bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impaired Response of Plasma Renin Activity to Tilting after Renal Transplantation
Authors: Cunningham J. , Vandenburg M. J. , Holly J. M. P. , Goodwin F. J. 
Published: August 2015

1. Changes in plasma renin activity, plasma noradrenaline, pulse rate and blood pressure after tilting were measured in normal subjects and in patients with renal transplants.
2. There was a marked difference between the renin responses in the two groups, the increases in plasma renin activity in the control subjects being much greater than those in the transplanted patients.
3. Activation of the sympathetic nervous system after tilting, as indicated by changes in pulse rate, blood pressure and plasma noradrenaline, was similar in the two groups.
4. We conclude that the ability of the transplanted kidney to increase plasma renin activity after tilting is impaired, probably as a result of sympathetic denervation of the kidney during transplantation. The results suggest a dominant role of the sympathetic nervous system in the mediation of renin release after tilting.
Effect of Propranolol Therapy on Aldosterone Responses to Angiotensin II and Adrenocorticotropic Hormone in Essential Hypertension
Authors: Golub M. S. , Tuck M. L. , Fittingoff D. B. 
Published: August 2015

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120–240 mg/day) in eight patients with essential hypertension.
2. Basal supine plasma renin activity was decreased (P &lt; 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P &lt; 0.05) after propranolol.
3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy.
4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after β-adrenoceptor antagonism in essential hypertension.
Ki+-Na+o Countertransport in Erythrocytes of Patients with Essential Hypertension
Authors: Adragna N. , Canessa M. , Bize I. , Solomon H. , Tosteson D. C. 
Published: August 2015

1. We describe in this paper a new ouabain-insensitive pathway for Na+ and K+ in human erythrocytes. K+ efflux was measured in cells loaded by the p-chloromercuribenzene-sulphonate (PCMBS) procedure to contain approximately equal amounts of Na+ and K+. K+ efflux was stimulated by external Na+ in the presence of ouabain and frusemide. Na+-stimulated K+ efflux was 0.35 ± 0.12 (mmol h−1 l−1 of cells) in eight normal subjects and 0.64 ± 0.13 in 13 patients with essential hypertension.
2. The Na+-stimulated K+ efflux was not observed in cells loaded in the presence of EGTA. This inhibition by EGTA suggests that K+ efflux is dependent on intracellular calcium. The Ki+-Nao+ countertransport of hypertensive patients was also inhibited by EGTA. The elevated K+—Na+ countertransport of hypertensive patients could be due to a higher intracellular Ca2+ content (Cai2+) or to an increased affinity for Cai2+. The relationship of this pathway to the Gardos effect is not clear since Na+-stimulated K+ efflux occurs without metabolic depletion or inhibition of the Ca2+ pump. As a tentative hypothesis, we relate the Ca2+-dependent downhill movement of K+ and Na+ to the Ca2+-dependent channels described in muscle and nerve, but other hypotheses cannot be excluded at this stage of our research.
Increased Erythrocyte Lithium-Sodium Countertransport in Essential Hypertension: Its Relationship to Family History of Hypertension
Authors: Canali M. , Borghi L. , Sani E. , Curti A. , Montanari A. , Novarini A. , Borghetti A. 
Published: August 2015

1. Erythrocyte lithium—sodium counter-transport was measured in 46 normotensive healthy controls without family history of hypertension, 15 subjects with essential hypertension, but without evidence of family history of high blood pressure, and 43 subjects with essential hypertension and at least one hypertensive first-degree relative.
2. Mean values (mmol h−1 l−1 of erythrocytes) were 0.248 ± 0.092 in controls, 0.258 ± 0.087 in hypertensive subjects without family history (not significant vs controls), 0.360 ± 0.115 in hypertensive subjects with family history of hypertension (P &lt; 0.001 vs controls), 0.334 ± 0.117 in all hypertensive subjects, both with and without family history (P &lt; 0.001 vs controls).
3. Our data confirm the finding of an increased erythrocyte lithium-sodium counter-transport, but with a significant overlap between essential hypertension and control values. Lithium-sodium countertransport is higher only in hypertensive subjects with at least one hypertensive first-degree relative.
4. We suggest that the increase of lithium-sodium countertransport in erythrocytes is not a consistent marker of essential hypertension. It seems to be associated with the family prevalence and/or the hereditability of hypertension, rather than with high blood pressure per se.
Changes in Plasma Renin Activity after Hypoglycaemia in Sympathectomized Man
Authors: Frier B. M. , Corrall R. J. M. , Pritchard J. L. , Sever P. S. 
Published: August 2015

