bluuebunny/crossref_metadata_2025_split huggingface dataset:
Noradrenaline Reactivity in Patients with Phaeochromocytoma before and after Surgical Correction
Authors: Leonetti G. , Terzoli L. , Bianchini G. , Rupoli L. , Lipira R. , Zanchetti A. 
Published: August 2015

1. For comparable blood pressures, plasma noradrenaline is disproportionately higher in patients with phaeochromocytoma than in those with essential hypertension.
2. The ‘pressor-dose’ of noradrenaline or its reciprocal, the reactivity index, were abnormal in patients with phaeochromocytoma before surgery and made normal by surgical removal of the phaeochromocytoma.
3. There was a significant correlation between blood pressures and the logarithm of plasma noradrenaline concentrations.
4. The higher dose of exogenous noradrenaline required in patients with phaeochromocytoma for a given rise in blood pressure seems to be the expression of the higher levels of endogenous noradrenaline rather than true decreased reactivity.
Differences In Utero in Activities of Catecholamine Biosynthetic Enzymes in Adrenals of Spontaneously Hypertensive Rats
Authors: Teitelman G. , Ross R. A. , Joh T. H. , Reis D. J. 
Published: August 2015

1. We sought to determine if catecholamine biosynthetic enzymes of spontaneously hypertensive rats (SHR) differed from those of normotensive Wistar—Kyoto (WKY) and Sprague—Dawley (SD) control rats before birth.
2. By immunocytochemical and biochemical methods we compared strains for the time of appearance and maturation of the enzymes tyrosine hydroylase (TH), dopamine-β-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT) in sympathetic ganglia and adrenals.
3. The time of appearance of enzymes was identical in all three strains: TH and DBH first appeared in sympathetic ganglia on embryonic day 11 (E11) and in adrenal medulla on E16. PNMT, restricted to adrenal medulla, appeared later on E18.
4. The activity of adrenal TH prenatally on E18 and E21 and at day of birth (P1) in SHR was approximately two fold that in WKY or SD rats. In contrast PNMT was lower in SHR but only on E18.
5. Thus, although the timing of the first expression of adrenergic phenotypes is similar in SHR and normotensive controls, the differences in TH activity in adrenals suggest an enhanced biosynthetic capacity for catecholamines in this strain before birth.
6. We conclude that SHR differ from normotensive rats from the first expression of some of the genes controlling catecholamine biosynthesis.
Central Dopaminergic Mechanisms in Young Patients with Essential Hypertension
Authors: Kolloch R. E. , Stumpe K. O. , Ismer U. , Kletzky O. , Dequattro V. 
Published: August 2015

1. Central dopaminergic pathways are possibly related to noradrenergic tone and may be important in the pathogenesis of essential hypertension. Basal plasma prolactin levels have been used as a marker of dopaminergic activity in the hypothalamus. The prolactin response to thyrotropin-releasing hormone (TRH) gives evidence of the dynamics of prolactin secretion.
2. To evaluate further the role of dopaminergic mechanisms in hypertension three groups of young male hypertensive patients were studied and compared with healthy male volunteers. In group 1 prolactin secretion was evaluated overnight at 60 min intervals from 22.00 to 06.00 hours. In group 2 we measured plasma prolactin concentrations before and sequentially after intravenous injection of 200 μg of TRH. In group 3 we measured prolactin, plasma and urinary noradrenaline and normetadrenaline during various degrees of physical and mental activity.
3. Basal prolactin, noradrenaline and normetadrenaline levels were higher in the hypertensive patients as compared with normotensive controls. In the hypertensive patients the prolactin response to TRH was significantly attenuated. Treatment with bromocriptine, a centrally acting dopaminergic agonist, lowered the blood pressure and suppressed the elevated prolactin and noradrenaline levels in the hypertensive patients. During bromocriptine therapy the prolactin response to TRH was not different in normotensive and hypertensive subjects.
4. These results suggest an abnormal regulation of the prolactin secretion in young hypertensive patients with evidence of increased sympathetic tone, supporting the concept that central dopaminergic mechanisms may be involved in the development or maintenance of essential hypertension.
Studies of the Biosynthesis of Renin with a Cell-Free Translation System
Authors: Dzau V. J. , Ouellette A. , Pratt R. 
Published: August 2015

1. Poly(A)+ mRNA from mouse submaxillary gland encodes a polypeptide of molecular weight 48 000 (48K polypeptide) which is abundant in the male.
2. This polypeptide is selectively absent in the translation products of mRNA from a strain of genetically renin-deficient mice C57 BL/10J.
3. The 48K polypeptide binds and co-elutes in identical fashion with pure authentic renin on pepstatin affinity chromatography.
4. Immunoprecipitation of translation products of male glandular mRNA with renin-specific antibody yielded this 48K band upon analysis by SDS/polyacrylamide gel electrophoresis and fluorography. Pure renin of molecular weight 37 000 blocked the binding of this polypeptide to antirenin antibody.
5. Mouse submaxillary gland synthesizes a renin precursor. The renin mRNA is androgenically regulated.
Specific Nuclear Binding of Angiotensin II by Rat Liver and Spleen Nuclei
Authors: Re R. N. , MacPhee A. A. , Fallon J. T. 
Published: August 2015

