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)

Secretory granules isolated from ox neurohypophyses released their content of vasopressin in the presence of ATP and Mg2+. A half maximal ATP concentration of 0.25 mM was found. Ca2+ was not necessary for the effect. High concentrations of ADP, AMP and ITP were shown to mimic the effect of ATP. Utilizing this effect of ATP combined with iodonitrotetrazolium treatment to make mitochondria heavier, a method is described to obtain granule "ghosts" in a purified form. They were shown to be phosphorylated when granules were incubated with [gamma-32P] ATP.
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PMID:ATP-induced release of vasopressin associated with phosphorylation of isolated bovine neurohypophyseal secretory granule membranes. 2 18

A 74-year-old woman with miliary tuberculosis had moderately severe hyponatremia due to inappropriate secretion of antidiuretic hormone (SIADH) and very severe thrombocytopenia without other hematologic abnormalities. She was treated with isoniazid, rifampin, ethambutol, prednisone, vincristine and fluid restriction and recovered completely. The SIADH may have been a response by the posterior pituitary to a decrease in intravascular volume resulting from the extensive pulmonary disease or associated hypoxia, or the tuberculous lung may have released ADH or an ADH-like substance. The thrombocytopenia may have resulted from a direct or indirect toxic effect of infection or, less likely, the tuberculosis may have activated latent idiopathic thrombocytopenic purpura.
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PMID:Miliary tuberculosis presenting with hyponatremia and thrombocytopenia. 99 Oct 33

Diabetes insipidus (DI) is a disorder characterized by polyuria, polydipsia and increased thirst [1] while pituitary DI is a syndrome that is known to result from deficient release of the antidiuretic hormone (ADH) [2,3]. Trauma to the neurohypophysis (operational or accidental) is the most common cause of DI. Primary or metastatic intracranial tumors are the second most common cause of DI. Among the less frequent causes are the granulomatous lesions or infections of the central nervous system, drugs and vascular lesions [2]. In 30-40% of the patients, there is no identifiable cause (idiopathic DI). Idiopathic thrombocytopenic purpura (ITP) is an immunologically mediated destructive thrombocytopenia. The clinical diagnosis is made after excluding the presence of other disorders that are known to be associated with shortened platelet survival [4]. In this paper two cases of DI and ITP are described.
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PMID:Coexistence of diabetes insipidus and idiopathic thrombocytopenic purpura. 139 2

PMS is probably a group of entities which include various symptoms that occur during the 7 to 10 days before menstruation and disappear a few hours after the onset of menstruation. The definition of PMS lacks objective criteria. The most common symptoms are irritability, bloating, aggressiveness, mastodynia, and headaches. The prevalence of PMS is estimated at 30 to 40 per cent. PMS is more prevalent among women working outside the home, alcoholics, women of high parity, and women with toxemic tendency; it probably runs in families. The etiology of PMS is no less obscure to us than when it was first described by Frank in 1931. No single theory has been established to explain the entire diversity of PMS symptomatology. The multitude of possible etiologic factors includes psychosocial bases, progesterone deficiency, prolactin excess, thyroid hypofunction, renin angiotensin alternations, antidiuretic hormone excess, decreased colloidosmotic pressure, endorphin activity alternations, serotonin metabolism alternations, prostaglandin action, vitamin deficiency, and such unconventional theories as the ovarian infection or the "yeast overgrowth" theory. A partial resolution of this divergence of hypotheses comes from the biopsychosocial model developed by Keye and Trunnel. According to this model, a biologic, perhaps genetically determined, predisposition to PMS is realized when past and present life experiences, attitudes, beliefs, coping styles, and social forces interact to stress a woman. The diagnosis of PMS is based on establishing a relationship between the luteal phase of the cycle and the symptoms. The evaluation of PMS patients includes the use of a monthly diary to scale the symptoms, a physical examination, and biochemical studies to rule out other disorders. Management includes education, reassurance, and drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The premenstrual syndrome. 218 58

