bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of pindolol on plasma renin activity in patients with essential hypertension
Authors: TÉNYI I. , NÉMETH M. , JÁVOR T. , NEMES J. , CZIMER J. 
Published: March 2008

Abstract. Twenty‐two patients with essential hypertension were treated for 3 months with pindolol, and blood pressure and plasma renin activity were measured at rest and after stimulation (upright posture stimulation and insulin induced hypoglycaemia stimulation).Beta‐receptor blockade produced a significant decrease in systolic and diastolic blood pressure.After treatment with pindolol the plasma renin activity was significantly lower. Under conditions of renin stimulation such as orthostasis and insulin produced hypoglycaemia, plasma renin activity was significantly lower in treated patients.There was no correlation between the fall of plasma renin activity and the decrease of blood pressure. Renin suppression is probably only one of the factors involved in the reduction in the blood pressure in these patients.
The effect of beta‐adrenergic blockade on patterns of urinary sodium excretion, blood pressure and plasma renin activity in patients with essential and renovascular hypertension
Authors: SALVETTI A. , SASSANO P. , POLI L. , PEDRINELLI R. , ARZILLI F. 
Published: March 2008

Abstract. The effects of β‐adrenergic blockade, using oxprenolol, were studied on plasma renin activity, urinary sodium excretion and blood pressure in ten normal subjects and in 120 patients with essential and renovascular hypertension.Blood pressure was reduced by oxprenolol administration. The hypotensive action of the drug was independent of either the basal plasma renin activity or of the plasma renin activity response.Oxprenolol decreased plasma renin activity in normal subjects and in patients with essential hypertension with normal or high basal plasma renin activity. Patients with low plasma renin activity may show a lack of response to the beta‐blockade.In patients with renovascular disease the response of plasma renin activity to oxprenolol was not a discriminant factor between patients cured or not cured by surgery. Some renovascular patients were unresponsive to beta‐blockade with oxprenolol.
Adrenaline‐sensitive adenylate cyclase of human fat cell ghosts: properties and hormone‐sensitivity
Authors: KATHER HORST , GEIGER MAGDALENE 
Published: March 2008

Abstract. Some of the properties of the human fat cell adenylate cyclase were studied in fat cell ghosts prepared from subcutaneous adipose tissue of twenty‐three patients. Under standard assay conditions (1 mmol/l ATP, 5 mmol/l mg2+, pH 8.5), the basal activity ranged from 0.6 nmol to 4.4 nmol of 3′,5′‐cyclic AMP formed per mg protein per 15 min.Peptide hormones (ACTH, glucagon) were ineffective in stimulating adenylate cyclase. Adrenaline, however, induced a 1.5–5‐fold enhancement of 3′‐5′‐cyclic AMP formation.The rates of basal and hormone‐stimulated enzymic activity were maximal at pH 8.5. The relative extent of hormonal stimulation, however, was greater at pH 7.4.ATP in excess of magnesium had an inhibitory effect on basal and hormone‐stimulated enzymic activity. Magnesium in excess of ATP caused a concentration‐dependent increase of both expressions of enzymic activity.Of the guanine nucleotides, GTP (0.1 mmol/l) augmented hormone sensitivity via a preferential inhibition of basal activity. 5′‐Guanylyl‐imidodiphosphate, however, caused a 2–5‐fold increase of basal and adrenaline‐stimulated activities.The results show that human fat cell ghosts contain an adrenaline‐sensitive adenylate cyclase system, whose hormone sensitivity is profoundly influenced by ATP, magnesium ions, pH, and guanine nucleotides. Artificial cofactors such as 5′‐guanylyl‐imidodiphosphate or α‐blocking agents are not essential for the expression of hormone sensitivity.
Renin levels and spironolactone treatment in general practice: similar blood pressure lowering effect of spironolactone in low and normal renin patients
Authors: SUNDSFJORD J. A. , ØDEGAARD A. E. 
Published: March 2008

