UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The central osmoregulation mechanism for vasopressin (VP) release was studied in the streptozotocin diabetic (STZ-DM) rat. Electrical activities of the VP-producing cell in the supraoptic nucleus (SON) were recorded extracellularly and compared with those in the control rat both in vivo and in vitro. Neuronal activities in the periventricular area (PVA) were also recorded in the in vitro experiment. Hyperosmolar stimulation which was done with an intraperitoneal injection of 1.0 M NaCl (4 ml/kg) resulted in an increase in plasma osmolality both of STZ-DM (increased by 14 +/- 2 mOsml/kg H2O) and control rats (15 +/- 3 mOsmol/kg H2O). Increased plasma osmolality caused significant increase in the mean discharge rate of VP-producing cells in the control animals, but only an insignificant change in STZ-DM rats. In the hypothalamic slice preparations incubated in the artificial cerebrospinal fluid (301 +/- 2 mOsml/kg H2O), VP-producing cells in control rats increased their discharge rate linearly as the osmolality (310 +/- 2 and 320 +/- 1 mOsmol/kg H2O) or concentration (10(-8) and 10(-6) M) of angiotensin II (AGII) of the perfusate was increased stepwise, but there was no change in response to either stimulus in STZ-DM rats. On the other hand, there was no difference in sensitivity to osmolality and AGII of PVA neurons in both animal groups. These data indicate that lower sensibility to osmotic change of VP-producing cells in STZ-DM rats may depend, at least partially, upon the disturbance of osmo- and AGII-sensitivity in VP-producing cells themselves, and that these changes seem to be restricted to SON VP-producing cells.
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PMID:Hypothalamic osmoregulation for vasopressin release in streptozotocin-diabetic rats in vivo and in vitro. 161 81

The contribution of hormone-stimulated glycogenolysis to hepatic glucose production was studied in hepatocytes from streptozotocin diabetic rats. To this end, the activation of glycogen phosphorylase by glucagon, vasopressin, and the alpha 1-adrenergic agonist phenylephrine was compared in hepatocytes from normal and diabetic rats and related to glycogen content, glucose production, and microsomal glucose-6-phosphatase activity. Streptozotocin-induced diabetes reduced the glycogen content and the amount of total (a + b) phosphorylase in hepatocytes proportionally to the severity of the disease. In cells from severely diabetic rats (group 1), the responsiveness of activation of phosphorylase to the hormones was reduced by about half, consistent with a 45% reduction in total phosphorylase. In addition, the sensitivity of phosphorylase activation to all hormones investigated was decreased by about 1 order of magnitude or more in cells of this group. In hepatocytes from rats with milder diabetes (group 2), maximal phosphorylase activation reached an intermediate value between that of the control group and of group 1. In response to all hormones investigated, group 2 diabetic rat hepatocytes produced less glucose than control rat liver cells, while in group 1 there was no increase in glucose production at all, presumably because glycogen concentration was too low. However, in group 2 diabetic rat hepatocytes, glucagon-stimulated glucose production, unlike phosphorylase activation, did not show decrease sensitivity, presumably because glucose-6-phosphatase activity is increased by diabetes. Our results thus indicate that hormone-stimulated liver glycogenolysis is unlikely to contribute to enhanced glucose production in insulin-deficient diabetes, despite increased glucose-6-phosphatase activity.
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PMID:Hormone-stimulated glucose production from glycogen in hepatocytes from streptozotocin diabetic rats. 165 43

Rats were administered streptozocin (STZ; 50 or 75 mg/kg i.v., tail vein) or vehicle. Approximately 2 wk later, venous and arterial catheters was implanted for subsequent (24 h later) vasopressin, electrolyte, and hemodynamic measurements. STZ-induced diabetic (STZ-D) rats demonstrated a dose-dependent increase in the plasma glucose concentration, plasma osmolality, and plasma vasopressin concentration. Mean arterial blood pressure (MABP) was unchanged, but heart rate was reduced. Diabetes-prone BB rats, maintained on or withdrawn from insulin treatment for 24-48 h, and diabetes-resistant rats were instrumented and studied as above. Spontaneous-diabetes-prone rats demonstrated increase in plasma glucose concentration and plasma osmolality similar to STZ-D rats but had significantly greater plasma vasopressin concentrations. The significant decrease in MABP observed in these animals probably contributed to the enhanced vasopressin response. We conclude that both osmotic and cardiovascular parameters play important roles in vasopressin secretion in diabetic rats.
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PMID:Vasopressin in rats with genetic and streptozocin-induced diabetes. 290 12