Ventricular dysfunction due to an abnormality of the heart which is associated with typical hemodynamic, renal and hormonal reactions, characterizes the clinical syndrome heart failure. The traditional definition of heart failure as the inability to pump an amount of blood sufficient to cover the metabolic needs of the body in the presence of adequate venous return, emphasizes mainly the reduction in cardiac output but not the increase in intracardiac pressures. Pressure or volume overload, decreased contractility, loss of muscle mass or restricted filling represent the most important pathological processes leading to heart failure. The disturbance of systolic ventricular function due to pressure or volume overload or diminished contractility is characterized by a decrease in the ejection fraction, the disturbance in diastolic ventricular function associated with restricted filling is characterized by elevated chamber stiffness. Decreased contractility is most commonly responsible for the development of heart failure. Impairment of diastolic ventricular function can only be regarded as the dominant mechanism leading to heart failure in the presence of a small noncompliant ventricle. Impairment of diastolic ventricular function in an enlarged heart is always associated with an impairment of systolic ventricular function and is, then, relegated to a subordinate role. Common causes of heart failure are coronary artery disease, hypertension, cardiomyopathies, valvular heart diseases and congenital heart diseases, for the incidence of which coronary artery disease is most frequently responsible. Most of these diseases lead to heart failure not via a single, but rather several of the specified pathophysiological processes. Possible mechanisms for loss of contractility include structural changes as well as alterations in excitation-contraction coupling. Possible mechanisms responsible for impaired diastolic ventricular function encompass, in addition to altered calcium flux, structural changes such as fibrosis and hypertrophy and factors such as asynchrony and abnormal loading conditions. With increasing derangement of cardiac function, there is recruitment of the compensatory mechanisms: hypertrophy of the cardiac muscle, Frank-Starling mechanism, activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system and the arginine-vasopressin system. The goal is maintenance of adequate blood pressure and cardiac output whereby blood flow is redistributed in favor of the heart and brain and away from the skin, musculature and visceral organs. Activation of the neurohumoral system can lead to excessive vasoconstriction as well as sodium and water retention resulting in an undesired elevation of preload and afterload which, in turn, leads to further worsening of the heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiologic and diagnostic aspects of heart failure]. 219 15

The hemodynamic situation in congestive heart failure (CHF) is greatly influenced by compensatory mechanisms within the heart itself as well as released from the central nervous system and from the kidneys. These measures are intended to maintain the cardiac output at a level as beneficial as possible and to distribute the blood flow to regions with the largest metabolic demands. Thus the hemodynamic consequences of CHF are reflected in the central circulation as well as in the periphery. Within the heart the Frank-Starling mechanism, adrenergic stimulation causing increase of heart rate and contractility, and during the chronic course also myocardial hypertrophy are operating. The central nervous and peripheral adaptive measures include increased sympathetic outflow bringing about an increased vasomotor tone with augmentation of pre- and afterload, and activation of the renin-angiotensin-aldosterone system, where angiotensin II further augments vasoconstriction directly and through central nervous stimulation. This vasoconstriction may be counteracted by humoral factors with vasodilatory properties, such as dopamine, bradykinin, acetylcholine and the metabolic products adenosine and lactic acid. The exact role of these and the possible importance of the antidiuretic hormone, arginine vasopressin, the prostaglandin system and the recently discovered atriopeptin remains to be established. As the compensatory mechanisms may maintain a fairly satisfactory hemodynamic situation at rest, investigations should be performed not only at rest but also during exercise to get an over-all impression of the cardiac functional state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of cardiac failure. Pathophysiologic aspects--hemodynamics. 294 44

