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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck causes a profound natriuresis and a suppression of the renin-aldosterone system, it was of interest to assess whether the diuresis induced by immersion was mediated by an analogous inhibition of ADH. The effects of water immersion on renal water handling and urinary ADH excretion were assessed in 10 normal male subjects studied following 14 h of overnight dehydration on two occasions, control and immersion. The conditions of seated posture and time of day were identical. During control ADH persisted at or above prestudy values. Immersion resulted in a progressive decrease in ADH excretion from 80.1 plus or minus 7 (SEM) to 37.3 plus or minus 6.3 muU/min (P smaller than 0.025). Cessation of immersion was associated with a marked increase in ADH from 37.3 +/- 6.3 muU/min to 176.6 +/- 72.6 muU/min during the recovery hour (P smaller than 0.05). Concomitant with these changes urine osmolality decreased significantly beginning as early as the initial hour of immersion from 1044 +/- 36 to 542 +/- 66 mosmol/kg H2O during the final hour of immersion (P smaller than 0.001). Recovery was associated with a significant mean increase in Uosm of 190 +/- 40 mosmol/kg H2O over the final hour of immersion (P smaller than 0.001). The suppression of ADH occurred without concomitant changes in plasma tonicity. These studies are consistent with the suggestion that in hydrated subjects undergoing immersion suppression of ADH release contributes to the enhanced free water clearance, which has been previously documented.
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PMID:Suppression of ADH during water immersion in normal man. 114 Nov 16

Isolated frog urinary bladder epithelial cells, upon dissociation lose their polarity and develop microridges and occasional microvilli in a global fashion. These cells, when exposed only to isotonic Ringer's solution manifest a membrane conformation with smooth discontinuous microridges, a cytoplasm with numerous free ribosomes, rough ER, thin Golgi cisternae, mitochondria, small vacuoles, electron-dense granules, few microtubules, and numerous microfilaments and intermediate filaments with an apparent random distribution, the dissociated cells, when treated with ADH or calcium ionophore (A23187), have the appearance of numerous elongated microvilli over the entire cell surface. The cytoplasm, under these conditions, is occupied by large vacuoles with a distribution of long profiles of aggrephores and associated vesicles. The peripheral cytoplasm as well as the cavities of the elongated microvilli of these cells contain large concentrations of microfilaments often showing a strong axial orientation to the long axis of the microvilli. Many of these filamentous elements appear in contact with the apical membrane of these microvilli with an alignment with the external glycocalyx. There is an indication that these morphocytological changes as revealed by SEM and TEM studies, correlated with a redistribution and realignment of microfilaments and possibly microtubules as detected by fluorescent microscopy using immunofluorescent antibody labeling for actin and tubulin. Cells treated with verapamil, a calcium antagonist, presented dwarf and stout microvilli with little detectable alterations in the cytoplasmic compositions from that of non-hormonal treated cells. Verapamil prevented ADH induction of microvilli, with the membrane, under these conditions, appearing as compact microridges. The results indicate that calcium ionophore, like ADH, produces intense formation of microvilli in dissociated cells, mobilization and realignment of microfilaments, microtubules, increase in the density of vesicles, aggrephores and possibly secretory granules, whereas the calcium antagonist, verapamil, opposes these actions. The results suggests a prominent role of calcium in the morphological changes induced by ADH.
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PMID:Morphometric analysis of epithelial cells of frog urinary bladder, II. Effect of ADH, calcium ionophore (A23187) and verapamil on isolated dissociated cells. 313 21