Abstract. We examined the predictive value of plasma renin activity (PRA) in ambulatory patients in the selection of hypertensive patients for treatment with spironolactone. The patients were classified as frusemide responders or non‐responders according to their PRA response to 80 mg frusemide orally.After an initial 4 weeks placebo period forty‐five patients with the clinical diagnosis of benign hypertension (WHO stage I‐II) entered a 4 × 4 week double blind treatment period during which they received spironolactone (Aldactone®) 400, 300, 200 and 100 mg/day, respectively.Five out of the forty‐five patients who started the trial were withdrawn on account of side‐effects and five patients for other reasons. Of the thirty‐five patients who completed the study eighteen belonged to the group of non‐responders to frusemide, seventeen to the responders.A gradual and significant decrease in mean blood pressure occurred during the period with the high doses of spironolactone, without any significant difference between the groups. The blood pressure lowering effect obtained with the initial high doses was maintained during the consecutive periods when the doses was reduced to a half or even a fourth, in both groups.We conclude that PRA measurement in ambulatory patients is of little, if any, value for the selection of hypertensives for spironolactone treatment; this in contrast to similar selections performed on hospitalized patients.
Thyroid hormone concentrations and inhibition of thyroid stimulating hormone secretion in euthyroid subjects with autonomous thyroid nodules
Authors: CARPI A. , BIANCHI R. , ZUCCHELLI G. C. , TONI M. G. , COLI A. , LEVANTI C. , MARIANI G. 
Published: March 2008

Abstract. Sixty‐four euthyroid patients with autonomous thyroid nodules and normal thyroxine (T4) concentrations and tri‐iodothyronine resin uptake have been studied. The serum tri‐iodothyronine (T3) concentration of the patients was 2.24 (±0.67) ng/ml, significantly higher than in a group of fifty‐seven euthyroid control subjects (1.58 ± 0.30 ng/ml). When no extranodular tissue was visible on the basal thyroid scan, the T3 was 2.31 (±0.63) ng/ml, significantly higher than in patients with some extranodular uptake on the basal scan (1.91 ± 0.42 ng/ml). There was no significant difference in the serum T4 concentrations of the patients (7.37 ± 2.10 μg/100 ml) compared to the control group (6.88 ± 1.89 μg/100 ml). The T4 concentrations were not correlated with total or partial inhibition of the extranodular tissue. The thyroid hormone concentrations were not directly correlated to the size of the nodule assessed by scan imaging. The thyroid stimulating hormone (TSH) concentration of the patients (1.52 ± 0.38 μU/ml) was significantly lower than in normals (2.49 ± 0.96 μU/ml). No significant difference was found in the TSH concentrations of patients with partial or total inhibition of extranodular tissue irrespective of the T3 concentration. A thyrotrophin releasing hormone stimulation test in twelve patients did not increase the serum TSH, irrespectively of the T3 concentration.These data show the high frequency of elevated serum T3 concentrations despite normal serum T4 concentration in euthyroid patients with autonomous thyroid nodules. They confirm that inhibition of TSH secretion can occur when thyroid hormone concentrations are in the normal range.
Effects of the angiotensin II antagonist 1‐sar‐8‐ala‐angiotensin II in hypertension in man
Authors: FAGARD R. , AMERY A. , LIJNEN P. , REYBROUCK T. 
Published: March 2008

Abstract. The angiotensin II antagonist 1‐sar‐8‐ala‐angiotensin II (saralasin) was infused in forty‐six patients with hypertension of various aetiology (essential, renal arterial or parenchymal disease, primary hyperaldosteronism), before and/or during sodium volume depletion obtained by chlorthalidone and low sodium diet. When saralasin was infused in twenty‐five patients ingesting 130 mmol of sodium per day, including patients with proven renovascular hypertension, the changes in mean arterial pressure ranged from +10 to ‐7 mmHg (mean: +0.20 mmHg) and were not related to the plasma renin concentration (PRC) (r= ‐0.11). During sodium volume depletion, saralasin induced changes in mean arterial pressure, ranging from +21 to ‐76 mmHg, which were closely related to log PRC (n= 32; r= ‐0.87). Combined sodium depletion and antagonism of angiotensin II ‘normalized’ mean arterial pressure (≤100 mmHg) in twenty‐one of the thirty‐two patients, while pressure remained between 106 and 147 mmHg in eleven ‘poor’ responders, so that pressor mechanisms other than sodium volume and angiotensin must be responsible for the remaining elevation of pressure in these patients.The study indicates that arterial pressure is not dependent on the immediate pressor effects of angiotensin II in sodium replete patients, and in sodium deplete subjects whose PRC remains low, while it is at least partly angiotensin II dependent during sodium volume depletion in the others. The results cast doubts on the clinical usefulness of saralasin in the investigation of patients with hypertension, when studied in the conditions of the present study.
The role of adrenaline and of the vagus in gastrin release and acid secretion in dogs
Authors: BRANDSBORG O. , ØRNSHOLT J. , BRANDSBORG M. , CHRISTENSEN N. J. 
Published: March 2008