1. The changes in blood glucose, plasma noradrenaline and plasma renin activity were measured in 11 normal subjects and in six tetraplegic subjects with a transection of the cervical spinal cord (preganglionic sympathectomy), in response to acute insulin-induced hypoglycaemia (0.15 unit/kg).
2. After hypoglycaemia, a pronounced rise in plasma noradrenaline was observed in the normal subjects but was absent in the tetraplegic group; plasma renin activity increased markedly in both groups.
3. It is concluded that the stimulation of renin release in response to hypoglycaemia can occur independently of any activation of the sympatho-adrenal system.
Intralymphocytic Sodium Concentration as An Index of Response to Stress and Exercise in Young Subjects with Borderline Hypertension
Authors: Ambrosioni E. , Costa F. V. , Montebugnoli L. , Borghi C. , Magnani B. 
Published: August 2015

1. A highly significant correlation between intralymphocytic sodium concentration and basal diastolic blood pressure can be found only in patients with sustained essential hypertension.
2. In subjects with borderline hypertension and in normotensive subjects with familial hypertension a highly significant correlation can be found between intralymphocytic sodium concentration and the increase in diastolic blood pressure induced by mental arithmetic or handgrip exercise.
3. The increase in diastolic blood pressure recorded during mental arithmetic and handgrip in patients with borderline hypertension and in genetic normotensive subjects is significantly greater if intralymphocytic sodium concentration is greater than 26 mmol/kg.
Effect of Extracellular Potassium on the Transport of Sodium and Potassium in Rat Thymocytes
Authors: Jones R. B. , Patrick J. , Hilton P. J. 
Published: August 2015

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro.
2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l.
3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump.
4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied.
5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.
3-Methylbutanal Metabolism in the Adult Rat
Authors: Kubow S. , Anderson G. H. , Blendis L. M. , Goldberg E. 
Published: August 2015

1. 3-Methylbutanal is a normal constituent of human plasma and is elevated in patients with hepatic encephalopathy. Therefore these studies examined the possible source and site of synthesis of 3-methylbutanal and its effect on the central nervous system of adult rats.
2. 3-Methylbutanal was found to be a normal constituent of rat plasma and increased two to five times when leucine comprised 5% of the diet. Neomycin in the diet prevented the leucine-induced rise in plasma 3-methylbutanal. When this was injected at a dose of 120 mg/kg abnormal EEG patterns and sleep-like behaviour occurred, whereas smaller amounts (30 mg/kg) increased brain serotonin concentrations.
3. 3-Methylbutanal is a normal component of rat plasma: it may be derived in part from colonic bacterial breakdown of leucine and may influence central nervous system function. A possible relationship of 3-methylbutanal to the pathogenesis of hepatic encephalopathy is suggested.
Plasma Levels of Vitamin D Metabolites in Diphosphonatetreated Rats
Authors: Trechsel U. , Taylor C. M. , Eisman J. A. , Bonjour J.-P. , Fleisch H. 
Published: August 2015

1. Protein-binding assays have been used to measure plasma 1,25-dihydroxy-vitamin D [1,25-(OH)2D] as well as 25-hydroxy-vitamin D [25-(OH)D] in rats given 10 mg of phosphorus (P) day−1 kg−1 as ethane-1-hydroxy-1,1-diphosphonate (EHDP).
2. In control animals given a normal laboratory chow plasma 25-(OH)D and 1,25-(OH)2D were about 40 nmol/l and 300 pmol/l respectively.
3. EHDP produced a decrease of plasma 1,25-(OH)2D to below 50 pmol/l in 2 days.
4. Both in control and in EHDP-treated rats plasma 1,25-(OH)2D increased when dietary calcium (Ca) was restricted to 0.1%, or dietary P to 0.2%, indicating that the well-known stimulatory effect of Ca or P deprivation was at least partially effective in EHDP-treated rats.
5. In response to an increase of the oral supply of vitamin D3 to 65 nmol/day the plasma level of 25-(OH)D rose in both control and EHDP groups. Plasma 1,25-(OH)2D was not increased above the normal value in control rats. In EHDP-treated rats, however, plasma 1,25-(OH)2D rose to a level equal to that in controls, suggesting that the effect of EHDP on plasma 1,25-(OH)2D can be overcome at high precursor concentration.
The Effect of Indomethacin on Vasopressin-Induced Antidiuresis in Man
Authors: Padfield P. L. , Grekin R. J. 
Published: August 2015

