bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tamm—Horsfall Glycoprotein Release from Rat Kidney Cortex Slices in Vitro
Authors: Wirdnam P. K. , Milner R. D. G. 
Published: August 2015

1. Rat kidney cortex slices were incubated for 30 min at 37°C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain.
2. Tamm—Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content.
3. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide.
4. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release.
5. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.
Effect of Acetylsalicylic Acid and of Indomethacin on Diuresis in Man: The Role of Cyclo-Oxygenase Inhibition
Authors: Vierhapper H. , Jörg J. , Waldhäusl W. 
Published: August 2015

1. The effect of acetylsalicylic acid (ASA, 3 g/day for 3 days) and of indomethacin (IND, 150 mg/day for 3 days) on diuresis and on the excretion of prostaglandin E2 (PGE2) was studied in six healthy, male volunteers. After overnight deprivation the subjects received an oral water load (20 ml/kg) and hourly urine volumes were replaced by an equivalent volume of water by mouth for 4 h.
2. Pretreatment with both ASA and IND induced a comparable suppression (P&lt;0.05 to &lt;0.001) in the excretion of PGE2, but only IND also reduced (P&lt;0.05) diuresis, free water clearance and the excretion of sodium. The excretion of creatinine was uninfluenced by both ASA and IND.
3. These data indicate that a mechanism other than cyclo-oxygenase inhibition is involved in the effect of IND and ASA on diuresis in man.
Effect of Two Models of Portal Hypertension on Splanchnic Organ Blood Flow in the Rat
Authors: Lebrec D. , Blanchet L. 
Published: August 2015

1. Splanchnic organ blood flow and cardiac output were measured by the microsphere method in fasted rats with prehepatic portal hypertension due to portal vein stenosis, in rats with intrahepatic portal hypertension due to bile duct ligation, and in unoperated normal rats.
2. Portal venous pressure was higher in both groups of portal hypertensive rats than in normal rats. Cardiac output was significantly higher in portal hypertensive rats than in normal rats.
3. In rats with portal vein stenosis, splanchnic blood flow was higher than in controls. This increase was caused by increased perfusion of all organs drained by the portal vein, and by increased hepatic arterial blood flow. In rats with bile duct ligation, splanchnic blood flow was not significantly higher than in normal rats: haemoperfusion of all organs contributing to the portal circulation decreased, whereas hepatic arterial blood flow increased. As cardiac output rose similarly, the differences observed between the two types of portal hypertension depend mainly on the difference in distribution of flow within the splanchnic bed.
Intracellular Chloride in Essential Hypertension
Authors: Zidek W. , Losse H. , Lange-Asschenfeldt H. , Vetter H. 
Published: August 2015

1. In 25 patients with untreated essential hypertension and 25 healthy controls, erythrocyte intracellular Cl− concentration and activity as well as Na+ activity were measured.
2. Intracellular Cl− concentration in essential hypertensive patients was 70.6 ± 11.3 as compared with 84.4 ± 9.5 mmol/l in the controls (P&lt;0.001).
3. Intracellular Cl− activity was 77.5 ± 13.0 mmol/l of cell water in hypertensive patients, the control value being 100.8 ± 11.0 mmol/l of cell water (P&lt;0.001).
4. In the hypertensive group intracellular Na+ activity was 14.3 ± 4.1 as compared with 7.1 ± 1.8 mmol/l of cell water in the normotensive group (P&lt;0.01).
5. From these results it is suggested that in essential hypertension not only disturbances of cation metabolism, but also of anion metabolism, occur. Possibly the Cl− changes reflect a decreased Cl− inward transport due to an altered Na-K co-transport.
Cholestasis induced by Sulphated Glycolithocholic Acid in the Rat: Protection by Endogenous Bile Acids
Authors: Kuipers Folkert , Havinga Rick , Vonk Roel J. 
Published: August 2015