The effect of arginine vasopressin (ADH) on water permeability and transepithelial voltage was examined in cortical collecting tubules from a specific pathogen-free line of male Sprague-Dawley rats (75-125 g body weight). Tubules were bathed in a medium resembling serum ultrafiltrate (310 mOsm/kg H2O) at 38 degrees C. Osmotic water permeability (Pf, micron/sec) was determined by the volume flow occurring with a hypo-osmotic perfusate (210-220 mOsm/kg H2O) and diffusional water permeability (Pd, micron/sec) was calculated from the lumen-to-bath flux of tritiated water using an isosmotic perfusate. In the absence of ADH, both Pf and Pd were low, 17 +/- 6 and 9.0 +/- 0.6 (SEM), respectively. ADH added to the bath at concentrations above 0.5 microunits/ml increased Pf, with a maximal response at 40 microunits/ml or greater. With 100 microunits/ml ADH, Pf and Pd were, respectively, 994 +/- 117 and 37.0 +/- 2.4. Without ADH, the transepithelial voltage was variable (range, -5.4 to +2.5 mV; mean, -1.9 +/- 0.4); however, with 100 microU/ml ADH, it hyperpolarized (lumen-negative) by 4.2 +/- 0.8 mV. In contrast to findings in the rabbit, both the hyperpolarization and the increased water permeability persisted for at least 3 hr. The higher water permeabilities are consistent with the shorter length of the cortical collecting tubule in the rat, and may reflect the importance of attaining osmotic equilibration within the cortex during maximal antidiuresis.
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PMID:Sustained response to vasopressin in isolated rat cortical collecting tubule. 609 38

The effect of antidiuretic hormone on urinary electrolyte excretion was investigated by clearance techniques in conscious rats in metabolic cages. Brattleboro rats with hereditary diabetes insipidus (DI) (no ADH) were studied in the absence of exogenous ADH (control group = C, n = 4), and after several weeks of continuous dDAVP infusion (period A) followed by discontinuation of dDAVP (period B) (experimental group = E, n = 6). dDAVP, a non-pressor antidiuretic analogue to ADH, induced 1) a high urine concentration (2,645 +/- 44 (SEM) in group E vs 131 +/- 6 mosmol/kg H2O in group C), P less than 0.001; 2) no significant change in plasma osmolality (288 +/- 2 vs 297 +/- mosmol/kg H2O respectively) and in plasma concentration of major electrolytes, Na, K, Cl, Mg, and Ca; 3) a large decrease in urinary excretion of calcium and magnesium and no change in other electrolyte or total osmolar excretion. Fractional excretions in rats of groups C and E during period A were, respectively, for Na: 0.59 +/- 0.03 (SEM) and 0.51 +/- 0.33% (NS), for Ca: 2.92 +/- 0.62 and 0.34 +/- 0.05% (P less than 0.001) and for Mg: 7.75 +/- 0.83 and 1.38 +/- 0.28% (P less than 0.001). After treatment discontinuation, plasma osmolality in group E rose to 304 +/- 2 mosmol/kg H2O (P less than 0.01 compared to period A) with slight increases in plasma Na and Cl concentrations. Urine osmolality fell below, and urine flow rate rose above values observed in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of tubular reabsorption of magnesium and calcium by antidiuretic hormone in conscious rats. Study in Brattleboro rats with hereditary hypothalamic diabetes insipidus. 652 52

The effect of prostaglandin on diffusional water permeability has been studied in collecting ducts in an isolated rat papilla. PGE2 increased water permeability. The effect was significant at a concentration of 10(-8) mol 1(-1) and was maximal with a concentration of 10(-6) mol 1(-1). The maximal increment of 0.94 +/- 0.10 (SEM) micron s-1 was approximately half that produced by maximal stimulation with antidiuretic hormone (2.18 +/- 0.12 micron s-1). A concentration of 10(-8) mol 1(-1) produced an increase in basal water permeability and 24 mu unit ml-1 ADH, which without PGE2 present gave a similar increase, had no incremental effect. ADH 100 mu unit ml-1 increased permeability to a value similar to that observed in the absence of PGE2. Thus PGE2 and ADH both increase water permeability but the increments are not additive. Indomethacin in a concentration that inhibited prostaglandin production altered the response of the collecting duct to ADH. The dose response curve was shifted to the left and the maximal increase in water permeability and the lowest dose at which a response occurred took place at concentrations less than 1/2 those required in its absence. Prostaglandins influence the action of ADH and it is likely that in life they regulate and modulate the change in water permeability induced by anti-diuretic hormone.
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PMID:The effect of prostaglandin E2 and ADH on diffusional water permeability in collecting duct of an isolated rat papilla. 694 74