1. Homogenates of neural lobes of bovine pituitary glands were fractionated by differential and density-gradient ultracentrifugation and the distribution of adenosine triphosphatase (ATPase) activity was studied. It was shown that all the activity was membrane-bound. 2. On the basis of ionic requirements the ATPase activity was grouped into three categories: (a) Mg(2+)-dependent, (b) Ca(2+)-dependent and (c) Mg(2+)+Na(+)+K(+)-dependent (ouabain-sensitive) ATPases. The activity in the absence of bivalent cations was negligible. The ratio between the activities of the three ATPases varied between the different subcellular fractions. 3. Preincubation of the subcellular fractions with deoxycholate increased the activity of the Mg(2+)+Na(+)+K(+)-dependent enzyme, whereas the Mg(2+)- and Ca(2+)-activated ATPases were either unaffected or slightly inhibited. Triton X-100 solubilized the Mg(2+)- and Ca(2+)-ATPases; however, the activity of the Mg(2+)+Na(+)+K(+)-ATPase was abolished by the concentration of Triton X-100 used. 4. All the subfractions displayed unspecific nucleotide triphosphatase activity towards GTP, ITP and UTP. These substrates inhibited the hydrolysis of ATP by all three ATPases. ADP also inhibited the ATPases. 5. Polyacrylamide-gel electrophoresis of extracts containing the Mg(2+)- and Ca(2+)-dependent ATPase activity solubilized by Triton X-100 revealed the presence of two enzymes; one activated by either Mg(2+) or Ca(2+) and the other activated only by Ca(2+). 6. In sucrose density gradients the distribution of vasopressin was different from that of all three types of ATPases. It is therefore suggested that the neurosecretory granules do not possess ATPase activity.
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PMID:Adenosine triphosphatase activity in the neural lobe of the bovine pituitary gland. 428 6

In the present study, we examined the effects of guanine nucleotides on vasopressin-induced osmotic water flow and sodium transport in the 14-h preincubated frog bladder. We also examined the effects of the adenylate cyclase-cyclic AMP and cyclic AMP-dependent protein kinase system in the bladder's epithelial cells. Gpp(NH)p significantly enhanced vasopressin-induced water flow while it did not affect cyclic AMP-induced water flow. However, Gpp(NH)p did not enhance the vasopressin-induced increment of sodium transport across the frog bladder. The adenylate cyclase activity of the crude homogenate was enhanced by vasopressin, Gpp(NH)p and NaF. The effects of Gpp(NH)p and vasopressin, at their maximum doses, on the enzyme activities were additive, while other combinations were not. Specific Gpp(NH)p binding sites were found in the pellet fraction after 2,400 X g centrifugation. No direct effect on the protein kinase activity was observed in the presence of 10(-6) M nucleotides, such as GTP, GDP, GMP, CTP, UTP, ITP and Gpp(NH)p. Cyclic AMP stimulated the phosphorylation of discrete protein bands, however, Gpp(NH)p did not influence cyclic AMP-dependent protein phosphorylation of crude homogenate of the bladder's epithelial cells. These results suggest the guanine nucleotides stimulate the vasopressin-induced osmotic water flow in frog bladder by enhancing the vasopressin-mediated adenylate cyclase activity, so that accumulated cyclic AMP might activate cyclic AMP-dependent protein kinase.
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PMID:Effects of guanine nucleotides on vasopressin-induced water flow and sodium transport of the frog bladder. 660 7

