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)

1. Extracellular action potentials were recorded from forty antidromically identified single units in the supraoptic nucleus of lactating, urethane-anaesthetized female rats. The activity was monitored both during reflex milk ejection and during an increase of 10-15 m-osmole/kg in plasma osmotic pressure induced by intraperitoneal injection of 1 ml. of 1.5 M-NaCl solution.2. About half (eighteen) the cells showed a burst of activity before reflex milk ejection and were dubbed oxytocin cells. Oxytocin cells responded to a hypertonic injection with a smooth sustained threefold increase in firing rate.3. The remainder (twenty-two) showed no burst of activity before reflex milk ejection and were dubbed vasopressin cells. Vasopressin cells doubled their firing rate as plasma osmotic pressure increased. Neither cell type increased its firing rate after injections of isotonic NaCl.4. A phasic firing pattern was rarely seen in slow firing vasopressin cells (< 2 spikes/sec) but was seen in almost all vasopressin cells (twelve out of fourteen) firing between 3 and 8 spikes/sec. Above 8 spikes/sec, some vasopressin cells fired continuously. Phasic firing was only once encountered in an oxytocin cell.5. The firing rate of both oxytocin and vasopressin cells decreased when plasma osmotic pressure was reduced 10-15 m-osmole/kg by an intragastric water load of 10 ml.6. Hypothalamic cells lying just outside the supraoptic nucleus did not show a consistent response to injection of hypertonic NaCl.7. Clearly, both oxytocin and vasopressin cells are osmoresponsive, but phasic firing is characteristic of stimulated vasopressin cells. Thus, osmotic activation allows discrimination between oxytocin- and vasopressin-secreting neurones.
J Physiol 1977 Sep
PMID:Characterization of the responses of oxytocin- and vasopressin-secreting neurones in the supraoptic nucleus to osmotic stimulation. 56 5

Platelets lose their ability to aggregate when deprived of divalent cations. This usually was studied by incubating human citrated platelet-rich plasma with EDTA or EGTA and then adding enough CaCl2 to combine with the chelating agent. Incubation for 5-7 min at 37 degrees C caused irreversible loss of the platelets' ability to adhere to glass and to aggregate with ADP, epinephrine, A23187, vasopressin, or serotonin or upon rewarming after chilling and markedly reduced aggregation with collagen or thrombin. Control samples incubated with saline, CaEDTA, or CaEGTA were not inhibited. Untreated platelets washed and incubated in solutions treated with resins that remove divalent cations lost their ability to aggregate in 30 min. More than about 0.26 mM Mg2+ partially protected the platelets. Unlike aggregation, ADP-induced shape change, clot retraction caused by thrombin or ADP plus reptilase, and thrombin-induced 14C-serotonin release were not inhibited after incubation. Aggregability was not restored by prolonged incubation with CaCl2, adding normal plasma, or washing the platelets. Its loss was temperature and pH dependent, occurring in 2 min at 43 degrees C but not in 7 min at 30 degrees C, and at pH 7.8 but much less at pH 7.2. The defect was not associated with an increase in platelet cyclic AMP, a decrease in metabolic ATP, or the presence of free ADP.
Blood 1978 Sep
PMID:Nonreversible loss of platelet aggregability induced by calcium deprivation. 67 68

Modification of the natural vasopressin molecule to form desmopressin acetate (DDAVP) resulted in a compound with prolonged antidiuretic activity and virtual elimination of vasopressor activity. Twenty-one patients with central diabetes insipidus who ranged in age from 3 to 68 years were treated with DDAVP, which was administered intranasally in a dosage ranging from 10 microgram every 12 hours to 20 microgram every eight hours. Effective control of symptoms was obtained in all cases. There were no consequential toxic effects. As previously reported, DDAVP appears to be the preferred drug for the management of central diabetes insipidus. Biochemical alteration of hormones may enhance desired therapeutic activity and eliminate toxic effects. The development of DDAVP is an example of the potential for development of useful therapeutic peptides.
Arch Intern Med 1978 Sep
PMID:Treatment of central diabetes insipidus in adults and children with desmopressin. 68 29

Studies demonstrating the antagonism by prostaglandins (PGs) of antidiuretic hormone (ADH) action led to the proposal that renal medullary PGs may act to attenuate the physiologic effects of ADH via a negative-feedback loop. Therefore, we examined urinary PG excretion, an indicator of renal PG synthesis, in rats with hereditary diabetes insipidus (DI) utilizing gas chromatography-mass spectrometry. The DI rats, devoid of ADH, excrete much less prostaglandin E2 (PGE2) than normal Long-Evans rats (39 +/- 5 vs. 228 +/- 53 ng/24 h, means +/- SE, P less than 0.005). DI and normal rats were treated for 35 days with ADH while separate groups of DI and normal controls received vehicle only. The ADH treatment increased urinary PGE2 excretion in DI rats to 233 +/- 35 ng/24 h whereas PGE2 excretion was unaffected by vehicle treatment. ADH treatment in normal rats similarly increased PGE2 excretion from 215 +/- 49 to 410 +/- 63 ng/24 h (P less than 0.05). To determine whether the rise in PGE2 excretion is the result of the rise in papillary osmolality, we subjected DI rats to dehydration, which increased urine osmolality from 130 +/- 10 to 302 +/- 12 mosmol/kg H2O but left urinary PGE2 unaffected. We conclude that ADH stimulates renal medullary PGE2 synthesis in vivo.
Am J Physiol 1978 Sep
PMID:Antidiuretic hormone increases renal prostaglandin synthesis in vivo. 69 28