Enhanced prostaglandin production is postulated to contribute to altered vascular reactivity and glomerular hyperfiltration in early insulin-deficient diabetes mellitus. Rats with streptozocin-induced diabetes (STZ-D) show glomerular hyperfiltration and develop renal disease. BB rats with genetic diabetes (BB-D) also hyperfilter but have only minor renal lesions. We therefore compared glomerular and mesangial prostaglandin E2 (PGE2) production and glomerular contractility in response to pressors as a reflection of in vitro vascular reactivity in these models. Glomeruli isolated from rats with 3 wk of STZ-D produced significantly more PGE2 under basal and ionophore A23187-stimulated conditions than those from control rats. Glomeruli from BB-D rats under basal and stimulated conditions, however, generated amounts of PGE2 that were comparable to either those of nondiabetic littermates or of normal Wistar rats. Mesangial cells cultured from glomeruli of STZ-D, BB-D, and control rats all had identical prostaglandin profiles judged by conversion of [14 C]arachidonic acid. They also produced comparable amounts of PGE2 under basal conditions and after stimulation with angiotensin II or A23187, as determined by radioimmunoassay. Planar surface area of glomeruli isolated from control rats showed a dose-dependent decrease in response to angiotensin II (10(-11)-10(-9) M). This response to angiotensin II was at least as great in glomeruli from STZ-D rats. Contraction of glomeruli from control and STZ-D rats was also comparable after vasopressin or norepinephrine. Similarly, glomeruli from BB-D and BB control rats contracted in a comparable fashion to angiotensin II and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of glomerular and mesangial prostaglandin synthesis and glomerular contraction in two rat models of diabetes mellitus. 311 6

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

Electrical activities of the vasopressin (AVP)-producing cell in the supraoptic nucleus of the streptozotocin diabetic (STZ-DM) rat were recorded extracellularly and compared with those in the control rat. Higher hematocrit (45.3 +/- 0.5%, mean +/- SE) and lower mean blood pressure (MBP) (89.5 +/- 2.1 mmHg) suggested that STZ-DM rats were hypovolemic and hypotensive. The mean discharge rates of AVP cells were 15.2 +/- 3.1 Hz (STZ-DM) (p < 0.05 vs. control) and 8.8 +/- 0.8 Hz (control), respectively. Pressor and depressor responses were caused by phenylephrine (1.5 and 2.9 micrograms/kg, i.v.) and nitroprusside (1.5 micrograms/kg, i.v.), respectively, during the recording the AVP cells. Pressor and depressor responses linearly (STZ-DM; gamma = -0.7071, control; gamma = -0.9262) decreased and increased the discharge activity of the cells in both experimental groups, respectively. The MBP-neuronal activity relationship in STZ-DM did not differ statistically from that in the control. These results suggest that cardiovascular regulation of AVP release is well retained in STZ-DM rats.
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PMID:Baroreceptor control of vasopressin-producing cells in streptozotocin diabetic rats. 851 61

In diabetes mellitus (DM), the high urine flow rate suggests that urinary concentrating capacity is impaired. However, several studies have shown that vasopressin is elevated in DM and the consequences of this elevation have not yet been characterized. This study reevaluated renal function and water handling in male Wistar rats with Streptozotocin-induced DM, and in control rats. During five weeks after induction of DM, urine was collected in metabolic cages and a blood sample was drawn during the third week. Control rats (CONT) were studied in parallel. On week 3, urine flow rate was tenfold higher in DM than in CONT rats and urinary osmolality was reduced by half along with a markedly higher osmolar excretion (DM/CONT = 5.87), due for a large part to glucose but also to urea (DM/CONT = 2.49). Glucose represented 52% of total osmoles (90.3 +/- 6.5 mmol/d out of 172 +/- 14 mosm/d). Free water reabsorption was markedly higher in DM rats compared to CONT (326 +/- 24 vs 81 +/- 5 ml/d). In other rats treated in the same way, urinary excretion of vasopressin was found to be markedly elevated (15.1 +/- 4.1 vs 1.44 +/- 0.23 ng/d). In DM rats, glucose concentration in urine was 17 fold higher than in plasma, and urea concentration 14 fold higher. Both urine flow rate and free water reabsorption were positively correlated with the sum of glucose and urea excretions (r = 0.967 and 0.653, respectively) thus demonstrating that the urinary concentrating activity of the kidney increased in proportion to the increased load of these two organic solutes. These results suggest that vasopressin elevation in DM contributes to increase urinary concentrating activity and thus to limit water requirements induced by the metabolic derangements of DM. The possible deleterious consequences of sustained high level of vasopressin in DM are discussed.
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PMID:Vasopressin and urinary concentrating activity in diabetes mellitus. 1049 90

