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)

Study of metabolic alterations that occur during space flight can provide insight into mechanisms of physiologic regulation. Results of medical experiments with astronauts reveal rapid loss of volume (2 L) from the legs and a transient early increase in left ventricular volume index. These findings indicate that, during space flight, fluid is redistributed from the legs toward the head. In about 2 days, total body water decreases 2 to 3%. Increased levels of plasma renin activity and antidiuretic hormone while blood sodium and plasma volume are reduced suggest that space flight-associated factors are influencing the regulatory systems. In addition to fluid and electrolyte loss. Skylab astronauts lost an estimated 0.3 kg of protein. Endocrine factors, including increased cortisol and thyroxine and decreased insulin, are favorable for protein catabolism. The body appears to adapt to weightlessness at some physiologic cost. Readaptation to Earth's gravity at landing becomes another physiologic challenge.
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PMID:Metabolic changes observed in astronauts. 176 22

The experiments presented here have been designed to investigated whether the age-related attenuation of the vagal reactivity to emotional stressors and its modulation by amphetamine (Amph) or arginine-vasopressin (AVP) can be generalized for other physiological response patterns. We therefore studied the vagal control of the endocrine pancreas during food intake. Young (3 months old) and aged (27 months old) male Wistar rats were provided with permanent cardiac catheters allowing free movement and repeated, stress-free blood sampling. The vagally mediated preabsorptive insulin response (PIR) in relation to food intake as seen in young rats was reduced in aged ones. Blood glucose increments were the same at both ages. Administration of Amph (0.5 mg/kg; s.c.) 30 min before, or AVP (10 micrograms/kg; s.c.) 60 min before presentation of a test meal led to an elevation of the magnitude of insulin secretion in young rats but reduced the response in aged rats. Moreover, the PIR was not reinstated in aged rats. Blood glucose increments were not influenced by the treatments. The results are interpreted in terms of age-related general reduction of parasympathetic reactivity. The differential effect of amphetamine and AVP treatment on the insulin response suggests that the central aminergic or peptidergic drive of vagal output to the endocrine pancreas is also age-related.
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PMID:Reduced preabsorptive insulin response in aged rats: differential effects of amphetamine and arginine-vasopressin. 176 18

Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.
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PMID:[Transient polyuria in pregnancy in diabetes insipidus and gestational diabetes]. 177 Sep 4

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

To clarify a possible mechanism whereby the perception of thirst may be associated with diabetes mellitus, we measured plasma levels of vasopressin (AVP), angiotensin II (ANG II), atrial natriuretic peptide (ANP) and plasma renin activity (PRA) in non-insulin-dependent (NIDDM) diabetic patients with or without thirst. Thirteen male NIDDM patients complaining of thirst had a significantly high blood hematocrit, plasma urea nitrogen and creatinine concentrations and plasma osmolality, indicating a reduction in plasma volume. In addition, the patients had a significantly high mean plasma concentrations of AVP (3.20 +/- 1.27 pmol/l) ANG II (33.8 +/- 31.4 pmol/l) and PRA, but a low mean plasma ANP concentration (8.9 +/- 4.5 pmol/l). After treatment with diet and/or sulfonylurea, plasma levels of AVP, ANG II and PRA decreased with a concomitant increase in plasma volume and disappearance of thirst. In contrast, 13 NIDDM patients (9 females and 4 males) without thirst had normal plasma urea nitrogen and creatinine concentrations, and the hematocrit did not change significantly after treatment. Plasma AVP (0.95 +/- 0.34 pmol/l), ANG II (14.7 +/- 8.8 pmol/l) and ANP (10.7 +/- 4.9 pmol/l) concentrations, and PRA were normal in this group of patients. There was no significant difference between the two groups of patients, however, in fasting glucose concentration and HbA1c. We conclude from these results that a reduction in plasma volume may be the major factor responsible for the induction of thirst sensation and for increased AVP secretion in NIDDM patients. The mechanism underlying a reduction in plasma volume remains unclear.
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PMID:Thirst and plasma levels of vasopressin, angiotensin II and atrial natriuretic peptide in patients with non-insulin-dependent diabetes mellitus. 182 24

