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

Aspects of the relationships between cellular composition and transepithelial sodium transport across toad urinary bladder are reviewed. Changes in cellular sodium produced by amiloride, vasopressin, aldosterone, hypoxia, ouabain, and sodium-free media are consistent with a cellular sodium transport pool. Metabolic studies suggest that this pool gains its sodium from the mucosal medium and that there is little recycling of sodium between cell and serosal medium. One-third of the cellular potassium equilibrates readily with serosal potassium. The rate of exchange of potassium is much less than the rate of sodium transport supporting the contention that sodium transport in this tissue is electrogenic. Studies with 36Cl suggest that chloride does not cross the apical cellular membranes, but exchanges with serosal chloride. Possible relationships between transepithelial sodium transport and cellular volume regulation are discussed.
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PMID:Epithelial cell electrolytes in relation to transepithelial sodium transport across toad urinary bladder. 73 78

Changes in the excretion of water and electrolyte in one kidney after exclusion of its partner have been studied in anesthetized dogs and rabbits. Complete clamping of the contralateral kidney pedicle or ureter results in a rapid increase in the excretion of water, sodium, potassium, chloride, calcium, phosphate and bicarbonate. This response is also observed in denervated kidneys. Pretreatment with the loop inhibitor, furosemide, does not preclude adaptation which, however, is blunted by acetazolamide, an inhibitor of proximal sodium and bicarbonate reabsorption. Free-water reabsorption during hypertonic saline diuresis is normal in the remaining kidney. Compensatory adaptation, thus, appears to be located in the proximal tubule. The regulatory response to contralateral kidney exclusion is already fully developed in one-month-old rabbits. Compensatory adaptation of electrolyte excretion is not accounted for by changes in extracellular fluid volume, plasma composition, glomerular filtration rate, effective renal plasma flow, aldosterone or vasopressin.
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PMID:Studies on compensatory adaptation of renal functions. 73 47

1. We have investigated the water transport and short-circuit current (s.c.c.) response to vasopressin (1 mu./ml. and 100 mu./ml.) in isolated toad urinary bladders (Bufo marinus) following overnight incubation in the presence or absence of steroid-containing Ringer solution. 2. The water transport response to the lower dose of vasopressin (1 mu./ml.) was considerably reduced in 'steroid depleted' conditions, wheras the response to the higher dose of vasopressin (100 mu./ml.) was not similarly affected. 3. Aldosterone 3. Aldosterone 3. Aldosterone (10(-7)M) potentiated the water transport response to the lower dose of vasopressin (1 mu./ml.) but had no effect on the response to the higher dose (100 mu./ml.). 4. There was no effect of 'steroid depletion' or aldosterone treatment on the vasopressin s.c.c. response when measured as a percentage increase above basal levels. 5. In 'steroid depleted' conditions vasopressin (1 mu./ml.) maximally stimulated Na+ transport (s.c.c.) but a higher dose of vasopressin (100 mu./ml.) was required for maximum water transport. 6. We have failed to obtain any potentiation effect of corticosterone (10(-7)M) on the water transport or s.c.c. response to vasopressin (1 mu./ml.).
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PMID:Effect of steroid depletion on the response of toad bladder to vasopressin. 81 May 80

Two cell-types of toad bladder epithelium show uncommon plasma membrane organization in freeze-fractured specimens. One type, the granular cell, contains a plasma membrane in which the A-face is poorly particulate luminally while the B-face discloses multiple large particles at this site. In contrast, the lateral and basal portions of the granular-cell membrane are typical in that more particles occupy the A-face than the B-face. In the other cell-type, which is mitochondria-rich, the plasma membrane, luminally, laterally, and basally, contains rod-shaped and a few globular particles in the A-face. We suggest that these two peculiar membrane organizations be considered in the localization of both vasopressin and aldosterone action in toad bladder.
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PMID:Patterns of membrane organization in toad bladder epithelium: a freeze-fracture study. 81 28