1. Sulphated glycolithocholic acid (SGLC) causes cholestasis in experimental animals, despite its sulphated form. In the present study, the cholestatic potency and the pharmacokinetics of SGLC were investigated in rats under two conditions: (a) in the presence of an intact circulating bile acid pool and (b) after exhaustion of the bile acid pool by 24 h of bile diversion.
2. Intravenous administration of SGLC (8 μmol/ 100 g body weight) to rats with an intact bile acid pool did not cause cholestasis. However, biliary phospholipid and cholesterol concentrations were reduced by 40% and 29% respectively during the first hour after administration. When the same dose of the bile acid was injected in rats with a 24 h biliary drainage, a complete cessation of bile production was observed within 1 h. Twelve hours after the onset of cholestasis, bile production gradually increased again, showed a marked overshoot, and reached control levels after 3 days. In the recovery phase, biliary phospholipid and cholesterol concentrations were greatly reduced.
3. The absence of endogenous bile acids did not change the hepatic clearance rate of a tracer dose of radiolabelled SGLC, but markedly decreased its biliary excretion rate.
4. It was concluded that the hepatotoxic effect of SGLC is much more pronounced in rats with an exhausted bile acid pool, possibly due to a slower biliary excretion of the toxic compound. This phenomenon may have clinical implications for patients with a contracted bile acid pool.
Potentiation of Cardiac Vagal action by Cold
Authors: Potter Erica K. , Parker Pamela , Caine A. C. , Lumbers Eugenie R. 
Published: August 2015

1. The effect of cold on vagal action at the heart was studied in sheep, dogs and an isolated guinea pig atrial preparation.
2. During cardiac output measurements in un-anaesthetized sheep, by the thermodilution method, bradycardia was evoked on injection of cold indicator in eight of 12 sheep studied. This bradycardia was consistently evoked when blood pressure was increased, but not at normal blood pressure levels.
3. In the guinea pig atrial preparation, which has one vagus nerve attached, bradycardia was evoked by electrical stimulation of the vagus nerve. When the preparation was cooled this bradycardia was potentiated.
4. In anaesthetized dogs, the cut peripheral end of one vagus was stimulated electrically at different frequencies. The linear relationship between pulse interval and vagal frequency was then compared at deep body temperatures of 35, 37, 39 and 41°C. This comparison showed that the vagus prolonged pulse interval more effectively when the animal was cool (35°C) than when it was warm (41°C).
Determination of the Rate of Urea Synthesis from Serial Measurements of Plasma Urea Concentration after an Alanine Load: Theoretical and Methodological Aspects
Authors: Geiseler D. , Kay J. D. S. , Oberholzer V. G. , Seakins J. W. T. , Hjelm M. 
Published: August 2015

1. A method is described by which the rate of synthesis of urea can be calculated from the change of plasma concentration of urea after an alanine load.
2. The results can be expressed in terms of f, the maximum increase in the rate of urea synthesis, and t, the time at which urea synthesis reaches its maximum.
3. These parameters are calculated by an algebraic curve-fitting technique which is suitable for a desk computer.
4. The method removes the need for isotopic analysis and urine collections.
5. The effect of various errors and experimental conditions on the calculated synthesis parameters is investigated.
Dopaminergic regulation of natriuretic response to acute volume expansion in dogs
Authors: McClanahan M. , Sowers J. R. , Beck F. W. J. , Mohanty P. K. , McKenzie T. 
Published: August 2015

1. Effects of carbidopa, a dopa (3,4-dihydroxy-phenylamine) decarboxylase inhibitor, on the renal, haemodynamic and hormonal responses to acute volume expansion were examined in six healthy mongrel dogs which were infused intravenously with 0.9% sodium chloride solution (saline; 30 ml h−1 kg−1) over 2 h.
2. Saline infusion studies were performed in the absence (control) and in the presence of carbidopa given by nasogastric tube in a dose of 1 mg/kg every 8 h beginning 24 h before the infusion.
3. Saline infusion resulted in an increase in renal excretion of dopamine (3,4-dihydroxy-phenylethylamine) and a decrease in renal excretion of noradrenaline.
4. Carbidopa treatment decreased urinary sodium excretion and eliminated the increase in renal production of dopamine in response to saline infusion without affecting renal or haemodynamic response to acute vascular volume expansion with saline.
5. Carbidopa treatment obliterated the suppression of aldosterone produced by saline infusion.
6. Thus, dopamine appears to play a significant role in mediating both the natriuretic and aldosterone response to acute volume expansion.
Apparent compartmentation of body nitrogen in one human subject: its consequences in measuring the rate of whole-body protein synthesis with 15N
Authors: Fern Edward B. , Garlick Peter J. , Waterlow John C. 
Published: August 2015