1. The effect of 3 days' treatment with indomethacin on the renal response to infused vasopressin was assessed in eight healthy volunteer subjects.
2. Indomethacin produced significant weight gain and an increase in serum potassium without a change in creatinine clearance.
3. Although indomethacin reduced maximum free water clearance in five subjects, the antidiuresis produced by an incremental infusion of physiological amounts of vasopressin was no different whether indomethacin had been taken or not.
4. Indomethacin, in the dose we have used, is known to reduce prostaglandin production and we therefore conclude that endogenous prostaglandins do not inhibit the effect of physiological amounts of vasopressin on water clearance, which makes it unlikely that prostaglandins are important in the day-to-day modulation of the response to vasopressin.
Comparison of Intrarenal and Extrarenal Converting-Enzyme Inhibition by SQ 20 881 on Canine Renal Blood Flow
Authors: Wong P. C. , Zimmerman B. G. 
Published: August 2015

1. Successive infusions of SQ 20 881 given intra-arterially (i.a.) to the kidney at 0.4 and 0.8 μg min−1 kg−1 for 50 min each did not alter renal blood flow and renal vascular resistance in spite of 40–47% blockade of the angiotensin I (ANG I i.a.)-induced vasoconstrictor response.
2. SQ 20 881 administered intravenously (i.v., 0.5 mg/kg) after the higher intra-arterial dose did not further decrease the renal response to ANG I (i.a.), but caused an increase in renal blood flow and a decrease in renal vascular resistance.
3. These results indicate that SQ 20 881 has limited efficacy in blocking the renal response to ANG I (i.a.). Under the conditions of these experiments, the renal vasodilator response to SQ 20 881 appears to be due to inhibition of extrarenal rather than intrarenal converting enzyme.
On the Mechanism of Plasma Cholesterol Reduction in the Rat Given Probucol
Authors: Balasubramaniam S. , Beins D. M. , Simons L. A. 
Published: August 2015

1. The effects of the cholesterol-lowering drug probucol on lipoprotein metabolism and on the key enzymes that regulate hepatic cholesterol metabolism in the rat were studied.
2. Probucol given for 2 weeks was accompanied by a significant reduction in plasma concentrations of low-density and high-density lipoproteins (LDL, HDL). The fractional catabolic rates of the apolipoproteins of HDL and LDL (apoHDL, apoLDL) were not affected by probucol, although the absolute rates of catabolism of both the apolipoproteins were significantly reduced.
3. The activities of 3-hydroxy-3-methyl-glutaryl-coenzyme A (CoA) reductase and cholesterol 7α-mono-oxygenase, as well as the rate of hepatic sterol synthesis, were unchanged during the first 2 weeks of probucol. More prolonged probucol led to inhibition of the activity of these enzymes and reduction in sterol synthesis, although the liver cellular content of cholesterol significantly increased.
4. It is postulated that a principal mode of action of the drug is to reduce the rate of lipoprotein synthesis.
Role of Prostaglandins in Bile Salt-Induced Changes in Rat Colonic Structure and Function
Authors: Rampton D. S. , Breuer N. F. , Vaja S. G. , Sladen G. E. , Dowling R. H. 
Published: August 2015

