bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inactive Renin in Rabbit Plasma: Effect of Haemorrhage
Authors: Richards H. K. , Grace S. A. , Noble A. R. , Munday K. A. 
Published: August 2015

1. Renin activity in rabbit plasma increases after acidification (pH 3·3), probably due to activation of an inactive form of renin.
2. Both active and inactive renin in plasma increase after haemorrhage. This stimulus does not change the relative proportions of the two forms.
3. After ligation of the renal blood vessels neither form of renin increases in response to haemorrhage.
4. One day after bilateral nephrectomy no inactive renin could be demonstrated in plasma.
5. In the rabbit, therefore, the kidney is a major source of the inactive renin in plasma.
Hypertension with Mineralocorticoid Administration to the Long-Evans Rat
Authors: Holland O. B. , Gomez-Sanchez C. , Ziegler T. 
Published: August 2015

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile.
2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 μmol) of DOCA pellets/rat or 250 μg (0·65 μmol) of 2α-methyl-9α-fluorocortisol/day subcutaneously.
3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2α-methyl-9α-fluorocortisol.
4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.
Evidence for Activation of Circulating Inactive Renin by the Human Kidney
Authors: Derkx F. H. M. , Wenting G. J. , In't Veld A. J. Man , Verhoeven R. P. , Schalekamp M. A. D. H. 
Published: August 2015

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide.
2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10–14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol.
3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one.
4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a β-adrenoreceptor might be involved in this activation process.
Glycerol-Induced Acute Renal Failure in Brattleboro Rats with Hypothalamic Diabetes Insipidus
Authors: Konrads A. , Hofbauer K. G. , Bauereiss K. , Möhring J. , Gross F. 
Published: August 2015

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure.
2. In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (61 mmol/l).
3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h.
4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol.
5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently.
6. These data support the idea that in glycerol-induced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.
Inhibition of Mitochondrial Electron Transfer in Rats by Ethanethiol and Methanethiol
Authors: Vahlkamp T. , Meijer A. J. , Wilms J. , Chamuleau R. A. F. M. 
Published: August 2015

1. We have investigated the effects of ethanethiol, methanethiol and dimethyl sulphide on some metabolic processes of isolated rat hepatocytes, isolated mitochondria from liver and brain and ox-heart submitochondrial particles.
2. Ethanethiol, but not dimethyl sulphide, inhibited both gluconeogenesis and ureogenesis from various substrates in rat hepatocytes, depressed cellular ATP content and caused an increased reduction of the mitochondria.
3. Ethanethiol inhibited respiration in isolated rat-liver mitochondria with several substrates, both in the presence of ADP and phosphate or in the presence of an uncoupling agent. Ethanethiol also inhibited respiration in isolated rat-brain mitochondria. Dimethyl sulphide was much less effective in inhibiting mitochondrial respiration.
4. In ox-heart submitochondrial particles ethanethiol inhibited electron transfer between cytochrome c and oxygen.
5. Purified cytochrome c oxidase was inhibited by ethanethiol in a non-competitive manner.
6. Methanethiol inhibited cytochrome c oxidase and was an effective inhibitor of mitochondrial electron transfer, both in liver and brain.
7. The difference in inhibitory properties between ethanethiol, methanethiol and dimethyl sulphide observed in our experiments coincides with the difference in potency to elicit coma in rats. We suggest that inhibition of mitochondrial electron transfer by mercaptans may be relevant to the mechanism by which energy production in brain is depressed during hepatic coma.
The Role of the Baroreceptor Reflex in the Cardiovascular Effects of Propranolol in the Conscious Spontaneously Hypertensive Rat
Authors: Struyker-Boudier H. A. J. , Smits J. F. , Van Essen H. 
Published: August 2015

1. The role of baroreceptors in the cardiovascular mechanism of action of dl-propranolol has been studied by comparing the acute effects of subcutaneous injection of 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) of this drug in conscious baroreceptor-denervated spontaneously hypertensive (SH) rats with those in sham-operated control SH rats.
2. At 5 mg/kg (16·5 × 10−6 mol/kg) propranolol caused a small, but significant, increase in blood pressure in sham-operated SH rats, whereas both after 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) immediate hypotension was observed in baroreceptor-denervated animals.
3. Heart rate dropped rapidly after injection of 1 or 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) propranolol both in the baroreceptor-denervated and sham-operated SH rats. Bradycardia was significantly larger in the baroreceptor-denervated animals after an injection of 5 mg/kg (16·5 × 10−6 mol/kg).
4. It is concluded that the lack of an early hypotensive effect of propranolol in intact animals is caused by an increased baroreceptor reflex activity as a consequence of the fall in cardiac output.
Kallikrein—Kinin System in One- and Two-Kidney Goldblatt Hypertensive Rats
Authors: Albertini R. , Rosas R. , Croxatto H. R. , Roblero J. 
Published: August 2015