Abstract. Serum gastrin, gastric acid secretion and plasma adrenaline in response to intravenous injection of 2‐deoxy‐D‐glucose and to insulin were measured in six dogs with gastric fistulae before and after denervation of the antrum and the intestine (antral‐intestinal vagotomy). Serum gastrin and gastric acid secretion were also measured in the same dogs during intravenous infusion of adrenaline in doses which produced an elevation of plasma adrenaline to levels occurring during hypoglycaemia and after the injection of 2‐deoxy‐D‐glucose.Antral‐intestinal vagotomy reduced basal gastrin concentration slightly and basal gastric acid secretion considerably. The rise in serum gastrin in response to 2‐deoxy‐D‐glucose and hypoglycaemia was abolished while the increase in gastric acid secretion was reduced after antral‐intestinal vagotomy. Beef meal‐stimulated gastrin secretion was the same before and after vagotomy. Intravenous infusion of adrenaline had no effect on either serum gastrin or gastric acid secretion.It is concluded that in the dog, in contradistinction to man, gastrin release after insulin is dependent on an intact vagus. Release of gastrin by adrenaline in the dog does not appear to be physiological since it is not achieved by the amount of adrenaline released in response to hypoglycaemia.
Urinary kallikrein and changes in endogenous aldosterone in the rat
Authors: MIMRAN ALBERT , BAUDIN GÉRARD , CASELLAS DANIEL , SOULAS DOMINIQUE 
Published: March 2008

Abstract. Urinary kallikrein excretion was studied during changes in sodium intake. The effect of short‐term (5 days) and long‐term (4 weeks) sodium restriction was also investigated. In order to provide additional evidence for a primary role of endogenous aldosterone on the renal kallikrein system, the effect of dietary potassium restriction was studied in chronically sodium depleted rats.

Chronic (4 weeks) sodium restriction was associated with high urinary kallikrein excretion (6.21 ± 0.31 i.u./24 h/100 g body weight). Urinary kallikrein was lower in high salt and normal salt rats (2.38 ± 0.18 and 2.71 ± 0.18 i.u./24 h/100 g bw). A negative correlation (r= ‐0.88, P<0.001) between urinary kallikrein and the logarithm of natriuresis was obtained.
Positive correlations between urinary kallikrein and diuresis were obtained within each group of rats equilibrated with different sodium intakes.
When chronically sodium loaded rats were given a low sodium diet for a 5‐day period, urinary kallikrein increased from 1.99 ± 0.17 to 3.64 ± 0.3 i.u./24 h/100 g bw (P<0.001). The mean value achieved after 5 days of sodium restriction was significantly lower (P<0.001) than the value obtained in long‐term (4 weeks) sodium depleted rats.
When low sodium rats were fed a low sodium‐low potassium diet for 7 days, urinary kallikrein decreased by 34 ± 8% (P<0.005) and urinary aldosterone fell from 112 ± 27 to 43 ± 11 ng/24 h (P<0.01). Natriuresis remained constant throughout the study.

These results suggest that endogenous aldosterone is one of the main determinant of renal kallikrein activity. Kallikrein may participate in the regulation of water excretion. In addition, the kallikrein‐kinin system may be involved in the renal adaptation to long‐term sodium restriction in the rat.
Effects of prostaglandin‐E1 on ST segment elevation and regional myocardial blood flow during experimental myocardial ischaemia in dogs
Authors: RIEMERSMA RUDOLPH A. , TALBOT RICHARD C. , UNGAR ALEX , MJØS OLE D. , OLIVER MICHAEL F. 
Published: March 2008

Abstract. The effects of prostaglandin E1 (PGE1) on myocardial ischaemia (as measured by epicardial ST segment changes), myocardial flow and substrate exchange has been studied in dogs. Myocardial ischaemia was induced by intermittent external clipping of a branch of the left anterior descending coronary artery.During occlusion with a continuous intravenous infusion of isoprenaline, elevated epicardial ST segments (∑ST), were raised to 46 ± 6 mV (mean ± SEM). Pretreatment with PGE1 reduced ∑ST to 34 ± 6 mV (P<0.001), but had no effect on mean aortic blood pressure (AP¯) or on regional myocardial blood flow. Isoprenaline infusion increased plasma free fatty acids (FFA) to 1925 ± 150 μmol/l and this was reduced to 1320 ± 220 μmol/l by PGE1 (P<0.005).During occlusion without isoprenaline, PGE1 did not effect ∑ST or plasma FFA when infused intravenously or into the left atrium. Mean aortic blood pressure decreased from 131 ± 7 to 108 ± 10 (PGE1 i.v.) or 109 ± 8 mmHg (PGE1 i.a.) (P<0.001). This was associated with a decrease in regional myocardial blood flow, both in the ischaemic and non‐ischaemic myocardium. However, when blood pressure was maintained constant, intravenous PGE1 tended to decrease occlusion‐induced ST segment elevation.These results suggest that PGE1 can reduce isoprenaline‐stimulated myocardial ischaemia through its antilipolytic action but in the absence of catecholamine stimulation the main effect is to reduce blood pressure thereby counterbalancing any potentially beneficial effects on the ischaemic myocardium.
Studies on the degradation of lipoprotein‐X
Authors: PATSCH W. , PATSCH J. R. , KUNZ F. , SAILER S. , BRAUNSTEINER H. 
Published: March 2008