1. The role of prostaglandins in mediating bile salt-induced diarrhoea was investigated with a colonic perfusion technique in vivo in rats either untreated or pretreated with the prostaglandin (PG) synthesis inhibitor, indomethacin.
2. Colonic perfusion with sodium deoxycholate (1 and 2 mmol/l) reduced net water and sodium absorption, whereas at a concentration of 5 mmol/l it caused net fluid secretion. Deoxycholate dose-dependently increased protein and deoxyribonucleic acid (DNA) output into the perfusion fluid and, at a concentration of 5 mmol/l, produced histological evidence of colonic mucosal damage (mucus release, goblet cell depletion, patchy epitheliolysis and inflammatory cell infiltration); histological change was less with deoxycholate at 2 mmol/l and did not occur at 1 mmol/l.
3. Output of immunoreactive prostaglandin E2 (PGE2) into the colonic perfusion fluid rose eight-, 10- and 270-fold after deoxycholate at 1, 2 and 5 mmol/l respectively.
4. Colonic perfusion with added PGE2, in concentrations 10 times lower (2.8 nmol/l) and 10 times higher (0.28 μmol/l) than those found in the perfusate after deoxycholate at 5 mmol/l did not alter mucosal function or structure. However, PGE2 in much higher concentration (0.28 mmol/l) reduced net absorption of water and sodium, increased protein output threefold and, as seen with light microscopy, produced excess surface mucus with minimal goblet cell depletion and no tissue damage.
5. Pretreatment with indomethacin reduced the colonic PGE2 output of rats perfused with deoxycholate at 2 and 5 mmol/l by 56 and 87% respectively, but the bile salt-induced changes in net water and sodium transport and DNA output were not significantly affected. The PG synthesis inhibitor reduced protein loss, goblet cell depletion and surface mucus seen after perfusion with deoxycholate at 2 mmol/l, although it did not prevent the more marked structural changes caused by deoxycholate at 5 mmol/l.
6. These results suggest that in rats prostaglandins (i) are not important mediators of the deoxycholate-induced impairment of colonic water and electrolyte transport, (ii) may contribute to the mucus secretion and goblet cell depletion produced by perfusion with deoxycholate in concentrations below those causing gross tissue damage, and that (iii) overt mucosal damage is not an essential prerequisite for prostaglandin release.
Calcium Antagonists Decrease Adrenal and Vascular Responsiveness to Angiotensin II in Normal Man
Authors: Millar J. A. , McLean Kathleen , Reid J. L. 
Published: August 2015

1. The effect of the calcium antagonist nifedipine on the pressor and aldosterone responses to angiotensin II was studied in six normal subjects.
2. Blood pressure, pulse rate and plasma aldosterone, potassium and cortisol were measured during paired consecutive infusions of angiotensin II (5, 10 and 20 ng min−1 kg−1) on two separate occasions. Nifedipine (20 mg by mouth) was given, 30 min before the second set of infusions.
3. After nifedipine there were reciprocal changes in supine resting blood pressure (−7 mm Hg) and pulse rate (+18 min−1) and a significant decrease in the pressor response to angiotensin II (P &lt; 0.05; Wilcoxon signed rank test).
4. Basal levels of aldosterone were not changed by nifedipine, but the response to angiotensin II was significantly attenuated (P &lt; 0.05). Nifedipine had no effect on plasma potassium or cortisol.
5. Transmembrane movement of calcium is involved in the aldosterone response to angiotensin II in man. Calcium antagonists may lower blood pressure via decreased adrenal responsiveness to angiotensin II as well as by peripheral vasodilatation.
Sulphamidase Activity in Leucocytes, Cultured Skin Fibroblasts and Amniotic Cells: Diagnosis of the Sanfilippo a Syndrome with the Use of a Radiolabelled Disaccharide Substrate
Authors: Hopwood J. J. , Elliott Helen 
Published: August 2015

1. Sulphamidase activity was assayed by incubation of the radiolabelled disaccharide O-(α-2-sulphamino-2-deoxy-d-glucopyranosyl)-(1 → 3)-l-[6-3H]idonic acid with homogenates of leucocytes and cultured skin fibroblasts and concentrates of urine derived from normal individuals, patients affected with sulphamidase deficiency disorder [mucopolysaccharidosis type IIIA (MPS IIIA): the Sanfilippo A syndrome], parents of such patients and patients affected with other mucopolysaccharidoses and lysosomal enzyme deficiencies.
2. the assay clearly distinguished affected homozygotes from normal controls, heterozygotes and other mucopolysaccharidoses types.
3. Sulphamidase displayed remarkable thermal stability; reaction rates were constant for at least 24 h at 60°C for leucocyte and 20 h at 37°C for cultured fibroblast preparations. Apparent Km values for fibroblast sulphamidase were 71 μmol/l at 37°C and 100 μmol/l at 50°C; the corresponding Vmax. values were 21 and 71 pmol min−1 mg−1 of protein respectively. an incubation temperature of 60h°C was used for the routine assay of sulphamidase activity in leucocytes, urine and amniotic supernatant preparations. the specific activities of fibroblast and amniotic cell sulphamidase, assessed at incubation temperatures of 37°C, were more than 10-fold the leucocyte enzyme activity at 60°C.
4. We recommend the use of radiolabelled disaccharide substrate for the assay of sulphamidase in leucocytes, skin fibroblasts and urine, for the routine enzymic detection of the sulphamidase deficiency disorder of the Sanfilippo A syndrome.
Creatinine Excretion as An Index of Myofibrillar Protein Mass in Dystrophic Mice
Authors: Murray C. E. , Warnes D. M. , Ballard F. J. , Tomas F. M. 
Published: August 2015