1. The rate of protein synthesis in the whole body was measured in one fed subject with seven 15N-labelled amino acids (intravenous and oral doses) and two 15N protein mixtures (oral doses only). The rates were determined individually from the urinary excretion of ammonia and total urea over a 12 h experimental period.
2. Except with oral glycine and alanine, the synthesis rates given by ammonia and urea were appreciably different within each study when calculated on the assumption of a single pool of metabolic nitrogen in the body. In general, intravenous administration of the tracers gave higher rates with urea and the oral route gave higher rates with ammonia.
3. The differences between intravenous and oral doses of 15N could be reduced significantly by calculating synthesis rates from either the arithmetic or harmonic average of flux rates given by ammonia and urea. The averages correspond to estimates of the total flux in a two-pool model of metabolic nitrogen when it is assumed either that both pools receive an equal amount of tracer (arithmetic) or that both have the same rate of nitrogen turnover (harmonic).
4. By so reducing the effect of physical separation of nitrogen in the body, the metabolic aspects of compartmentation of the tracer could be examined. The results show that the absolute value obtained for protein synthesis depends on the source of labelled nitrogen. The data are discussed in this empirical context.
Leukaemic promyelocytes and normal bone marrow cells release a passive sodium transport modifier (inhibitin)
Authors: Morgan Kevin , Spurlock Gillian , Mir M. Afzal 
Published: August 2015

1. Previous studies have shown that leukaemic immature cells, specifically promyelocytes but not mature leucocytes, contain and release an inhibitor of ouabain-insensitive sodium transport (inhibitin).
2. In the present study, medium from cultured leukaemic promyelocytes significantly reduced the ouabain-insensitive sodium efflux from erythrocytes, whereas medium from the same cell line which had been made to differentiate did not have this effect.
3. Culture medium from normal bone marrow cells (containing promyelocytes) also significantly (P &lt; 0.001) reduced ouabain-insensitive sodium efflux.
4. These data suggest that inhibitin is secreted by primitive but not by mature leukaemic cells and normal bone marrow cells.
Neuropeptide Y: a novel renal peptide with vasoconstrictor and natriuretic activity
Authors: Allen J. M. , Raine A. E. G. , Ledingham J. G. G. , Bloom S. R. 
Published: August 2015

1. A novel vasoconstrictor peptide, neuropeptide Y (NPY), has been identified in considerable quantities in the renal artery and kidney. Within the kidney, NPY was confined to the cortex and corticomedullary interface, the regions where the juxtaglomerular apparatus is most numerous.
2. In the isolated perfused rat kidney, NPY caused a prompt dose-dependent increase in perfusion pressure and reduction in flow, with only a small fall in glomerular filtration rate (GFR). In spite of the reduced renal perfusion, a dose-dependent natriuresis was observed. This response contrasts to the response of this preparation to noradrenaline, which causes sodium reabsorption.
3. The presence of a potent vasoconstrictor and natriuretic peptide within the rat renovascular system suggests that it may play a significant role in the control of renal function.
Maternal zinc and intrauterine growth retardation
Authors: Simmer Karen , Thompson R. P. H. 
Published: August 2015

1. The levels of zinc in plasma, erythrocytes, polymorphonuclear (PMN) and mononuclear (MN) white cells were measured after delivery in women giving birth to appropriate-for-gestational-age (AGA) babies (group I mothers), or small-for-gestational-age (SGA) babies (group II mothers) and in non-pregnant controls.
2. Mean maternal plasma zinc and albumin levels 24-48 h after delivery were lower than in controls, but PMN and MN zinc levels were unchanged. PMN zinc levels were lower than those of MN cells.
3. PMN and MN zinc levels were significantly lower in group II mothers than in group I, irrespective of smoking habits. There were no racial differences in peripheral white cell zinc levels.
4. PMN, and to a lesser degree MN, zinc levels were lower in smoking than in non-smoking mothers.
5. Erythrocyte zinc did not correlate with other zinc measurements nor with the size of the babies. Fetal erythrocyte zinc levels were one-third of maternal levels.
6. A combination of smoking and/or low PMN zinc levels selects 85% of mothers having small-for-gestational-age babies.
The human eccrine sweat gland adenylate cyclase system: response to agonists
Authors: Khullar A. K. , Schwarz V. , Wilson P. D. 
Published: August 2015