A microassay was developed to measure the binding of the labelled monoiodinated analogue [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine, 4-threonine, 8-ornithine, 9-125I-tyrosylamide]vasotocin [125I-d(CH2)5[Tyr (Me)2, Thr4, Tyr-NH(2)9]OVT] to isolated nephron segments microdissected from collagenase-treated rat kidneys. When determined using 1.7 nM labelled ligand at 4 degrees C, specific binding sites (expressed at 10(-18) mol 125I-d(CH2)5[Tyr (Me)2, Thr4, Tyr-NH(2)9]OVT bound/mm tubule length) were found in medullary thick ascending limbs (MTAL), 1.67 +/- 0.49; cortical thick ascending limbs, 2.20 +/- 0.80; cortical collecting ducts, 2.39 +/- 0.86; outer medullary collecting ducts (OMCD), 2.54 +/- 0.53 and inner medullary collecting ducts, 5.33 +/- 0.40, whereas no specific binding could be detected in glomeruli and proximal tubules. Specific 125I-d(CH2)5[Tyr (Me)2, Thr4, Tyr-NH(2)9]OVT binding to OMCD was saturable with incubation time and reversible after elimination of free labelled ligand (the association and dissociation rate constants at 4 degrees C were 1.06 x 10(7) M-1 min-1 and 1.95 x 10(-2) min-1 respectively). The stereospecificity of MTAL and OMCD binding sites was assessed in competitive experiments revealing the following recognition pattern for a series of eight vasopressin analogues:dDAVP greater than AVP greater than d(CH2)5-[Tyr (Me)2, Thr4, Tyr-NH(2)9]OVT = AVT = OT greater than d(CH2)5[Tyr(Me)2]AVP = [Thr4, Gly7]OT greater than [Phe2, Orn8]VT, whereas pharmacological concentrations of insulin and glucagon did not impair radioligand binding. These results indicate that the detected labelled binding sites might correspond mainly to physiological V2 vasopressin receptors.
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PMID:Receptors for neurohypophyseal hormones along the rat nephron: 125I-labelled d(CH2)5[Tyr(Me)2, Thr4, Orn8, Tyr-NH(2)9] vasotocin binding in microdissected tubules. 183 Mar 90

Serum growth hormone (GH) levels were measured in 3 brothers with Hunter syndrome. The secretion of GH was studied by means of insulin (ITT), glucose (GTT), lysine-vasopressin (LVP), and L-Dopa administrations. Mean basal GH levels during the 4 tests were high (x = 14.2 ng/ml) in all cases. In the ITT and LVP tests, GH responses correlated positively with the patients' ages. Contrarily, after L-Dopa administration, GH elevations were normal in the two younger and absent in the oldest case. During GTT, GH levels were suppressed in all cases as expected. Basal cortisol and prolactin serum levels during the tests were normal. In order to clarify these data, GH levels were then determined during 120 min. (20-20 min.) under basal conditions. The means (+/- SD) of GH were 178 +/- 0.15; 4.42 +/- 2.47; and 2.30 +/- 0.71, for cases 1, 2 and 3, respectively (normal values 0-5 ng/ml). Basal somatomedin-C levels were in low-normal ranges. As patients were not undernourished and albumin levels were normal, a slight dysfunction of hypothalamic-pituitary-GH-somatomedin-C axis might occurred in these cases. The hypothesis here offered is that a primary sub-production of somatomedin-C, mainly by liver and kidneys, could be present in Hunter syndrome. This situation would lead to normal-high GH serum levels, as seen in the present cases. GH serum measurements in Hunter syndrome were not documented previously.
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PMID:[Serum growth hormone levels in Hunter's syndrome]. 184 6

Skin fibroblasts from newborn spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were cultured to study their growth rate and their reactivity to various agonists in terms of mitogenic potency and inositol phosphate production. A marked enhancement of nuclear 3H-thymidine incorporation, occurring after stimulation of quiescent fibroblasts by fetal calf serum, correlated with the increased growth rate of these cells with regard to WKY ones. Insulin (1 microgram/ml) and epidermal growth factor (10 ng/ml) induced two and four times greater DNA synthesis in SHR fibroblasts compared to WKY cells, without activating the phospholipase C pathway. In contrast, angiotensin II, bradykinin, vasopressin which stimulated inositol phosphate production, and phorbol-12 myristate 13-acetate were unable to stimulate DNA synthesis. Higher levels of tritiated inositol phosphates were produced in SHR cells after serum, bradykinin and angiotensin II stimulation, but not in WKY cells after vasopressin. This enhanced mitogenic response of SHR skin fibroblasts is probably due to a genomic alteration and appears to be independent of the hyperactivation of the phospholipase C to some vasoactive agonists.
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PMID:Enhanced response to growth factors and to angiotensin II of spontaneously hypertensive rat skin fibroblasts in culture. 184 54

Blood vasopressin concentration, hypothalamic response to stress resultant from insulin hypoglycemia and to acute furosemide load were measured in 72 patients with neuro-endocrine-metabolic form of hypothalamic syndrome. Pathogenetic treatment was decided upon by sensitivity to dopaminergic drug parlodel and antiserotonin drug peritol. According to the sensitivity tests the patients received either parlodel (5 mg/day) or peritol (12 mg/day) for 3-6 months. There were also patients on symptomatic treatment aimed at reduction of body weight. Peritol treatment promoted a decline in basal blood level of vasopressin and better response to insulin hypoglycemia and furosemide test. Parlodel treatment normalized vasopressin blood concentration and hypothalamic response to stimulators. Routine symptomatic therapy did not induce differences in vasopressin level compared to active stage of the disease.
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PMID:[Effect of pathogenetic treatment on vasopressin secretion in patients with hypothalamic syndrome]. 186 62

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87


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