Abstract. Three patients suffering from prolonged obstructive jaundice were studied after surgical removal of biliary obstruction. Four days after surgery the initial cholesterol esterification rate in the plasma rose from very low activities to values three to four times higher than those found in normal subjects. During this time lipoprotein‐X decreased in concentration. The initial cholesterol esterification rate returned to normal values when plasma lipids and lipoproteins reached normal levels.During incubation of normal plasma with lipoprotein‐X, changes in the lipid composition of the incubation mixture were observed which appeared to be catalysed by lecithin:cholesterol acyltransferase. The formation of esterified cholesterol and lysophosphatidylcholine exceeded that of control experiments when lipoprotein‐X was replaced by buffer solution in the incubation mixture. Lipoprotein‐X disappeared as monitored by electrophoresis on agar and measured after zonal ultracentrifugation, and lipoproteins with flotation behaviour of high density lipoprotein2, enriched in polar lipids, appeared.When plasma was incubated separately with lipoprotein‐X1 and lipoprotein‐X2in vitro, the T1/2 of these lipoproteins were 24 h and 9 1/2 h, respectively. Addition of lipoprotein‐X2 to normal plasma resulted in an increased initial cholesterol esterification rate with a sigmoidal response curve. Lipoprotein‐X1 increased the initial cholesterol esterification rate also but to a lesser extent.Our findings indicate that incubation of normal plasma with lipoprotein‐X results in the disappearance of this abnormal lipoprotein and the appearance of a high density lipoprotein2‐like particle mediated by enzymic cholesterol acyltransfer.
Free fatty acid and carbohydrate metabolism of the working forearm muscle in type IV hyperlipoproteinaemia
Authors: OLSSON ANDERS G. , EKLUND BRITA , RICCARDI GABRIELE , WALLDIUS GÖRAN , KAIJSER LENNART 
Published: March 2008

Abstract. Substrate utilization of the working forearm was studied in nineteen patients with hypertriglyceridaemia (HLP) and compared to nineteen normolipidaemic (NLP) subjects, matched with regard to body weight, body height, intravenous glucose tolerance and age. Arterial‐deep venous differences of oxygen, carbon dioxide, free fatty acids (FFA), glucose, lactate and pyruvate was measured. The fractional extraction and oxidation of fatty acids was assessed by intravenous infusion of albumin‐bound [3H]palmitate and [14C]oleate. Measurements were made both in the postabsorptive state and after plasma FFA lowering by nicotinic acid.The HLP subjects had, before nicotinic acid, higher arterial concentrations, higher turnover rates of palmitate and oleate and higher plasma glycerol concentrations indicating a greater mobilization of FFA. However, the forearm extraction and oxidation of FFA as well as the calculated total body fatty acid oxidation was similar in HLP and NLP subjects. Nicotinic acid decreased arterial concentrations and turnover rates of FFA to the same extent in HLP and NLP groups, the effect being the same for palmitic and oleic acid. Fractional extraction both of palmitic and of oleic acid increased after nicotinic acid in the NLP but not in the HLP group. Plasma glycerol decrease after nicotinic acid was of the same magnitude in HLP and NLP groups.Thus, (1) an increased uptake of FFA in HLP subjects must occur in other tissues than skeletal muscle and with another fate of the fatty acids than oxidation. The explanation might be an increased incorporation of fatty acids into triglycerides which are subsequently secreted from the liver. (2) The impaired triglyceride removal in skeletal muscle which has been found in HLP subjects is more likely due to an impaired lipolytic activity than to an abnormality in uptake and utilization of hydrolysed fatty acids.No abnormalities in carbohydrate metabolism were found in these HLP subjects with normal glucose tolerance.
Metabolic and hormonal changes after surgery: hyperinsulinaemia during glucose infusion
Authors: SOERJODIBROTO W. S. , HEARD C. R. C. , JAMES W. P. T. , FEW J. D. , BLOOM S. R. 
Published: March 2008

