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)

Seven patients with a rare syndrome of diabetes insipidus (DI), diabetes mellitus (DM), optic atrophy (OA), neurosensory deafness (D), atony of the urinary tract, and other abnormalities (Wolfram or DIDMOAD syndrome) are reported. Of the seven patients, three siblings were followed up for 10-17 years. All seven patients had diabetes mellitus and optic atrophy; six had diabetes insipidus; and in the four patients investigated there was dilatation of the urinary tract. The severity of diabetes varied, and all required insulin for control of the hyperglycaemia. In one patient the course of the disease simulated maturity onset diabetes of the young; another presented with ketoacidosis; but none had haplotypes usually associated with insulin dependent diabetes mellitus. The diabetes insipidus responded to chlorpropamide, suggesting partial antidiuretic hormone deficiency. Onset of optic atrophy and loss of vision occurred relatively late and progressed slowly, although in one patient there was a rapid deterioration in visual acuity. Deafness was mild, of late onset, and of sensorineural origin. A degenerative process affecting the central and peripheral nervous system can explain all the manifestations of the syndrome except diabetes mellitus. The pathogenesis of the diabetes mellitus remains obscure.
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PMID:Association of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness. The Wolfram or DIDMOAD syndrome. 405 39

In rats with deoxycorticosterone acetate (DOCA) salt hypertension, induction of diabetes with streptozotocin did not aggravate the elevation in blood pressure, but pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were enhanced. Along with glycosuria and hyperglycemia, the other effects of streptozotocin-induced diabetes were: reduced body weight, increased fluid intake, and bradycardia. Despite enhanced responsiveness to hypothalamic stimulation, blood pressure increases produced by intravenous injections of norepinephrine, tyramine, or vasopressin were unaltered. When pressor responses were compared in diabetic rats drinking either tap water or isotonic saline solution, no appreciable differences occurred. It was considered possible that hypothalamic responsiveness was enhanced in diabetic-DOCA hypertensive rats by increases not only in sympathetic nerve firing but also in release of endogenous norepinephrine.
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PMID:Hypothalamic responsiveness in DOCA hypertensive rats augmented by streptozotocin-induced diabetes. 618 70

To determine whether diabetes predisposes rats to hypertension, tail-cuff systolic pressures were measured in male rats made diabetic by pretreatment with streptozotocin. From Weeks 2 through 7, diabetic rats weighed less but had higher systolic pressures than nondiabetic ones. Further comparisons made while the rats were anesthetized with urethane showed that pressor and sympathetic nerve responses to ventromedial hypothalamic stimulation, as well as pressor responses to injected vasopressin, were significantly reduced in the diabetic group. A generalized reduction of cardiovascular reactivity was considered unlikely because systemic pressor responses to norepinephrine and tyramine were unimpaired. Yet reflex bradycardia elicited by norepinephrine was enhanced indicating that baroreceptor resetting had not occurred. Thus, diabetic rats were characterized by hypertension, narrowed pulse pressure, bradycardia with increased reflex responses to norepinephrine, and reduced pressor responses to hypothalamic stimulation and to vasopressin. The successful induction of diabetes was confirmed not only by the presence of hyperglycemia, hypoinsulinemia, glycosuria, and abnormal glucose tolerance, but also by reductions in pancreatic weight, insulin, and beta-cell content. Although our results suggest that diabetic rats are predisposed to become hypertensive, other mechanisms such as hypothalamic depression may be activated to restrict further elevations in blood pressure.
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PMID:Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness. 621 80

Deficiencies of corticotrophin (ACTH), growth hormone, and prolactin were documented in a woman with diabetes mellitus and Sheehan's syndrome. The patient's ACTH deficit appeared to be secondary to a hypothalamic abnormality since on two occasions the patient had a marked plasma ACTH response to vasopressin but not to insulin induced hypoglycaemia. It is postulated that the deficits of these three adenohypophysial hormones were instrumental in causing a severely impaired aldosterone secretory capacity in response to sodium restriction and an angiotensin infusion. In addition, the patient had an unusual form of thyroid dysfunction that was in part reversed with hydrocortisone replacement. The patient's unfortunate death during a hypoglycaemic crisis allowed correlation between her extensive antemortum endocrine testing and her pathologic anatomy.
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PMID:Corticotrophin, growth hormone and prolactin deficiencies with hypoaldosteronism and corticosteroid-reversible hypothyroidism in Sheehan's syndrome. Clinical and anatomical correlations. 625 5