1. Urinary kallikrein, renal tissue kininogenase activity, and plasma kininogen were measured during the development of hypertension in rats, either with left renal artery clamped and contralateral kidney intact (Goldblatt 2-kidney) or removed (Goldblatt 1-kidney). Plasma urea, plasma volume and blood volume were also measured.
2. In Goldblatt 2-kidney rats, urinary kallikrein was not significantly different from that of sham-operated rats up to the 5th post-operative week even though at this time the Goldblatt 2-kidney animals were hypertensive. Urinary kallikrein started to decrease at week 8. Plasma kininogen was significantly elevated 5 and 10 weeks after surgery and returned to normal by week 15. No changes in renal tissue kininogenase activity were observed. Plasma urea and plasma and blood volumes were normal 5 weeks after, but significantly increased at 10 and 15 weeks after surgery.
3. In Goldblatt 1-kidney rats from the fifth week urinary kallikrein and renal kininogenase activity were significantly decreased compared with unilaterally nephrectomized rats, whereas plasma kininogen, plasma urea and plasma and blood volumes were significantly elevated.
4. These results show important differences in the kallikrein system between the Goldblatt 1-kidney and 2-kidney models of renovascular hypertension in rats.
Inhibition of Rat Liver Mitochondrial 3-hydroxy-3-methylglutaryl-CoA Lyase by Succinyl-CoA
Authors: Deana Renzo , Rigoni Fernanda , Galzigna Lauro 
Published: August 2015

1. Succinyl-CoA inhibits 3-hydroxy-3-methylglutaryl-CoA lyase (EC 4.1.3.4) when added to purified preparations of the enzyme.
2. The apparent Ki value is 2·1 × 10−4 mol/l and the inhibition has the features of a partially competitive inhibition.
3. The effect of succinyl-CoA both added and enzymically produced on the lyase activity of sonically disrupted rat liver mitochondria results in decreased acetoacetate formation.
4. This occurs with mitochondria obtained from normal, starved and streptozotocin-diabetic rats.
Riassunto
1. Il succinilCoA inibisce la 3-idrossi-3-metilglutarilCoA liasi (EC 4.1.3.4) se viene aggiunto a preparazioni di enzima purificato.
2. Il valore della Ki è 2·1 × 10−4 mol/l ed i dati indicano una inibizione parzialmente competitiva.
3. Il succinilCoA, aggiunto o prodotto enzimaticamente, provoca una diminuzione nella produzione di acetoacetato nei mitocondri sonicati di fegato di ratto.
4. Lo stesso fenomeno si verifica con mitocondri di ratti normali, digiuni e diabetici da streptozotocina.
Correlation of Ethanol Concentrations in Blood and Saliva
Authors: McColl K. E. L. , Whiting B. , Moore M. R. , Goldberg A. 
Published: August 2015

1. The concentrations of ethanol in blood, mixed saliva obtained before and after rinsing and drying the mouth and parotid saliva have been monitored in 12 healthy subjects after the ingestion of alcohol.
2. A highly significant linear correlation was found between blood and the three types of saliva examined from 20 min after completion of drinking.
3. Blood and mixed saliva samples were obtained from 20 patients attending the Casualty Department with evidence of ethanol intoxication. A similar correlation was obtained.
4. These results show that salivary ethanol may be used as an index of blood ethanol concentrations, provided that the salivary sample is not obtained within 20 min of the ingestion of alcohol.
Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat
Authors: Campbell W. B. , Schmitz J. M. , Itskovitz H. D. 
Published: August 2015