Spreading and flattening of glomerular podocyte cell bodies and major processes and an apparent lack of foot processes were observed by scanning electron microscopy in a reversible pedicle-clamping model of acute renal failure in ADH-treated rabbits and in biopsy specimens taken 1 hour after transplantation from patients who later showed clinical signs of "acute tubular necrosis." Glomerular changes were quantified by morphometry in A) normal rabbit kidneys, B) rabbit kidneys obtained 2 hours after 1 hour of left pedicle clamping and right nephrectomy, C) kidneys similar to Group B except that the animals were treated with an agent that reliably lessens the eventual severity of renal failure (clonidine, 30 microgram/kg given intravenously 1/2 hour before unclamping), D) 1-hour-posttransplantation biopsy specimens from human kidneys that functioned well after transplantation (recipient serum creatinine less than 2.5 mg/dl on Day 3), and E) 1-hour-posttransplant biopsy specimens from kidneys that later manifested posttransplantation ischemic acute renal failure (recipient serum creatinine greater than or equal to 2.5 mg/dl on Day 3). The fraction of glomerular capillary surface covered only by podocyte processes smaller than 1 mu (and not by cell bodies and wider processes) was .65 +/- .02 (SEM) in A; .48 +/- .03 in B; .64 +/-.03 in C; .57 +/- .01 in D; and .38 +/- .04 in E (A vs B, P less than .01; B vs C, P less than .02; D vs E, P less than .01). In Groups D and E there was a significant negative correlation between the fraction of glomerular capillary surface covered only by podocyte processes less than 1 mu in width and serum creatinine on the third posttransplantation day (r = --.86, P less than .01 by the Spearman rank test). It is concluded that podocyte changes are seen by scanning electron microscopy early in clinical and experimental postischemic acute renal failure and are more pronounced in those groups that eventually develop more severe renal failure. It is unclear whether these changes reflect a decrease in glomerular hydraulic permeability or an increase in glomerular permeability to protein.
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PMID:Glomerular epithelial cell changes in early postischemic acute renal failure in rabbits and man. 701 70

A radioimmunoassay of ADH has been applied to the study of plasma ADH levels in various conditions. The validity of the assay has been evaluated by the usual quality control parameters of RIA and by the measure of plasma levels in 12 upright water deprived normal volunteers (mean 9.5 pg/ml, SEM +/- 1.5) in 8 resting and hydrated normal volunteers (1.3 +/- 0.4 pg/ml), in a case of diabetes insipidus (1.6 pg/ml), in 8 cases of SIADH Syndrome (range 13-77 pg/ml) and in 4 anesthetized dogs before (33.7 +/- 9.2 pg/ml) and after acute haemorrhage (66 +/- 9.5 pg/ml, p less than 0.02). The osmotoic challenge to ADH secretion has been studied in 8 patients with no overt endocrine pathology by salt perfusion and showed a significant rise (p less than 0.05) of plasma ADH from 6.3 +/- 3.1 pg/ml before, to 20.6 +/- 7.9 pg/ml during salt infusion corresponding to the significant (p less than 0.0001) rise of plasma osmolality from 273 +/- 2.8 to 288.2 +/- 1.1 m Osm/kg.
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PMID:Assessment of a plasma ADH radioimmunoassay in experimental and physiologic or pathologic conditions. 737 70