Abstract. Serial measurement of blood and urinary hormones and metabolites were made on eleven patients before and after abdominal surgery. A complete nitrogen balance on three patients showed that after the operation there was a net loss of nitrogen equivalent to about 50 g protein per day for 5–6 days.This period coincided with elevated fasting plasma levels of glucagon and non‐esterified fatty acids (NEFA), and elevated 24 h urinary excretion of free cortisol and 17OH‐corticosteroids; total plasma amino acid levels were diminished but the concentrations of the branchedchain amino acids were increased. Fasting plasma concentrations of glucose, insulin and cortisol were increased only on day 1 after the operation. A 2 h glucose infusion (0.35 g kg‐1 h‐1) was carried out on each patient on day 1 and on ‘recovery’ (9–21 days). The mean glucose levels reached (12.1 mmol and 10.3 mmol/l, respectively) did not differ significantly; they were much higher than in young normal subjects (6.1 mmol/l). Glucose infusions, both on day 1 and on ‘recovery’ resulted in significant depression of glucagon and NEFA levels. Plasma insulin levels during glucose infusion were significantly higher on day 1 than on ‘recovery’, suggesting improving sensitivity to insulin. Possible explanations are discussed. Attention is drawn to the practical implications of the choice of nutrients in the parenteral nutrition of postoperative patients.
Enhanced sympathetic nervous activity after intravenous propranolol in ischaemic heart disease: plasma noradrenaline splanchnic blood flow and mixed venous oxygen saturation at rest and during exercise
Authors: HANSEN JØRGEN FISCHER , HESSE BIRGER , CHRISTENSEN NIELS JUEL 
Published: March 2008

Abstract. To study the mechanisms by which acute beta‐adrenergic blockade may change the activity of the sympathetic nervous system we have measured haemody‐namic responses including splanchnic blood flow in twenty‐three patients with ischaemic heart disease at rest and during supine exercise before and after i.v. injection of 0.039 mmol (10 mg) dl‐propranolol.After propranolol both at rest and on exercise blood pressure, cardiac output and heart rate decreased, while splanchnic vascular resistance increased; mixed venous oxygen saturation decreased whilst arterial oxygen saturation and oxygen uptake were unchanged. Plasma noradrenaline increased after propranolol, values correlating with mixed venous oxygen saturation and splanchnic vascuIar resistance, both at rest and during exercise before and after propranolol, only at rest was there any correlation with arterial blood pressure. The increase in sympathetic nervous activity after propranolol may be due to a reduction in cardiac output and thereby alteration of the metabolic state (oxygen or related factors) in tissues. Afferent neural signals from the tissues may play a significant role in the regulation of sympathetic nervous activity.
Serum prolactin levels in eighty patients with sarcoidosis
Authors: NAKAO KIYOHIDE , NOMA KEIZO , SATO BUNZO , YANO SABURO , YAMAMURA WICH , TACHIBANA TERUO 
Published: March 2008

Abstract. Serum prolactin levels were measured by radio‐immunoassay in eighty patihts (thirty‐four males, forty‐six females) with sarcoidosis before treatment. In twelve patients (15%) serum prolactin levels were more than two standard deviations above the mean of normal subjects. Hyperprolactinaemia was found most frequently (22%) in patients with radiological stage 11; however, 14% of patients with stage I also had elevated serum prolactin levels.In most cases serum prlactin levels fell to within the normal range after treatment with corticosteroid in parallel with improvement of intrathoracic lesions. These findings suggest that hyperprolactinaemia may be due to hypothalamic involvement by sarcoid granulomata.We conclude that the measurement of basal serum prolactin levels using radioimmunoassay is a sensitive and practical method for screening patients with sarcoidosis for hypothalmic lesions.
Magnesium metabolism in patients with coronary heart disease
Authors: BODDY K. , ROBERTSON I. , MAHAFFY M. E. , KATOCH D. S. , MURRAY R. G. , DUNN F. G. , HUTTON I. 
Published: March 2008

Abstract. 1. The oral absorption of magnesium, its myocardial uptake and exchangeable magnesium have been studied in patients with coronary heart disease and controls using the radioactive isotope magnesium‐28.2. No significant difference in oral absorption or myocardial uptake was found between patients and controls.3. The exchangeable magnesium per kg body weight was significantly lower in the patients than in the controls.