides is imaginable. Decrease in immunoreactive cathepsin L in vasopressin-deficient rats points to a possible involvement of the enzyme in the control of fluid homeostasis.
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PMID:Cathepsin L immunoreactivity in the hypothalamus of normal, streptozotocin-diabetic and vasopressin-deficient Brattleboro rats. 800 46

The endocrine status of the pancreas and the hypothalamic neurosecretory nuclei were studied by radioimmunoassay, immunocytochemical, morphometric and histochemical methods in Wistar rats of both sexes with experimental diabetes mellitus. The development of diabetes mellitus was characterized by beta-cell destruction and insulin concentrations reduction in these cells and the blood, by increase of glucagon and somatostatin levels in the alpha- and delta-cells, respectively, as well as by the growth of these substances concentrations in the peripheral blood. These changes were parallelled by activation of the vasopressin-, oxytocin and corticoliberin-synthesizing neurones of the paraventricular and supraoptic nuclei of the hypothalamus, as evidenced by morphometric findings and by increase of the blood vasopressin and corticoliberin concentrations and oxytocin level in the hypothalamus. Experimental diabetes mellitus was found to be characterized by activation of the hypothalamo-hypophyseo-adrenal system. Functional differences in the contribution of vasopressin- and oxytocin-synthesizing neurones of the hypothalamic nuclei in the pathogenesis of the disease is shown, as are their sex-specific reactions.
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PMID:[Status of vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in experimental diabetes mellitus in rats of different sexes]. 805 64

The Brattleboro rat with hypothalamic diabetes insipidus (BDI) has an abnormal aversion to drinking quinine-adulterated water compared with normal rats of the parent Long Evans (LE) strain. This BDI animal tolerates marked hypovolemia and decreased body weight in preference to drinking the quinine-adulterated fluid, indicative of a reduced motivation to drink. Acute or chronic treatment of BDI rats with desamino-8D arginine vasopressin (DDAVP) restored to normal their drinking response to quinine solution. Partial restoration of fluid turnover in BDI rats with hydrochlorothiazide, which has an antidiuretic effect in diabetes insipidus (when vasopressin is absent), failed to abolish the abnormal drinking response to quinine-adulterated solution in 8 out of 12 animals. In contrast, induction of diabetes mellitus in LE rats, which resulted in a marked polydipsia and polyuria even though vasopressin was still present, did not impair the drinking response to quinine solutions. These results suggest that the abnormal drinking response to quinine-adulterated fluid in BDI rats is reversed by treatment with the vasopressin V2-receptor agonist DDAVP but is unlikely to be a consequence of the restoration of fluid turnover to normal levels by a renal action. A possible central action involving vasopressin and the motivation to drink is discussed.
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PMID:The abnormal quinine drinking aversion in the Brattleboro rat with diabetes insipidus is reversed by the vasopressin agonist DDAVP: a possible role for vasopressin in the motivation to drink. 819 Jul 53

The relationship between erythrocyte sodium lithium countertransport activity (SLC), total exchangeable sodium (NaE), and hormonal control of renal function was examined in 40 normotensive, normoalbuminuric, non-neuropathic Type 1 diabetic subjects, of whom 8 had elevated SLC (> 0.40 mmol Li h-1l-1 rbc). Eleven health controls with normal SLC, who were of comparable age, body mass, and blood pressure were also studied. By contrast with healthy controls, SLC in Type 1 diabetes was not associated with plasma renin activity (PRA), aldosterone, systolic blood pressure or lean body mass. SLC was also unrelated to atrial natriuretic peptide (ANP) (Type 1 diabetes only) and NaE. NaE was not correlated with any other variables. The relationships between PRA and aldosterone in healthy controls were retained in Type 1 diabetes (R2 0.37 supine, p = 0.00001, and 0.27 ambulant, p = 0.0005), as were respective direct and inverse relations between vasopressin and ANP and both PRA (rs 0.54 to 0.57, rs -0.43 to -0.53), and aldosterone (rs 0.78 to 0.80, rs -0.71 to -0.80). Fasting free serum insulin and vasopressin were both inversely related to ANP (rs -0.91 and -0.71, respectively). In the absence of autonomic dysfunction, hypertension or early nephropathy in Type 1 diabetes, increased SLC or exchangeable sodium were unrelated to each other or with hormonal control of sodium balance, but the homeostatic factors controlling hormonal interaction appear to be maintained. The interaction between insulin and hormonal control of sodium and water balance may be modified by circulating free insulin concentrations.
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PMID:Increased red cell sodium lithium countertransport activity, total exchangeable sodium, and hormonal control of sodium balance in normoalbuminuric type 1 diabetes. 828 27

For subjects on a normal diet, urea is the major urinary solute and is markedly concentrated in the urine compared with in the plasma. Because urea is not known to undergo active secretion, its excretion rests on filtration lessened to a variable extent by tubular reabsorption. It is well established that the efficiency of urea excretion drops with increasing urinary concentration and decreasing urinary flow rate (from approximately 60% of filtered load, above 2 mL/min, to approximately 20% below 0.5 mL/min) because the prolonged transit time in the distal nephron favors passive urea reabsorption. Thus, a higher urinary concentration is achieved at the expense of a reduced efficiency of urea excretion. Recent experimental observations suggest that GFR could actually increase in parallel with the urinary concentrating activity, thus ensuring a normal urea excretion in the face of a high, concentration-dependent urea reabsorption, with only a moderate increase in plasma urea. A possible mechanism is proposed that could explain how the vasopressin-induced intrarenal recycling of urea (which contributes to improvement in urinary concentration), but not an exogenous urea administration, could indirectly depress the tubuloglomerular feedback and hence increase GFR. An increased concentration of an osmotically active solute in the thick ascending limb of Henle's loop (such as urea and, in some cases, glucose) could enable a lower NaCl concentration to be achieved at the macula densa by reducing the osmotically driven water leakage in this nephron segment. This mechanism could explain the hyperfiltration seen in various pathophysiologic situations such as chronic vasopressin infusion, high protein intake, severe burns, and diabetes mellitus. Whatever the mechanism, if the need to excrete relatively high amounts of urea in a concentrated urine leads to a sustained elevation of GFR, the price to pay for this water economy is higher than generally assumed. It is not limited to the energy spent in the sodium reabsorption providing the "single effect" for the urinary concentrating process. It also includes the consequences on the glomerular filter of sustained high pressure and flow and the energy spent in reabsorbing the extra load of solutes filtered. In chronic renal failure, the ability to form hypertonic urine declines but is nevertheless well preserved with respect to declining GFR, thus imposing on remnant nephrons an additional permanent stimulus for hyperfiltration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Is the process of urinary urea concentration responsible for a high glomerular filtration rate? 830 36

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
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PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89


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