Incubation of human colonic contents with various ethanol concentrations (2.75-44 mM) in vitro at 37 degrees C resulted in significant accumulation of acetaldehyde--a toxic and highly reactive compound. At pH 9.6, all samples produced notable acetaldehyde concentrations (58 (13) microM; mean (SEM)) even from the lowest (2.75 mM) ethanol concentration, and the production of acetaldehyde increased lin-early with rising ethanol concentration (r = 0.97; p < 0.005), reaching a peak concentration of 238 (37) microM at 44 mM ethanol. The formation of acetaldehyde took place rapidly, as almost 50% of acetaldehyde formed during the total eight hour incubation was detectable after one hour, and 75% of the total after four hours. Maximal acetaldehyde production from 22 mM ethanol occurred at pH 9.6 (160 (35) microM) but appreciable concentrations were also seen at pH 7.4 (110 (38) microM) and pH 6.0 (63 (19) microM). At pH 4.0, by contrast, acetaldehyde formation was negligible (17 (5) microM). 4-Methylpyrazole, a potent inhibitor of alcohol dehydrogenase, showed a decreasing effect on acetaldehyde production in vitro but first at a concentration of 100 mM. Considerable acetaldehyde production by human colonic bacteria--if it occurs also in vivo--could constitute a risk factor for rectal cancer in heavy drinkers and also provide a pathogenetic mechanism for alcohol induced diarrhoea.
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PMID:In vitro acetaldehyde formation by human colonic bacteria. 795 36

Vasopressin (ADH) increases transepithelial water flow in renal epithelia by a process that involves the insertion of water channels into the apical membrane. The objective of the present study was to examine membrane surface remodeling under conditions that promote the recovery of water channels. Hemibladders were set up as sacs with an imposed osmotic gradient. The control sacs received no hormone treatment, whereas the other sacs were stimulated with 100 mU/ml ADH for 10 or 15 min to induce exocytosis and enhanced water flow. ADH was then washed from the tissues with fresh buffer rinses to abolish the hormone actions. These tissues were then allowed to recover for 15, 30 and 60 min. During this time water channels are recovered intracellularly by a process of endocytosis. This time period was called the retrieval period. At specified time intervals, tissues were fixed and processed for SEM or embedded in epon for ultrathin sectioning for TEM studies. Control tissues, regardless of the length of time, showed little or no sign of surface remodeling that was indicative of endocytosis during pre- or post-buffer washes, whereas the ADH-treated tissues showed a time-dependent remodeling of the apical membrane during activation and following removal of the hormone during the retrieval period. At the 10 min retrieval period, greater than 47% of the granular cells showed extensive surface remodeling. By 30 and 60 min posthormone treatment during recovery, fewer than 23% of granular cells showed signs of surface membrane changes. During retrieval the apical membrane undergoes a transition with a loss of both microridges and microvilli prior to membrane restoration. These observations suggest that apical membrane remodeling is crucial for the restoration of membrane permeability following hormone activation and termination.
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PMID:Surface membrane remodeling following removal of vasopressin in toad urinary bladder. 802 24

By virtue of possessing alcohol dehydrogenase activity, cytosol prepared from Helicobacter pylori produces toxic acetaldehyde from ethanol in vitro. To approach the in vivo situation in the stomach, we have now investigation whether intact H. pylori--without addition of exogenous nicotinamide adenine dinucleotide--also forms acetaldehyde. Furthermore, to assess the energy metabolism of H. pylori, we determined whether the alcohol dehydrogenase-catalyzed reaction can run in the opposite direction with ethanol as the end-product and thereby yield energy for the organism. Intact H. pylori formed acetaldehyde already at low ethanol concentrations (at 0.5% ethanol, acetaldehyde, 64 +/- 21 and 75 +/- 9 mumol/l (mean +/- SEM) for strains NCTC 11637 and NCTC 11638, respectively). H. pylori produced ethanol in concentrations that can be significant for the energy metabolism of the organism. Acetaldehyde production by H. pylori may be an important factor in the pathogenesis of gastroduodenal diseases associated with the organism. The primary function of H. pylori alcohol dehydrogenase may, however, be alcoholic fermentation and consequent energy production under microaerobic conditions.
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PMID:Acetaldehyde and ethanol production by Helicobacter pylori. 804 4


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