Vasopressin and oxytocin pathways were specifically localized in glutaraldehyde-paraformaldehyde fixed rat brains, with the use of the unlabelled antibody enzyme method and purification of the first antiserum. Vasopressin and oxytocin containing pathways were traced from the paraventricular nucleus towards the dorsal and ventral hippocampus, the nuclei of the amygdala, substantia nigra and substantia grisea, nucleus tractus solitarius, nucleus ambiguus and to the substantia gelatinosa of the spinal cord. In addition, a vasopressin containing pathway between the suprachiasmatic nucleus and the lateral habenular nucleus was demonstrated. The possible nature (axons or dendrites) and role of these extrahypothalamic fibres is discussed in relation to water balance, milk ejection and avoidance behaviour.
Cell Tissue Res 1978 Sep 26
PMID:Intra- and extrahypothalamic vasopressin and oxytocin pathways in the rat. Pathways to the limbic system, medulla oblongata and spinal cord. 69 26

This work proposes the use of (a) a commercially available homologous system AVP antibody-AVP (Arginine Vasopressin) standard and (b) new acquisitions for the improvement of sensitivity for AVP radioimmunoassay by separate or simultaneous use of two-phase sequential incubation and epsilon-aminocaproic acid (EACA). The antiserum used in the system described is very specific since none even cross-reacted with lysine vasopressin (LVP) and has an apparent affinity constant (K) of 0.909 +/- 0.047 X 10(12) l/mol. This is sufficiently high to detect 0.5 +/- 0.2 pg/tube, which is theoretically expected of biological AVP. The total assay time is less than 48 h.
Clin Chim Acta 1978 Sep 01
PMID:A practical proposal for arginine-vasopressin radioimmunoassay. 69 31

Two patients with hypodipsia and hypernatremia are described. The first patient, whose hypodipsia was of unknown cause, developed hypernatremia unless large volumes of fluid were urged upon him; upon treatment with chlorpropamide normal serum sodium levels were achieved with spontaneous fluid intake. The second patient had hypodipsia and diabetes insipidus resulting from a craniopharyngioma. Treatment with vasopressin and a prescribed daily water intake resulted in frequent hyper- and hyponatremia, but treatment with chlorpropramide yielded serum sodium values which were more often normal and less variable. In neither patient could the improved water regulation be attributed to an effect of chlorpropamide on renal water excretion. Possible mechanisms for the effect of chlorpropamide on thirst are discussed.
Clin Nephrol 1978 Sep
PMID:Successful treatment of hypernatremic thirst deficiency with chlorpropamide. 69 8

Cholera toxin, stereotaxically injected into the medial septal nucleus of the rat, leads within 24 h to a dramatic decrease in body weight and an increase in septal adenylate cyclase activity. Toxin-treated rats drink one-third the water of vehicle-treated animals while excreting two-and-one half times the urine. Food intake over the 24-h period is depressed to 13% of control but feces production was normal. The dramatic increase of urinary output suggests that cholera toxin activates a septal adenylate cyclase system which supressess the release of antidiuretic hormone. Cholera toxin injection into the septum may be a unique alternative to electrical stimulation for investigating septal involvement in the regulation of neuronal and metabolic processes.
Eur J Pharmacol 1978 Sep 15
PMID:Increased adenylate cyclase activity and rapid weight loss following intraseptal injection of cholera toxin. 69 80

In order to test the integrity of central receptors, spontaneously hypertensive rats (SHR) of the Okamoto strain and weight-matched control rats of the Wistar Kyoto (WKY) strain were given intracerebroventricular (i.vt.) injections of carbachol and norepinephrine. The rats, in an unanesthetized, unrestrained state, were tested for drinking, antidiuretic and pressor responses. Antidiuretic hormone release was determined by using water loaded, diuresing rats as their own antidiuretic hormone bioassay. Blood pressure was measured directly from a femoral artery catheter. Drinking responses to i.vt. carbachol and antidiuretic responses to i.vt. carbachol and norepinephrine infusions were not different between SHR and WKY while pressor responses were potentiated in SHR. The potentiated pressor responses to central carbachol and norepinephrine injections were the result of increased vascular responsiveness to the antidiuretic hormone released by these drugs. A second, neurally mediated, factor was also apparent to i.vt. carbachol injections. This additional factor could be increased sympathetic outflow to central drug stimulation, increased vascular reactivity to sympathetic outflow, decreased baroreflex responses or a combination of the above.
J Pharmacol Exp Ther 1978 Sep
PMID:Central cholinergic and noradrenergic stimulation in spontaneously hypertensive rats. 70 27

Regional blood flow responses to 1-deamino-6-carba-(8-arginine)-vasopressin (dCAVP) were investigated in pregnant guinea pigs by the radioactive microsphere technique. Intravenous injection of 0.1 microgram/kg body weight caused a moderate rise in mean arterial blood pressure from 6.8 to 7.9 kPa, a significant reduction in tissue perfusion of the stomach, mammary gland, urinary bladder and vagina, and a significant increase in renal and cerebral blood flow. In a small number of animals given 1.0 microgram/kg of dCAVP, which evoked a strong pressor response, it was also possible to demonstrate a reduction in cutaneous and pancreatic blood flow and an augmentation of adrenal blood flow. Uterine and maternal placental blood flow did not alter significantly following administration of this vasopressin analogue.
Acta Pharmacol Toxicol (Copenh) 1978 Sep
PMID:Actions of a new vasopressin analogue (1-deamino-6-carba-[8-arginine]-vasopressin) on regional blood flow in pregnant guinea pigs. 70 32


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