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)

Open-circuit voltage (PD) and short-circuit current (SCC) across toad skin were studied in in vivo conditions. An improved technique for fastening a lucite chamber on the abdominal region of the animal was developed. Saline bridges (230 mM NaCl in 4% agar solution) were placed subcutaneously to make the connections between the extracellular fluid and the half-cells. A clear relationship was observed between the electrical parameters and sodium transport by the skin, since PD and SCC were related to the sodium concentration of the bathing solution, and abolished by the presence of amiloride--a specific sodium transport inhibitor in epithelia. The initial control values of SCC in vivo were higher than those in vitro, which was attributed to hormonal stimulation. However, these high initial control values of SCC in vivo fell with time, reaching steady levels after a 2 hr period. Vasopressin failed to increase SCC in vivo when the external sodium concentration was 115 mM, being effective only when the sodium concentration was low (5 mM). On the other hand, in isolated preparations vasopressin significantly promoted an increase in both PD and SCC.
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PMID:The in vivo electrical parameters of toad skin. 613 17

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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PMID:The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. 624 83

Patients subjected to proctocolectomy together with an ileal resection will lose increased amounts of sodium with the ileostomy excreta and may develop sodium and water depletion. Studies of sodium balance and measurements of renin activity, aldosterone, and arginine vasopressin in plasma were made in 23 such patients, 8 of them under metabolic-ward conditions while receiving various salt loads. Salt loss never resulted in subnormal sodium levels in serum. The earliest sign of salt depletion was a nearly total inhibition of renal sodium excretion, which could precede activation of the renin-aldosterone axis in these patients. Secretion of vasopressin remained unaffected by sodium-water depletion and by activation of the renin system. The routine monitoring of these patients should include measurements of renal sodium excretion. Measurement of renin and aldosterone levels should be used for evaluation of the severity of a sodium deficiency.
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PMID:Factors regulating sodium balance in proctocolectomized patients with various ileal resections. 637 72

Saltwater-adapted ducks with functioning supraorbital salt glands were chronically implanted with a device for perfusion of the third cerebral ventricle (icv perfusion) with artificial cerebrospinal fluid (CSF) of different tonicities. The osmoregulatory responses to icv stimulation were studied at conditions of salt and water loading in which only the salt glands, both salt glands and urinary fluid excretion, or only urinary fluid excretion were stimulated; in the latter experiments plasma antidiuretic hormone (ADH) was measured with a radioimmunoassay. Hypertonic icv stimulation enhanced salt gland secretion and caused antidiuresis, due to the increase of plasma ADH. Hypotonic icv stimulation inhibited salt gland activity and caused diuresis, due to the decrease of plasma ADH. Salt gland activity, urine formation, and plasma ADH reacted more sensitively to changes of icv tonicity in the hypertonic than in the hypotonic range. The effect of icv hypotonic stimulation could be obtained also with icv perfusion of isosmotic artificial CSF deficient in NaCl content. Perfusion with artificial CSF exceeding plasma tonicity by 50 mosmol X kg-1 or more caused inhibition of salt gland secretion associated with enhanced urinary output in several experiments.
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PMID:Salt gland and kidney responses to intracerebral osmotic stimulation in salt- and water-loaded ducks. 650 49

We have studied the possible role of the hypothalamic-pituitary system in the control of the release of plasminogen activator (PA) into peripheral blood of male rats. Plasminogen activator was measured by euglobulin lysis time. Desamino-D- arginine vasopressin (dDAVP) and adrenaline injected i.v. induced an increase in plasma PA as did electrical stimulation of the median eminence (ME), but dDAVP had no effect on plasma PA in hypophysectomized rats. The PA response to ME stimulation was similar in Brattleboro rats (deficient in vasopressin) and adrenalectomized Wistar rats compared with intact Wistar rats, but was abolished by section of the pituitary stalk and was negligible in hypophysectomized rats. The 41-residue corticotropin releasing factor (CRF) had no effect on PA release. Saline extracts of anterior pituitary gland from both normal Wistar and Brattleboro rats produced a dose-dependent increase in plasma PA when injected into normal Wistar rats. The activity of pituitary tissue was abolished by boiling, but not by di-isopropyl fluorophosphate which inactivates PA itself. Thus the anterior pituitary gland of the rat contains a heat-labile factor which stimulates the release of PA from peripheral stores into the circulation. This pituitary factor is released by a hypothalamic factor that is neither vasopressin nor CRF.
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PMID:A hypothalamic-pituitary system that stimulates the release of plasminogen activator in the rat. 653 43

Using radioimmunoassay (RIA), the content of gastrin-cholecystokinin family peptide immunoreactivity (G-CCK-IR), in the posterointermediate lobe (PIL) of the rat pituitary, has been determined in several experimental conditions. G-CCK-IR levels are significantly higher in males than in females. Salt loading induces a significant decrease of G-CCK-IR in animals of either sex. In males, G-CCK-IR levels are lower than controls 21 days after either castration or daily subcutaneous oestradiol injections. Using immunocytochemistry, G-CCK-IR disappears from the external median eminence 21 days after adrenalectomy. Our results show that, in addition to sex difference, factors affecting the vasopressin and/or oxytocin levels in the posterior pituitary and external median eminence also affect G-CCK-IR in the same regions. Cholecystokinin may therefore be of importance in functions related to these hormones.
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PMID:Cholecystokinin varies in the posterior pituitary and external median eminence of the rat according to factors affecting vasopressin and oxytocin. 685 57