1. Cyclic AMP accumulation has been measured in whole human sweat glands. The mean rate in glands from 19 subjects was 0.519 ± 0.316 pmol of cyclic AMP formed 5 min−1 μg−1 of DNA, which is comparable with that reported for other tissues.
2. Cyclic AMP accumulation in the sweat gland is stimulated fourfold by prostaglandin (PG) E1 and fivefold by PGE2 (0.1 mmol/l), in accord with stimulation in renal tubules and medullary membranes.
3. Bradykinin (10 μg/ml) increases the rate threefold and this is substantially prevented by indomethacin (1.5 × 10−5 mol/l), as also is a five-fold stimulation by cyclic GMP (10−5 mol/l).
4. Mecholyl (10−2 mol/l) and isoprenaline (6 × 10−6 mol/l) increase the rate five- and four-fold respectively, and these agonist effects are largely abolished by atropine and propranolol.
5. The stimulation and inhibition pattern suggests a direct action of PGE, enhancement of prostaglandin synthetase by cyclic GMP and stimulation of guanylate cyclase by mecholyl and bradykinin. Isoprenaline presumably stimulates adenylate cyclase directly.
6. This complex chain of events, from cholinergic stimulation to an enhancement of adenylate cyclase, demonstrated in vitro, constitutes a potential for flexible and fine control of sweat gland function.
Changes in plasma catecholamines in response to reflex modulation of sympathetic vasoconstrictor tone by cardiopulmonary receptors
Authors: Grassi Guido , Gavazzi Cecilia , Cesura Andrea M. , Picotti Giovanni B. , Mancia Giuseppe 
Published: August 2015

1. The effects of selective deactivation and stimulation of cardiopulmonary receptors on plasma noradrenaline (radioenzymatic method) were studied in nine normotensive subjects by reducing and increasing central venous pressure for 20 min via lower body suction and leg-raising manoeuvres that did not alter arterial blood pressure and heart rate.
2. Deactivation of cardiopulmonary receptors was accompanied by a rise in plasma noradrenaline that achieved a peak within 5 min (91.8 ± 22%, mean ± se) and was then sustained. Stimulation of cardiopulmonary receptors was accompanied by a fall in plasma noradrenaline (−16.6 ± 3.4%) that levelled off at the second minute and was then sustained.
3. On average the increase and the reduction in plasma noradrenaline had a time course and a magnitude similar to the increase (80.5 ± 10.5%) and the reduction (−28.4 ± 5%) in forearm vascular resistance (derived from plethysmographic flow measurement) concomitantly caused by cardiopulmonary receptors. Furthermore, analysis of individual data showed that changes in plasma noradrenaline and forearm vascular resistance were linked by a positive relationship (r = 0.64).
4. Thus the cardiopulmonary receptor reflex can produce rapid, marked and sustained changes in both plasma noradrenaline and forearm vasomotor tone. This is in sharp contrast with the previously observed inability of the carotid baroreflex to alter both these humoral and haemodynamic variables. Taken together these findings support the hypothesis that sympathetic tone to skeletal muscle is an important determinant of the concentration of plasma noradrenaline in blood.
The retention of cobalamin by the liver in the cobalamin-deficient rat
Authors: Owens Julie A. , Scott J. S. D. , Cooksley W. G. E. 
Published: August 2015