We sought to identify the areas that have altered neuronal activity within the hypothalamus of diabetic rats by mapping neuronal expression of c-fos protein (Fos) and Fos-related antigens. After a standard PAP immunocytochemical protocol, Fos-like immunoreactivity was observed in the paraventricular nucleus (PVN), supraoptic nucleus (SON), median preoptic area (MnPO), anterior hypothalamus (AH) and posterior hypothalamus (PH) of control (vehicle; n=6) and diabetic rats (Sprague-Dawley rats injected with STZ 65 mg/kg/ip 4 weeks prior to the experiment; n=6). Blood glucose levels were significantly elevated in the diabetic group (370+/-8 mg/dl) compared to control group (104+/-3 mg/dl). Diabetic rats had a significantly higher number of Fos-positive cells in PVN (2.5x), SON (7x) and MnPO (2x) compared to the control rats. However, diabetic rats had significantly fewer Fos-positive cells in the AH (0.3x) and no difference was observed in the PH between the diabetic and control rats. Despite the elevated number of Fos-positive cells in the diabetic rats, dehydration (water withdrawal for 24 h) or hypertonic challenge (1.5 ml of 0.1 M NaCl i.p. injection) produced a further increase in the number of Fos-positive cells in the PVN, SON and MnPO. Dehydration did not alter the number of Fos-positive cells in the AH or PH, but hypertonic challenge produced a significant increase in the Fos-positive cells in both the AH and PH of diabetic rats. This study demonstrates that: (1) there is increased basal neuronal activity in the PVN, SON and MnPO, a decrease in neuronal activity in the AH and no change in neuronal activity in the PH as indicated by Fos staining in diabetic rats; and (2) dehydration or hypertonic challenge produces a further increase in the number of Fos-positive cells in the PVN, SON, and MnPO which is comparable to control rats. These data support the conclusion that vasopressin producing neurons in the PVN and SON and autonomic areas within the lamina terminalis and hypothalamus are activated during diabetes and may contribute to the elevated levels of vasopressin and autonomic dysfunction during diabetes.
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PMID:Neuronal expression of fos protein in the forebrain of diabetic rats. 1244 95

Galanin-like peptide (GALP) is a 60-amino-acid peptide with structural similarities to galanin and a high affinity for galanin receptors. GALP is expressed by a discrete population of neurons in the arcuate nucleus (ARC) and median eminence of the hypothalamus of several species, including the rat. GALP neurons express leptin receptors and GALP mRNA levels are decreased slightly in fasted rats and stimulated significantly by acute leptin treatment in combination with fasting. In studies to further explore the leptin dependence of GALP expression, we examined GALP mRNA levels in the hypothalamus of obese Zucker and streptozotocin-induced diabetic (STZ-DM) rats. In leptin receptor-deficient obese Zucker rats, with 75% higher body weight than lean littermates, GALP mRNA levels in the ARC were decreased by 75%, while neuropeptide Y (NPY) mRNA levels were increased 7-fold (n = 5, p < 0.001), consistent with earlier reports. In hypoleptinemic diabetic rats with 4.5-fold higher blood glucose and 15% lower body weight than controls, GALP mRNA levels in the ARC were decreased by 90%, while NPY mRNA levels were increased 9-fold (n = 5, p < 0.001). GALP is also expressed by pituicytes in the neural lobe of the rat pituitary gland and GALP expression is increased by osmotic stimulation such as dehydration and salt loading. Thus, in STZ-DM rats that are in a hyperosmotic state with elevated plasma vasopressin levels, GALP mRNA levels were increased by approximately 20-fold in the neural lobe relative to control (n = 4, p < 0.001). The current findings are consistent with a strong tonic influence of leptin receptor signalling on hypothalamic GALP expression under normal conditions, and possible abnormalities in GALP neuronal signalling and their putative targets, thyrotropin-releasing hormone and gonadotropin hormone-releasing hormone neurons, under pathophysiological conditions such as diabetes and obesity. Our data in STZ-DM rats also clearly demonstrate that GALP gene expression is differentially regulated in neurons and pituicytes.
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PMID:Galanin-like peptide mRNA alterations in arcuate nucleus and neural lobe of streptozotocin-diabetic and obese zucker rats. Further evidence for leptin-dependent and independent regulation. 1525 10

Chronic diabetes mellitus (DM) induces hyperactivity of the hypothalamo-pituitary-adrenal axis (HPA). Our present study addresses the role of vasopressin (AVP) in maintaining adrenocortical responsiveness during DM. AVP-deficient mutant Brattleboro rats were used with heterozygous controls and the V2 agonist, desmopressin was infused to replace peripheral AVP. To induce DM the rats were injected by streptozotocin (STZ, 60 mg/ml/kg i.v.) and studied 2 weeks later. The acute stress stimulus was 60 min restraint. The signs of DM (the increase in water consumption and in blood glucose levels) were discovered in all rats. The diuretic effect of the lack of AVP was additional to the DM-induced osmotic diuresis. DM induced significant, chronic stress-like somatic changes on which AVP-deficiency had no effect and although desmopressin infusion normalized the water consumption and the body weight gain in AVP-deficient rats, it had no effect on DM-induced changes. The acute stress-induced plasma ACTH elevation was smaller in AVP-deficient or DM rats but these effects were not additive. Desmopressin did not normalize the decreased ACTH-elevation of AVP-deficient animals. The resting morning plasma corticosterone level was elevated both in DM and AVP-deficient rats without interaction. The restraint-induced corticosterone rise was influenced neither by the lack of AVP nor by DM and the basal and stress-induced prolactin levels were smaller in DM rats without any effect of AVP-deficiency. In conclusion, our data suggest that AVP does not play a crucial role in HPA axis regulation during DM-induced chronic stress. In contrast, the role of AVP seems to be more important during acute stress, however, it is restricted to the ACTH regulation. According to the water consumption data diabetes insipidus seems to be an additional risk factor for DM.
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PMID:The role of vasopressin in diabetes mellitus-induced hypothalamo-pituitary-adrenal axis activation: studies in Brattleboro rats. 1646 84

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