1. Twenty-one normotensive subjects were studied to assess any possible benefits of moderate salt restriction and of high potassium intake in the prevention of hypertension in man. 2. The effects of salt reduction from 200 to 50 mmol/day and/or of an increase of potassium intake from 80 to 200 mmol/day over a 2 week period, on blood pressure, plasma noradrenaline, adrenaline, vasopressin, renin and aldosterone, were measured both at rest and after mental stress. The effects of graded infusion of noradrenaline on blood pressure and heart rate were also studied. 3. Salt restriction lessened the increase of blood pressure during noradrenaline infusion; the combination with high potassium intake also reduced the pressure rise after mental stress. There were no major changes in plasma levels of vasopressin and adrenaline. Plasma noradrenaline increased during the low sodium diet. 4. High potassium intake improved baroreceptor function as revealed by the greater decrease in heart rate for a given rise in pressure after noradrenaline infusion. 5. The results of this study are compatible with a protective effect of a practicable low sodium/high potassium diet on the development of human hypertension.
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PMID:Effect of moderate salt restriction and high potassium intake on pressor hormones, response to noradrenaline and baroreceptor function in man. 700 23

A humoral factor has been implicated in Dahl salt-sensitive genetically hypertensive rats. The goal of this study was to evaluate the pressor role of vasopressin (AVP) in Dahl rats. Salt-sensitive (S) and resistant (R) rats were fed either high (8%) or low (.04%) NaCl diets for 6 to 8 weeks. Blood pressure was elevated in S rats fed high salt diets (p less than 0.05). Plasma AVP increased with high salt diet in both groups (p less than 0.05), but was higher in S than R rats (2.0 +/- 0.3 and 1.3 +/- 0.2 microU/ml respectively, mean +/- SE, p less than 0.05). With low salt diet, plasma AVP did not differ significantly in S and R rats (1.0 +/- 0.2 and 0.7 +/- 0.2 microU/ml respectively). Pressor responses to intravenous injection of AVP were greater in S than R rats (p less than 0.05), but this difference was also observed with pressor responses to norepinephrine (S greater than R, p less than 0.05); there was no difference in pressor responses to AVP in S rats fed high vs low salt diet. Injection of 50 micrograms of d(CH2)5 VDAVP, which selectively inhibits vasoconstrictor effects of AVP, failed to lower blood pressure in S and R rats fed high or low salt diets despite the fact that this dose decreased pressor responses to 8 microU of AVP more than 90%. Although plasma AVP and vasopressor responses to AVP and NE are slightly elevated in S rats fed high salt, results with d(CH2)5 VDAVP suggest that vasoconstrictor effects of AVP do not play an important role in the maintenance of hypertension in Dahl S rats.
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PMID:Does vasopressin contribute to salt-induced hypertension in the Dahl strain? 721 72

Salt-loading induces profound metabolic changes in magnocellular vasopressin (AVP)-containing neurons, including changes in levels of coexisting peptides and tyrosine hydroxylase (TH). Although many studies have been conducted on salt-loading, little information is available on the recovery processes following its cessation. In the present study, we investigated the changes in AVP, galanin (Gal), dynorphin B (Dyn-B), and TH immunoreactivities in the rat supraoptic nucleus (SON) and paraventricular nucleus (PVN) by immunocytochemistry using specific antisera against these substances. Salt-loading was induced in rats by dissolving 2% NaCl in their drinking water for 7 days. These animals were then allowed free access to fresh water for 2, 4, or 7 days prior to sacrifice. In the SON at the 7th day of salt-loading, AVP, Gal and Dyn-B immunoreactivities decreased in contrast to the marked increase in TH-immunoreactivity compared to those of control rats with free access to water. After a recovery period with free access to water, AVP and Gal immunoreactivities increased with time and returned to the control level at the 7th day. However, Dyn-B immunoreactivity did not recover even at the 7th day. Dehydration-induced TH-immunoreactive neurons almost disappeared at the 7th day. Immunoreactivities for these substances in the PVN showed a similar time course as that in the SON. These findings suggest that AVP and substances coexisting with it change with different time courses in magnocellular neurons following cessation of salt-loading.
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PMID:Rehydration process from salt-loading: recovery of vasopressin and its coexisting galanin, dynorphin and tyrosine hydroxylase immunoreactivities in the supraoptic and paraventricular nuclei. 753 8

1. We have previously described a progressive antidiuresis in response to low-dose vasopressin infusion during salt restriction in man, despite stable or even declining plasma vasopressin concentration. In the present study we examine the hypothesis that renal sensitivity to the antidiuretic effect of arginine vasopressin may be enhanced by salt restriction. 2. Extremely low-dose infusions of arginine vasopressin were given to normal subjects after equilibration to high (260 mmol/day) and low (20 mmol/day) sodium intakes. 3. Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min-1 kg-1 arginine vasopressin increased urine osmolality from 67.8 +/- 2.6 to 196.3 +/- 35.7 mosmol/l in the high-salt study and from 268.3 +/- 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Glomerular filtration rate, estimated from inulin clearance, was unchanged during arginine vasopressin infusion irrespective of salt intake (high salt 116.5 +/- 9.4 to 118.9 +/- 6.4 ml/min; low salt, 135.1 +/- 9.2 to 111.2 +/- 12.4 ml/min). Renal plasma flow, estimated from para-aminohippurate clearance, fell further during infusion of 2 fmol min-1 kg-1 arginine vasopressin in the low-salt study than in the high-salt study (low salt, from 555.7 +/- 22.7 to 298.3 +/- 27.6 ml/min; high salt, from 544.5 +/- 30.2 to 452.9 +/- 28.9 ml/min; P < 0.05 between sodium intakes).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary salt restriction on renal sensitivity to vasopressin in man. 767 66


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