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

The interrelationships between vasopressin and the renin-angiotensin system are reviewed. Vasopressin can inhibit the release of renin by the kidney. This effect can occur at physiological plasma concentrations of vasopressin. Centrally administered angiotensin II can stimulate the release of vasopressin, a response that may be partially mediated by brain prostaglandins. The significance of this action of angiotensin II depends on whether there is an effective brain renin-angiotensin system and on whether peripherally generated or administered angiotensin can reach sites in the brain where it can act on vasopressin release. Peripherally administered angiotensin II can under certain, but not all, conditions stimulate vasopressin release. Peripheral angiotensin II can also potentiate the vasopressin response to an osmotic stimulus and to dehydration, but has little effect the release of vasopressin and renin, there is a failure to demonstrate any correlation between the two. Blockade of the renin-angiotensin system fails to modify the vasopressin response to a reduction in blood volume. In conclusion, the physiological significance of the interactions between the vasopressin and the renin-angiotensin system is not as yet clearly established.
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PMID:Interrelations between vasopressin and the renin-angiotensin system. 45 12

Vasopressin was infused intra-arterially or intravenously during 12 portal bypass operations. In comparison with a control group (without vasopressin), there was a very significant reduction in blood loss and portal pressure, and a moderate increase in arterial blood pressure.
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PMID:[The use of vasopressin during portal bypass (author's transl)]. 46 Nov 61

The effects of vasopressin administered by continuous infusion (0.75 and 0.5 mU/m2/minutes) was studied in two groups of three normal and two groups of 5 and 8 malnourished children given 0.5 and 0.3 mU/m2/minute. The following parameters were analyzed: urine volume, osmolality, water reabsorption, PAH, urea and inulin clearances, Na and K urinary excretion. Malnourished children had a urine volume 3 to 5 times higher than the normal groups. Vasopressin increased urine volume initially, but a mild antidiuretic effect followed in the normal groups. In malnourished children with a high CH2O, antidiuresis showed quite important figures with vasopressin. A transient fall in PAH and inulin clearances was observed with vasopressin in both malnourished groups with a mild drop in the normal group. Natriuresis with a higher % of the filtered sodium excretion was observed in the malnourished groups and in normal children with 0.5 mU of vasopressin. These results show that vasopressin had similar effects, but at a different level in the normal and malnourished children that we studied.
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PMID:[Renal function in normal and malnourished children given different doses of vasopressin in continuous infusion]. 46 71

1. Isolated rat neural lobes were incubated in vitro and electrically stimulated to release vasopressin. The released vasopressin was assayed using a radioimmunoassay and there was a reasonably good correlation (r = 0.81) between results obtained with this assay and those obtained by bioassay with the rat blood pressure method.2. Regular stimulation at frequencies of 5, 10 and 20 Hz released progressively more vasopressin and the release could be blocked by addition of tetrodotoxin to the incubation medium.3. Stimulation with pulse patterns derived from tape recordings of phasically firing units in the supraoptic nucleus of dehydrated rats released more vasopressin than the same number of pulses regularly spaced in time. In the range 2-8 pulses/sec vasopressin release was related to the pulse frequency within the bursts (r = 0.90) and the number of short (< 100 msec) interpulse intervals (r = 0.92). Vasopressin released per pulse increased over the frequency range 3-6 pulses/sec, but above 6 pulses/sec vasopressin release per pulse tended to diminish.4. We conclude that phasic firing of vasopressin neurosecretory cells may enhance vasopressin release in vivo and that an important factor in determining release is the number of short interspike intervals.
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PMID:Phasic firing enhances vasopressin release from the rat neurohypophysis. 46 85

The concentration of blood vasopressin was investigated in apparently healthy persons and in patients with I--II degree hypertension, aged from 20 to 80 years. Vasopressin concentration was determined by the biological method according to the antidiuretic effect of ethanol-anesthetized and constantly hydrated rats on an original 5-channel apparatus. The results obtained showed the blood vasopressin concentration to increase with age. In patients with the I--II degree hypertensive disease the mentioned concentration was significantly higher than in healthy persons of the same age. Close correlation coefficient was revealed between the blood vasopressin concentration and minimal arterial blood pressure values.
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PMID:[Blood vasopressin concentration is patients of different ages with hypertension]. 47 71

Individual hypothalamic nuclei were microdissected from brain tissue of ten human subjects who had died suddenly while in apparent good health. Appreciable amounts of vasopressin and oxytocin immunoreactivity were found by specific radioimmunoassay in six hypothalamic nuclei including supraoptic and paraventricular nuclei. Vasopressin and oxytocin are presumed to be synthesized in supraoptic and paraventricular nuclei for axonal transport to the posterior pituitary for storage and release. Vasopressin and oxytocin in other hypothalamic nuclei may be a part of this system of neurosecretion or may serve some other function.
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PMID:Immunoreactive vasopressin and oxytocin: concentration in individual human hypothalamic nuclei. 55 8

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.
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PMID:Characterization of the responses of oxytocin- and vasopressin-secreting neurones in the supraoptic nucleus to osmotic stimulation. 56 5

Intraventricular injection of arginine-8-vasopressin and its analogues vasotocin and lysine-8-vasopressin into rat brain evoked a special rotational behavior resembling somatostatin-induced barrel rotation [1]. Oxytocin and oxypressin were less active while vasopressin fragments had no effect. Vasopressin-induced barrel rotation was accompanied by pathological symptoms indicating a disturbance of muscle tone regulation and is considered to be a non-specific and toxic effect. This rotational behavior was not prevented by atropine, propranolol, phentolamine, methylsergide or haloperidol but was reduced by chlorpromazine, probably due to the latter's muscle relaxing activity.
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PMID:Barrel rotation induced by vasopressin and related peptides in rats. 56 83

The administration of 5 I. U. oxytocin (by quick infusion) or of 5 I. U. vasopressin-lysine (intramuscularly) to healthy subjects was followed by a significant decrease in the plasma non-esterified fatty acid level. We regard this as evidence of inhibition of basal lipolysis in the adipose tissue. Vasopressin also completely blocked an increase induced in the plasma non-esterified fatty acid level by activating hormone-sensitive lipase in the adipose tissue by the infusion of 0.5 mg noradrenaline.
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PMID:Inhibition of lipolysis by oxytocin and vasopressin. 61 48

Fetal growth in utero demands a continuous flow of water and solutes across the placental barrier. We investigated the membrane parameters that control the influx of solutes that are not actively transported and the influx of water. The osmotic conductivity, and the Na+ and Cl- permeabilities of the membrane were measured in chronically instrumented fetal sheep. Transplacental salt flow and water flow were augmented by drainage of fetal urine to the exterior over extended periods of time. Calculation showed that the membrane parameters are: deltaNaCl = 0.83, P.SNaCl = 8.0 10-3 ml.sec-1 kg-1, and LPS = 4.7 10-8 cm5.dyne-1.sec-1.kg-1 (placental surface area S being expressed per kg fetal weight). The chronic infusion of vasopressin into the fetuses at 8 to 11 units per day per kg fetal weight reduced the reflection coefficient deltaNaCl to a mean of 0.63 (P less than 0.03). We concluded that the characteristics of the influx of NaCl and water are compatible with those of a diffusion filtration process, that fetal growth is constrained by the diffusional permeability of the placenta for inert electrolyte and that in the long run fetal growth can only accelerate because placental electrolyte permeability increases. Vasopressin appears to reduce the salt reflection coefficient of the placenta thus enabling the fetus to exert some short term control over its acquisition of water and electrolyte.
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PMID:Fetal homeostasis in relation to placental water exchange. 61 9


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