The effects of arginine-vasotocin and nucleotides on the steady-state kinetics of the adenylate cyclase activity in the epithelial cell membranes of the bullfrog (Rana catesbiana) bladder were studied. Arginine-vasotocin stimulated adenylate cyclase more effectively than oxytocin or arginine-vasopressin, with respect to both the maximal hormonal activation ratio relative to basal, and the hormone concentration yielding a half-maximal response (apparent Km). Arginine-vasotocin, GTP and its analogue guanyl-5'-yl imidodiphosphate (Gpp(NH)p) increased the Vmax of the basal adenylate cyclase activity, but showed no effect of the apparent Km of the system for ATP. In addition, Gpp(NH)p enhanced the arginine-vasotocin-stimulated adenylate cyclase activity, further increasing the Vmax, while GTP showed no statistically significant effect. Dual effects of GDP were apparent: it was stimulatory at 1 x 10(-5) mol/l and inhibitory at 1 x 10(-3) mol/l, on both the basal and the arginine-vasotocin-stimulated adenylate cyclase activity. Guanosine 5'-monophosphate, CTP, UTP and ITP showed no apparent effect on the enzyme activity. Sodium fluoride acted in the same manner as GTP on the adenylate cyclase system, increasing only basal activity. Adenylate cyclase activities exhibited pH optima that were less distinct in the presence than in the absence of Gpp(NH)p. The Arrhenius plot of the temperature experiment showed that a high-energy step was involved for activation by Gpp(NH)p or arginine-vasotocin. When the relative activation ratios by arginine-vasotocin at different ATP concentrations were studied, a distinct activation optimum was shown at 2.5 x 10(-4) mol ATP/l, either in the absence or presence of Gpp(NH)p. The possibility that GTP, GDP nd ATP play a regulatory role in the epithelial cells of the bullfrog bladder by adjusting the responsiveness of the system to a natural hormone, arginine-vasotocin, is discussed.
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PMID:Stimulatory and inhibitory effects of guanine nucleotides on arginine-vasotocin-sensitive adenylate cyclase in the epithelial cell membranes of the bullfrog bladder. 660 97

Four neuropeptides were identified from the brain and corpora cardiaca-corpora allata (CC-CA) of the mealworm beetle Tenebrio molitor using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and information derived from the genome of the red flour beetle, Tribolium castaneum. Leucomyosuppressin (a FLRFamide), previously associated with cockroaches, but also subsequently identified from honey bee seen as a prominent peptide in both brain and CC-CA of T.molitor. A coding sequence for this peptide is found in the genome of T. castaneum. In addition, three FXPRLamides (pyrokinins), provisionally Tenmo-PK-1, Tenmo-PK-2 and Tenmo-PK-3 (HVVNFTPRLamide, SPPFAPRLamide, HL(I)SPFSPRLamide) were identified in both CC-CA and brain of T. molitor, again on the basis of predicted occurrence or similarity in T. castaneum. The sequence of Tenmo-PK-2 is the same as the PK-2 of the cockroach, Periplaneta americana. Other peptides readily predicted from the genome of T. castaneum include two AKH/HrTH peptides (Trica-AKH-1; pELNFSTDWamide and Trica-AKH-2; pELNFTPNWamide), the second of which is identical to Pyrap-AKH, an AKH-related peptide (Trica AKH-L; pEVTFSRDWPamide), two CRF-related diuretic factors (Trica-DH 37 and Trica-DH 47), the latter identical to Tenmo-DH 47, a putative antidiuretic factor (Trica-ADFb; LYDDGSYKPHVYGF-OH), two sulfakinin-like peptides (Trica-SK-1; pETSDDY(SO(3))GHLRFamide, and Trica SK-2; GEEPFDDYGHMRFamide), a potential allatostatin-C (Trica-AS; pESRYRQCYFNPISCF-OH), six allatostatin-B/myoinhibitory peptides (Trica-AST-B-1,2,3,4,5 & 6; DWNKDLHIWamide, GWNNLHEGWamide, AWQSLQSGWamide, NWGQFHGGWamide, SKWDNFRGSWamide, EPAWSNLGIWamide), an allatotropin-like peptide (Trica-ATL; GIEALKYHNMDLGTARGYamide), four 'CAPA'-related peptides (Trica-CAPA-1,2,3,4; NKLASVYALTPSLRVamide, RIGKMVSFPRIamide, PGANSGGMWFGPRLamide, SENFTPWAYIILNGEAPIIREVHYSPRLamide), proctolin (RYLPT), a potential SIFamide (Trica-SIFa; TYRKPPFNGSIFamide), an arginine-vasopressin-related peptide (Trica-AVP; CLITNCPRGamide) and an ITP-related peptide (Trica-ITP). No evidence was found for the presence of 'A' allatostatins (Y/FxFGLamides) or corazonin, either in T. molitor, or in the genome of T. castaneum.
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PMID:Neuropeptides of the beetle, Tenebrio molitor identified using MALDI-TOF mass spectrometry and deduced sequences from the Tribolium castaneum genome. 1820 99


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