1. To investigate the relative roles of angiotensin II (AII) and des-Asp1-angiotensin II (angiotensin III) in the control of blood pressure and aldosterone release, the effects of seven angiotensin agonists on mean arterial blood pressure and serum aldosterone concentrations were compared in normal and sodium-depleted, conscious rats.
2. In normal rats, angiotensin I, α-Asp1-angiotensin II, β-Asp1-angiotensin II, and angiotensin II-amide were equipotent in elevating mean arterial blood pressure. Angiotensin III, des-Asp1-angiotensin I, and poly-O-acetylserine-angiotensin II were 25%, 25%, and 41% as potent as angiotensin II, respectively. After sodium depletion, pressor responses to these angiotensin peptides were reduced approximately 60–80% when compared with control responses. In contrast, pressor responses to noradrenaline were not significantly affected by sodium depletion.
3. Angiotensin II, β-Asp1-angiotensin II, angiotensin II-amide, and angiotensin III were equipotent in increasing serum aldosterone concentrations in normal animals. Angiotensin I was 59% and des-Asp1-angiotensin I only 5% as potent as angiotensin II in their abilities to release aldosterone. After sodium depletion, control serum aldosterone concentrations increased as did the slope of the dose—response curve for each angiotensin peptide. Angiotensin II was the most potent steroidogenic peptide in sodium-depleted rats with angiotensin III and β-Asp1-angiotensin II being 27%, angiotensin I 7%, angiotensin II-amide 3%, and des-Asp1-angiotensin I 1% as potent as angiotensin II in releasing aldosterone. Poly-O-acetylserine-angiotensin II has less steroidogenic effect than angiotensin II or III in both normal and sodium-depleted animals.
4. Infusions of the angiotensin II antagonist, Sar1-Ile8-angiotensin II, and the angiotensin III antagonist, Ile7-angiotensin III, enhanced aldosterone release in normal rats without altering blood pressure. After sodium depletion, Sar1-Ile8-angiotensin II decreased blood pressure without affecting aldosterone release whereas Ile7-angiotensin III diminished aldosterone release without altering blood pressure.
5. These data suggest that angiotensin II, independent of its conversion into angiotensin III, is an important regulator of steroidogenesis in the rat in normal sodium states. In sodium depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of angiotensin III to its steroidogenic effects is increased.
Increased Turnover of Muscle Contractile Proteins in Duchenne Muscular Dystrophy as Assessed by 3-Methylhistidine and Creatinine Excretion
Authors: Ballard F. J. , Tomas F. M. , Stern L. M. 
Published: August 2015

1. Myofibrillar protein degradation has been measured in patients with Duchenne muscular dystrophy, normal boys, adult males and Duchenne carriers by the rate of 3-methylhistidine excretion after transfer of subjects to a meat-free diet.
2. Although absolute rates of protein breakdown are lower in Duchenne patients, expression of the data to allow for differences in muscle mass gives fractional degradation rates 2–3 times higher than in age-matched controls.
3. Fractional rates of muscle protein synthesis are increased in the Duchenne patients to almost the same extent as protein breakdown.
4. Rates of muscle protein breakdown in obligate and presumed carriers of the Duchenne gene are not different from controls.
Studies on Mineralocorticoid ‘Escape’ in Cirrhosis
Authors: Wilkinson S. P. , Smith I. K. , Moodie Helen , Poston Lucilla , Williams R. 
Published: August 2015

1. The mineralocorticoid 9α-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an ‘escape’ from its sodium-retaining effects was observed, the other five continuing to retain sodium.
2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the ‘effective’ extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. These findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume.
3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.
Radioimmunoassay Measurement of Urinary Ligandin Excretion in Nephrotoxin-Treated Rats
Authors: Bass N. M. , Kirsch R. E. , Tuff S. A. , Campbell J. A. , Saunders J. S. 
Published: August 2015

1. A radioimmunoassay was used to establish normal urine excretion of ligandin, a renal tubular protein, in rats, and to study the pattern of ligandin excretion after nephrotoxin administration.
2. Validation of radioimmunoassay measurement of ligandin in urine is described. A normal range of 2–46 ng/h was obtained for ligandin excretion in rats (n = 24).
3. Mercuric chloride (HgCl2; 10 mg/kg) administration resulted in a significant increase in ligandin excretion within 6 h, preceding the onset of significant azotaemia. Serum ligandin concentrations were raised after 12 h, while renal ligandin concentration fell to 30% of control values by 24 h.
4. Rats given HgCl2 (5 mg/kg) developed massive ligandinuria between 6 and 12 h, which declined to normal values by 72 h. Potassium dichromate (K2Cr2O7; 7 mg/kg) administration produced a comparatively moderate increase in ligandin excretion after 24 h.
5. The time course of ligandin excretion in HgCl2- and K2Cr2O7-treated rats correlated with the histological sequence of damage to the pars recta and pars convoluta of the proximal tubule respectively.
6. The results of this study confirm that renal ligandin is confined mainly to the pars recta of the proximal tubule, and small quantities of this protein are present in the pars convoluta. Radioimmunoassay provides a sensitive and specific means for measuring ligandin in urine and provides a valuable tool for the detection and study of renal tubular damage.
Effect of Aging on Free Amino Acids and Electrolytes in Leg Skeletal Muscle
Authors: Möller P. , Bergström J. , Eriksson S. , Fürst P. , Hellström K. 
Published: August 2015