Investigations effected in 16 subjects of 20-69 years at bed rest after bone fractures demonstrated, in an interval of 10-27 days after surgery, normal plasma sodium concentration and a decreased urinary elimination, an increased plasma potassium concentration but a decreased urinary output. The osmotic changes were not significant. The plasma vasopressin activity was increased. Three urinary aldosterone determinations showed an increased output. The serum calcium level was within normal limits but its urinary output was initially slightly decreased, contrary to its augmented elimination after simple voluntary bed rest, as results from literature. The hydroxyproline elimination was increased, demonstrating an active collagen metabolism.
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PMID:Hydroelectrolytic changes caused by prolonged clinical recumbency. 81 41

Two days after a severe haemorrhage plasma calcium concentrations and bone marrow mitotic activity in rats were significantly increased and so remained for a further 5-6 days until the haematocrit had returned to normal. The first 48 h after bleeding were characterized by hypocalcaemia. During this phase two significant peaks in mitotic activity were observed at 4 and 18 h after haemorrhage. The mitotic surge 4 h after bleeding was still present in adrenalectomized and parathyroidectomized animals but in rats which were either hypophysectomized or had congenital diabetes insipidus this mitotic response was absent. Vasopressin was shown to stimulate bone marrow mitotic activity both in vivo and in vitro whereas angiotensin, aldosterone and erythropoietin had no rapid, direct mitogenic action on these cells. This novel hypophysial-bone marrow system suggests that vasopressin may assist in post-haemorrhagic recovery in blood cell numbers in the circulation.
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PMID:Role of vasopressin in the mitotic response of rat bone marrow cells to haemorrhage. 83 40

The brain has evolved a number of mechanisms to maintain body fluid balance. They include the sensation of thirst, which stimulates water intake, the secretion of vasopressin, which helps prevent water loss, and the secretion of aldosterone, which helps prevent sodium depletion. In the research described here, all three mechanisms are shown to be mediated by the actions of angiotensin on the brain.
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PMID:CNS regulation of salt and water intake. 83 97

In these experiments, two groups of animals were studies to evaluate the effect of altering renal tubular sodium-handling on the excretion of acute HCl load. In group, I, normal salt animals hypotonically expanded with antidiuretic hormone (ADH) (using a protocol known to stimulate aldosterone) presented large amounts of sodium to the distal tubule and excreted an acute HCl load much more efficiently than did animals pretreated with either a normal (NL) or low (LO) salt diet alone. In group II, 24 hr after acid-loading, the plasma bicarbonate concentrations were significantly lower in animals pretreated with sodium restriction plus furosemide (F) than in those maintained on a normal (NL) or high (HI) salt diet alone. Acid excretion was maximized (ADH) when distal sodium avidity was stimulated in the presence of adequate distal sodium delivery and minimized (F) when distal sodium delivery was limited (despite possible augmentation of distal sodium avidity). Alterations in urinary sodium excretion alone (LO, NL, HI) did not affect the rate of acid excretion. These data are compatible with the hypothesis that the excretion of an acute HCl load is mediated by existing levels of distal sodium delivery and distal sodium avidity.
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PMID:Evidence that alterations in distal sodium delivery and distal sodium avidity affect the rate of excretion of an acute HCl load. 84 69