Since the approval of lithium use in treatment of acute mania, there have been numerous clinical trials of lithium in medical and psychiatric disorders. This paper gives a brief review of the literature on lithium trials in approximately fourteen medical conditions. These are: hyperthyroidism, metabolizing thyroid cancer, syndrome of inappropriate secretion of antidiuretic hormone, premenstrual tension syndrome, anorexia nervosa, Felty's syndrome, chemotherapy-induced neutropenia, aplastic anemia, seborrheic dermatitis, eczematoid dermatitis, cyclic vomiting, diabetes mellitus and asthma. Most of the case reports cited showed the efficacy of the side effects from lithium salt in the management of the symptoms and signs of these disorders, however, well-designed and controlled studies give negative results. The positive results are reported in the group of disorders having an underlying subdromal affective syndrome such as premenstrual tension syndrome and anorexia nervosa. Other encouraging reports include the effect of lithium to induce leucocytosis in Felty's syndrome and chemotherapy-induced neutropenia.
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PMID:A review of clinical trials of lithium in medicine. 639 35

This study was designed to determine if vascular dysfunction and enhanced norepinephrine sensitivity occurring in early experimental juvenile diabetes (S. M. Mueller, T. M. Mueller, and P. J. Ertel, 1982, Amer. J. Physiol. 243, H139-H144) persist, improve, or worsen in adulthood. Alloxan was administered to rats at 4 weeks of age and they were studied 14 weeks later. After Seconal anesthesia, the hindquarters of diabetic and control rats were perfused at a constant flow rate per 100 g through the abdominal aorta with oxygenated Tyrode solution containing dextran. Efflux was from the ligated and severed inferior vena cava. In order to test the effect of a strong sympathetic stimulus producing reflex peripheral vasoconstriction, the cephalad portions of the rats were rapidly hemorrhaged. The time to the maximal increase was significantly longer in the diabetics (122 +/- 6 sec, P less than 0.05) than in the controls (102 +/- 5 sec) and the increase in perfusion pressure was markedly less in the diabetics (D) (48 +/- 9 mm Hg, P less than 0.01) than in the age-matched controls (C) (88 +/- 10 mm Hg). The threshold to norepinephrine in the perfusate was determined. The threshold was significantly lower in D than in age-matched C [0.112 +/- 0.026 (P less than 0.05) vs 0.265 +/- 0.057 micrograms/ml, respectively]. The maximum vasoconstrictor capacity of the vasculature was tested with supramaximal doses of vasopressin and was significantly lower in D than in C [190 +/- 10 (P less than 0.001) vs 284 +/- 15 mm Hg, respectively]. These data suggest that both vasculopathy and enhanced norepinephrine sensitivity persist in chronic uncontrolled experimental diabetes mellitus. However, when the severity of the abnormalities was compared to early experimental diabetes mellitus, mild improvement had occurred--an apparent adaptation to the diabetic state as the animal grew.
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PMID:Adult sympathetic and vascular dysfunction in experimental juvenile-onset diabetes mellitus. 674 60

Filtered proteins including insulin are absorbed in the proximal tubule by means of pinocytosis. The first step in this process is binding of the protein to brush border membrane. As it is not known whether absorption exhibits specificity, we set out to determine whether specific binding sites for insulin are present in brush border membranes. Rabbit-isolated brush border membranes were incubated with 125I-insulin and varying concentrations of cold insulin or other peptide hormones. Binding and degradation of 125I-insulin occurred in a time- and temperature-dependent manner. Native insulin competitively inhibited 125I-insulin binding, but calcitonin, arginine vasopressin, glucagon, and growth hormone (10(-6) M) were relatively ineffective. Nonspecific binding averaged one-third of the total radioactivity bound. Scatchard analysis of binding data revealed two classes of insulin receptors: high affinity, low capacity receptors and low affinity, high capacity receptors. Gel filtration analysis of 125I-insulin exposed to brush border membrane revealed the formation of low-molecular-weight products similar to that produced by intact kidneys. The degrading process exhibited some specificity, for cold insulin (10(-6) M) was more effective than calcitonin, vasopressin, glucagon, or growth hormone in inhibiting degradation (32% versus less than 13% inhibition; P less than 0.01). Whether this reflects inhibition of insulin specific binding before exposure to degradation or inhibition of specific enzymes is unclear. In summary, it appears that renal brush border membranes have a major insulin-specific receptor component that could potentially mediate tubular insulin absorption. In addition, there is a smaller nonspecific component that may also have the potential to mediate insulin absorption. Finally, it appears that brush border membranes have the ability to degrade insulin to low-molecular-weight products by a process that exhibits some specificity for insulin.
Diabetes 1982 Jul
PMID:Binding and degradation of insulin by isolated renal brush border membranes. 676 Dec