1. The concentrations of electrolytes and free amino acids in plasma and the quadriceps femoris muscle were studied in ten apparently healthy elderly men, 52–77 years of age. The results were compared with those previously recorded for men 20–36 years old.
2. The two groups of subjects did not differ with regard to serum electrolytes and intracellular water content but the extracellular water in the older subjects exceeded that of the younger group by about 50%. The muscle specimens of the elderly men were also characterized by a 40% elevation of their total contents of Na+ and Cl−, whereas the content of K+ and Mg2+ was almost identical in both groups.
3. The means recorded for the plasma concentrations of most amino acids tended to be higher in the elderly men. The differences reached statistical significance for tyrosine, histidine, valine, lysine and total essential amino acids. In keeping with the findings in plasma, the amino acid concentrations in the muscle of the older group tended to exceed those of the younger ones. The difference reached statistical significance with regard to total amino acids, essential and non-essential amino acids, aspartate, alanine, citrulline, histidine, arginine, leucine and lysine. The various mechanisms that may contribute to these findings are discussed.
Comparison of Two Rebreathing Methods for the Determination of Mixed Venous Partial Pressure of Carbon Dioxide during Exercise
Authors: Heigenhauser G. J. F. , Jones N. L. 
Published: August 2015

1. Duplicate measurements were made of mixed venous Pco2 (Pv̄, co2) by two rebreathing methods during steady-state exercise at three power outputs in seven subjects. One method employed a high initial bag CO2 concentration to obtain equilibrium of CO2 in the lung—bag system before recirculation (equilibrium method); in the other, a low initial bag CO2 concentration was used and a statistical method was applied to alveolar Pco2 measurements before recirculation, to obtain the asymptote from the exponential rise in end-tidal Pco2 during rebreathing (exponential method).
2. The reproducibility was similar; sd of duplicate determinations of Pv̄, co2 was 0·15 kPa (1·1 mmHg) for the equilibrium method and 0·20 kPa (1·5 mmHg) for the exponential method. Measurements of Pv̄, co2 by the exponential method were systematically lower than the equilibrium method. When the equilibrium Pv̄, co2 was corrected for the alveolar—arterial (‘downstream’) Pco2 difference, using published values, Pv̄, co2 was similar for both methods.
3. As an alveolar to arterial Pco2 difference did not appear to exist with the exponential method, it is concluded that the previously described disequilibrium between alveolar and arterial Pco2 during rebreathing in exercise is mainly related to prevention of net CO2 movement from the pulmonary capillary blood in the equilibrium method, and is not present when continuous CO2 evolution occurs in the exponential method.
Cardiac Effects of Angiotensin Antagonists in Normotensive Rats
Authors: Sen S. , Tarazi R. C. , Bumpus F. M. 
Published: August 2015

1. Angiotensin II (AII) antagonists, namely Sar1,Ile8-AII, Sar1,Ala8-AII and Sar1,Thr8-AII, were administered daily for 4 weeks to normotensive rats to study their effect on cardiac hypertrophy.
2. None of the antagonists altered blood pressure significantly but Sar1,Ile8-AII and Sar1,Ala8-AII produced a significant increase in heart weight, as compared with untreated age-matched control rats. Administration of Sar1,Thr8-AII did not produce cardiac hypertrophy.
3. A significant increase in catecholamine concentration was observed in the ventricles of rats treated with Sar1,Ile8-AII and Sar1,Ala8-AII but no change was found in the group treated with the Sar1,Thr8-AII analogue. The production of cardiac hypertrophy by Sar1,Ile8-AII was prevented by bilateral adrenalectomy, suggesting an important role for catecholamines in modulating cardiac hypertrophy.
Faecal Methylamine in Normal and Uraemic Subjects
Authors: Owens C. W. I. , Padovan W. 
Published: August 2015

1. A ninhydrin-reacting substance seen during ion-exchange chromatography of faecal dialysate obtained in vivo from normal and uraemic subjects has been isolated and identified as methylamine.
2. Faecal dialysate concentrations of methylamine were higher in uraemic subjects and were related to the degree of renal impairment (P &lt; 0·05).
3. Methylamine concentrations in faecal dialysate and centrifugate were not significantly different.