1. The effect of cobalamin deficiency on whole body cobalamin content and its turnover was examined in the rat. Quantitative and qualitative changes in hepatic cobalamin were also followed and the effect of deficiency on the turnover of this cobalamin was determined in the isolated perfused liver.
2. As cobalamin deficiency developed after total gastrectomy, whole body cobalamin content declined at a constant rate, indicating no attempt to conserve total body cobalamin stores even when depleted (5% of normal).
3. In contrast, the cobalamin concentration of liver declined more slowly, indicating conservation of hepatic cobalamin. Furthermore, the methylcobalamin (Me Cbl) content of liver was maintained or even increased.
4. Measurement of the rate of release of cobalamin by the isolated perfused liver at varying times after gastrectomy showed that as depletion of whole body and hepatic cobalamin stores proceeded, the rates of release of hepatic cobalamin into plasma and bile decreased. Regression analysis showed that the fractional rates of release of hepatic cobalamin into plasma (r = 0.9, P &lt; 0.001, n = 15) and bile (r = 0.65, P&lt;0.01, n = 15) were significantly correlated with hepatic cobalamin content.
5. It is concluded that conservation of hepatic cobalamin in deficiency is achieved, at least in part, by a specific decrease in the rate of release of hepatic cobalamin.
Human jejunal transglutaminase: demonstration of activity, enzyme kinetics and substrate specificity with special relation to gliadin and coeliac disease
Authors: Bruce S. E. , Bjarnason I. , Peters T. J. 
Published: August 2015

1. By use of a radiometric assay transglutaminase activity was demonstrated for the first time in human jejunal mucosa. The activity is similar to that in other tissues, with a pH optimum of 9.0, an absolute requirement for Ca2+ and an apparent Km for putrescine of 0.15 mmol/l.
2. Assay of jejunal transglutaminase activity with a variety of dietary proteins as acceptors showed high activity with gliadin, comparable with that of the standard substrate, dimethylcasein. Deamidation of the gliadin markedly reduced its acceptor activity. Collagen, ovalbumin, elastin and zein exhibited very low acceptor activities.
3. Increased transglutaminase activity was demonstrated in jejunal biopsies from four patients with untreated coeliac disease compared with 14 control subjects and eight patients with inflammatory bowel disease. Eight patients with coeliac disease in remission, with normal levels of brush border α-glucosidase, showed elevated transglutaminase activities compared with those of controls.
4. It is postulated that intestinal transglutaminase activity may be important in gliadin binding to tissues and thus in the pathogenesis of coeliac disease.
Interactions between neural mechanisms, the renin-angiotensin system and vasopressin in the maintenance of blood pressure during water deprivation: studies in Long Evans and Brattleboro rats
Authors: Gardiner S. M. , Bennett T. 
Published: August 2015

1. Plasma volumes and cardiovascular status were assessed in rats with a congenital deficiency in hypothalamic vasopressin (Brattleboro strain) and in the parent strain (Long Evans), in water-replete and water-deprived states.
2. Water-replete Brattleboro rats were not hypovolaemic; water deprivation (14 h in Brattleboro rats, 53 h in Long Evans rats) produced similar percentage reductions in plasma volumes in the two groups.
3. In the water-replete state, cardiovascular variables were similar in Long Evans and Brattleboro rats. Inhibition of ganglionic transmission (with pentolinium) or of the renin-angiotensin system (with captopril), separately, did not have a greater effect on blood pressure in Brattleboro rats than in Long Evans rats. Recovery from hypotension caused by pentolinium was characterized by large swings in blood pressure in both groups of rats. These pressor episodes were abolished by administration of captopril to Brattleboro rats. After administration of pentolinium and captopril to Long Evans rats there was a substantial, although intermittent, recovery in blood pressure that was abolished by an antagonist of the cardiovascular actions of vasopressin.
4. In the water-deprived state, blood pressures were similar in Long Evans and Brattleboro rats; both groups showed an elevation in diastolic blood pressure relative to the water-replete state. After administration of pentolinium, there was a more marked recovery in blood pressure than was seen in the water-replete state. Administration of Captopril alone had a slightly greater effect on blood pressure in Long Evans rats in the water-deprived, compared with the water-replete, state. However, in the former condition, Brattleboro rats showed a profound and progressive hypotension in response to captopril, indicating an indispensable role for the renin-angiotensin system in the maintenance of blood pressure in these animals during water deprivation.
5. Only when the renin-angiotensin system and neural activity were inhibited did vasopressin express its full, independent, pressor potential in Long Evans rats. However, evidence was obtained that vasopressin may exert important effects on cardiovascular regulation via neural mechanisms and through interactions with the renin-angiotensin system.