The effects of epinephrine, vasopressin, and A23187 on glycogen synthase and phosphorylase were examined in isolated rat liver parenchymal cells from fed animals. In normal calcium-containing hepatocytes, epinephrine, vasopressin, and A23187 were more potent at inactivating glycogen synthase, previously activated with 30 mM glucose, than at activating phosphorylase. In calcium-depleted hepatocytes (cells washed and incubated with 1 mM EGTA), the effect of epinephrine on both enzyme activities was impaired, while the effects of vasopressin and A23187 were completely abolished. Insulin was more effective at inhibiting the effects of epinephrine in calcium-depleted cells, but it was without effect on vasopressin and A23187 actions. The ability of epinephrine, vasopressin, and A23187 to elicit calcium efflux from cells was not altered by the presence of 30 mM glucose. These findings are consistent with the idea that the alpha-adrenergic inactivation of liver glycogen synthase may be a result of the increased stimulation of a calcium-dependent protein kinase, possibly phosphorylase b kinase.
Diabetes 1980 Aug
PMID:The role of calcium in alpha-adrenergic inactivation of glycogen synthase in rat hepatocytes and its inhibition by insulin. 677 24

Daily subcutaneous injections of lente insulin reduced the hypertension and bradycardia which developed consistently in streptozotocin diabetic rats. Insulin-treated rats also became less hyperglycemic, drank less water, and gained weight faster than untreated diabetic controls. Behavioral and tachycardiac effects elicited by electrical stimulation of the ventromedial hypothalamus while the rats were awake were similar, but attendant pressor responses were larger in those that had been treated with insulin. Under subsequent urethane anesthesia, pressor and sympathetic responses to hypothalamic stimulation, as well as pressor responses to tyramine and vasopressin, were augmented in insulin-treated rats. A generalized increase in cardiovascular reactivity caused by insulin seemed unlikely since pressor responses to norepinephrine were unaltered. Enhanced hypothalamic responsiveness was considered due to improvement of diabetic encephalopathy rather than to direct CNS stimulation by insulin because the injected insulin had mostly dissipated by the time pressor responses were recorded. By showing that insulin treatment produced changes opposite to those occurring during induction of diabetes our results suggest that insulin can alleviate cardiovascular and hypothalamic dysfunction in streptozotocin-induced diabetes.
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PMID:Insulin reverses hypertension and hypothalamic depression in streptozotocin diabetic rats. 684 67

Investigations in a 14 year old girl with arrested growth for 2 years, delayed pubertal development, hypernatraemia without thirst, diabetes mellitus and hyperlipaemia are reported. The hypernatraemia was accompanied by a low vasopressin concentration with an abnormal response to thirst, high plasma renin but normal plasma aldosterone concentrations. Treatment with vasopressin and increased fluid intake decreased serum sodium levels. Serum gonadotrophins were low; GH response during an insulin tolerance test was subnormal and basal serum Prl concentration was elevated. Bone age, thyroid function and adrenal function were normal. After initiation of bromocriptine treatment her growth accelerated and regular menstruations commenced. The serum gonadotrophin levels increased and showed pulsatile release. A hypothalamic disorder is suggested, but no cerebral lesion could be demonstrated.
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PMID:Hypernatraemia, diabetes mellitus, hyperprolactinaemia, retarded growth and delayed puberty in a 14 year old girl. Effect of bromocriptine treatment. 700 94


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