1. Daily creatinine excretion in the urine of normal and dystrophic mice was determined and then the carcass proteins were quantitatively extracted into soluble, myofibrillar and collagenous fractions.
2. on a live body-weight basis, total carcass protein was 15% lower in dystrophic than in normal mice. Relative to carcass weight, however, the amount of protein was significantly lower only in male dystrophic mice.
3. the myofibrillar protein fraction comprised 36.3 and 32.5% of the total protein in male and female dystrophic mice and 48.8 and 45.0% respectively in normal mice. the decrease in myofibrillar protein in dystrophic mice was accompanied by an increase in the residual collagenous fraction of proteins.
4. the rate of excretion of creatinine was strongly correlated (r = +0.98) with the myofibrillar protein mass in each mouse. This relationship was the same for both normal and dystrophic mice, each gram of myofibrillar protein being associated with 3.6 μmol of creatinine excreted/day.
5. the creatinine excretion rate is a valid index of contractile muscle mass in murine dystrophy.
Time-Course of Vascular Resistance Changes in Mineralocorticoid Hypertension of Man
Authors: Wenting G. J. , Man in 'T Veld A. J. , Schalekamp M. A. D. H. 
Published: August 2015

1. Repeated measurements of blood pressure, cardiac output (99mTc-labelled albumin dilution with single-probe precordial counting of radioactivity), plasma volume and extracellular volume were made in 20 subjects exposed to mineralocorticoid excess. Patients with aldosterone-producing adenoma (n = 14) were followed for 6 weeks during the recurrence of hypertension after spironolactone treatment had been stopped. Patients with adrenal insufficiency (n = 4) were followed for 6–9 weeks after treatment with dexamethasone (1 mg daily) and fludrocortisone (0.5 mg daily) was begun. Patients with severe orthostatic hypotension due to autonomic insufficiency (n = 2) were followed for 21 and 120 weeks while treated with fludrocortisone (0.25 mg daily). Measurements were made weekly during the first 6 weeks and with longer intervals thereafter.
2. All subjects showed increments of cardiac output, stroke volume, plasma volume and extracellular volume during the first 2 weeks with little or no increase in total peripheral resistance. Mean blood pressure rose from 104 ± 3 to 126 ± 5 mmHg (mean ± sem) (P &lt; 0.001, n = 14) in that period in primary aldosteronism and from 85 ± 4 to 94 ± 6 mmHg (P &gt; 0.05, n = 6) with fludrocortisone.
3. After 6 weeks hypertension was maintained by increased resistance in nine subjects, whereas cardiac output and plasma volume had returned towards normal (mean blood pressure at the end of the study 127 ± 4 mmHg). In the remainder hypertension was maintained by increased cardiac output and expanded plasma Volume for at least 6 weeks (mean blood pressure at the end of the study 131 ± 8 mmHg). The patients with the high-resistance pattern were older (56 ± 2 years) than the patients with the high-flow pattern (34 ± 2 years) (P &lt; 0.01).
4. Mean blood pressure and extracellular fluid volume were positively correlated (r = 0.63, P &lt; 0.001, n = 161). Cardiac output was positively correlated with plasma volume (r = 0.51, P &lt; 0.001, n = 161), and total peripheral resistance was inversely correlated with the plasma volume/interstitial fluid volume ratio (r = 0.47, P &lt; 0.001, n = 161).
5. The long duration of a high-flow state and the interindividual differences in progression of high-resistance hypertension argue against a cause-and-effect relation between flow and resistance through local metabolic factors (auto-regulation) as a hypertensive mechanism in sodium loading. The results are compatible with the view that fluid-shifts between the intravascular and extravascular compartments can influence the changes in cardiac output and resistance in early and sustained hypertension due to sodium overload. Cardiac output is increased when the proportion of fluid that is retained in the intravascular compartment is relatively high, and vascular resistance is increased when that proportion is relatively low.