1. A lithium chloride (1.1 g/kg) supplemented diet was given to Long Evans (LE) and Brattleboro (DI) rats to investigate its actions in the presence (LE) and absence (DI) of vasopressin. 2. During the first 24 h, Li-supplemented LE rats displayed an initial water deficit (drinking less than renal output), increased plasma antidiuretic (ADH) titres and slightly increased plasma renin activities (PRA) and plasma osmolarities. Such changes were qualitatively similar to those seen in rats fed a normal diet, but deprived of water for 24 hours. After 12 days, the Li-supplemented rats had elevated plasma ADH titres, but reduced pituitary oxytocic and antidiuretic activities. 3. The urinary losses of Na, K and Cl exceeded dietary intakes in LE rats on the introduction of the Li-supplement, and the urinary osmolarity fell by 50%. Electrolyte balances were gradually re-established, although drinking and urine production increased in parallel to reach twice the control values by day 12 of the supplement. 4. Aldosterone and corticosterone secretory rates and their peripheral plasma concentrations were unchanged both after 24 h and 28 days of the Li-supplement. 5. Li elicited no water deficit or saluresis in DI rats, and although the polyuria and polydipsia were exacerbated, urinary osmolarity did not change over the 12 day observation period. 6. Li increased Ca excretion in both rat types; after 12 days the PRA of DI but not LE animals were increased. 7. It is concluded that the overall renal actions of Li are tempered by vasopressin rather than adrenocorticosteroids.
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PMID:Time course of lithium-induced alterations in renal and endocrine function in normal and Brattleboro rats with hypothalamic diabetes insipidus. 85 9

Prolactin is an important osmoregulatory hormone in several lower vertebrate species. The present study was undertaken to clarify the effects of prolactin, if any, on human renal function. Eight normal adult male subjects on a 150 mEq sodium (Na), 60 mEq potassium (K) diet for 5 days were studied during 12 h of oral water (H2O) loading on 2 consecutive days. On day 1, after a 6 h control period, a 1 ml normal saline placebo was given im; on day 2, 25 mg of ovine prolactin (OP) was substituted. The subjects were supine and received a constant infusion of Na and K. After OP, serum prolactin rose from 6.9+/-0.8 ng/ml to 15.0+/-2.5 ng/ml (P less than .01) at 1 h, 27.6+/-4.0 ng/ml (P less than .002) at 2 h, 33.1+/-4.3 ng/ml (P less than .001) at 3 h and remained elevated for the remaining 3 h of study. The ovine prolactin had 20-25% of the potency of human prolactin in the human prolactin radioimmunoassay system. In response to OP, free H2O clearance (CH2O) promptly decreased from 10.1 +/- .06 ml/min to 6.1 +/- .05 ml/min (P less than 0.1) at 1 h, to a nadir of 5.1+/-.3 ml/min (P less than .001) at 2 h, and returned to control levels by 4 h. CH2O was unchanged after placebo, and urinary Na and K excretion, creatinine and osmolar clearance (COSM), plasma Na, K, osmolality and aldosterone were unchanged after OP or placebo. Control plasma vasopressin was 1.0+/-0.1 micronU/ml and was not changed after prolactin (1.1+/-0.1 micronU/ml at 1 h, 1.1+/-0.1 micronU/ml at 2 h and 1.1+/-0.1 micronU/ml at 3 h). The ovine prolactin contained 2 micronU of immunoassayable vasopressin per microng of powder. Aqueous vasopressin, 50 mU (containing in 25 mg of ovine prolactin), produced a decrease in CH2O not significantly different from prolactin in 6 water loaded subjects. Four different subjects given 100 mg of OP had decreased CH2O from 8.3+/-0.3 to 2.7+/-0.7 ml/min at 1 h (P less than .001) and to 2.8+/-0.7 ml/min at 2 h (P less than .01). Control plasma osmolality was 301+/-4 mOsm/1 and decreased to a maximum of 288+/-5 mOsm/1 4 h after OP (P less than .001). After prolactin administration, plasma vasopressin rose from 0.44+/-0.15 to 0.80+/-0.41 micronU/ml (P =NS) at 1 h. The transient antidiuresis in response to ovine prolactin is due to contamination of the preparation with vasopressin. Prolactin does not acutely influence renal electrolyte excretion and probably does not influence water excretion in man.
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PMID:The effects of ovine prolactin on water and electrolyte excretion in man are attributable to vasopressin contamination. 87 May 13


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