1. Nuclei were isolated from rat liver and spleen by a standard technique which preserved the nuclear membrane. Electron microscopy, DNA/protein ratios and 5′-nucleotidase determinations confirmed the purity of the preparation.
2. Both liver and spleen nuclei specifically bound 125I-labelled angiotensin II (ANG II) with high affinity (Kd ≅ 1.0 nmol/l). Saralasin ANG III and ANG II competed with tracer for ligand whereas ANG I did so less effectively and neurotensin not at all.
3. These results suggest the presence of specific nuclear intracellular ANG II receptors and raise important questions regarding the mechanism of action of this peptide.
Blood Pressure and the Renin—Angiotensin—Aldosterone System
Authors: Ljungman S. , Aurell M. , Hartford M. , Wikstrand J. , Berglund G. 
Published: August 2015

1. The relationships between blood pressure and the components of the renin-angiotensin-aldosterone system were studied in 49-year-old men (n = 120) who were selected at random from the total population so as to be representative of all blood pressure levels.
2. Only plasma aldosterone concentration was significantly correlated with blood pressure, both in the whole study group (r = 0.22; P &lt; 0.02) and in the hypertensive blood pressure range (r = 0.36; P &lt; 0.02). The hypertensive subjects had a significantly higher plasma aldosterone concentration than the borderline and normotensive subjects.
3. Multiple regression analysis including factors related to the renin—angiotensin—aldosterone system, showed that the 24 h urinary excretion of noradrenaline was the factor most strongly correlated to. plasma aldosterone.
4. The findings indicate that aldosterone may be the most important component of the renin—angiotensin—aldosterone system in the development and maintenance of essential hypertension.
Effects of the Oral Angiotensin-Converting Enzyme Inhibitor MK-421 in Human Hypertension
Authors: Gavras H. , Biollaz J. , Waeber B. , Brunner H. R. , Irene Gavras , Sackel H. , Charocopos F. , Davies R. O. 
Published: August 2015

1. The effects of the new oral angiotensin-converting enzyme (ACE) inhibitor MK-421 on blood pressure, plasma renin activity, angiotensin II, aldosterone and converting enzyme activity were assessed in 16 hypertensive patients followed for 6–18 weeks.
2. After an initial titration period, maintenance doses of 2.5–40 mg once daily produced satisfactory blood pressure control in 11 and a partial but significant decrease in the remainder.
3. Treatment was associated with no change in heart rate and no orthostatic hypotension. At 24 h after the first effective dose, blood pressure was still decreased, plasma ACE was suppressed to 16% of the baseline, plasma angiotensin to 58%, aldosterone to 42%, and plasma renin activity was elevated to 228% of the baseline.
4. Magnitude of blood pressure fall was significantly correlated with the height of pretreatment blood pressure but not with baseline levels of plasma renin activity.
Vasodepressor Effects of Arachidonic Acid and Prostacyclin (PGI2) in Hypertensive Rats
Authors: Dusting G. J. , Di Nicolantonio R. , Drysdale T. , Doyle A. E. 
Published: August 2015

1. Vasodepressor responses to prostacyclin and nitroprusside were compared in anaesthetized, spontaneously hypertensive rats of the Okamoto strain and Wistar—Kyoto controls, and also in one-kidney, one-clip hypertensive rats and unilaterally nephrectomized controls of the Sprague—Dawley strain. The responses, measured as a percentage of resting blood pressure, did not differ significantly between the hypertensive rats and the normotensive controls within each strain.
2. The effects of intravenous injections of arachidonic acid were also studied in each strain.
3. The vasodepressor effects of high doses of arachidonic acid (1 or 3 mg/kg) were much greater and more prolonged in both groups of hypertensive rats. These differences were abolished by indomethacin (2 mg/kg).
4. Comparisons between the strains showed that whereas Okamoto rats have significantly greater depressor responsiveness to nitroprusside and prostacyclin than Sprague—Dawley rats, the depressor effects of high doses of arachidonic acid (1 and 3 mg/kg) were smaller in the normotensive Wistar-Kyoto than in the Sprague—Dawley rats.
5. It is concluded that hypertensive rats have enhanced ability to transform exogenous arachidonic acid into vasodilator prostanoids. This occurs both in spontaneous hypertension and in experimental renal hypertension. However, rats of the Okamoto strain appear to have reduced ability to form prostacyclin when compared with Sprague—Dawley rats.
Central Haemodynamics and Plasma Prostaglandin E2 in Borderline and Sustained Essential Hypertensive Patients before and after Indomethacin
Authors: Safar M. E. , Hornych A. F. , Levenson J. A. , Simon A. Ch. , London G. M. , Bariéty J. L. , Milliez P. L. 
Published: August 2015

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 ± 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 ± 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 ± 1.4 pg/ml).
2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions.
3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index.
4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients.
5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment.
6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.
Association between the C3F-Gene and Essential Hypertension
Authors: Schaadt O. , Sørensen H. , Krogsgaard A. R. 
Published: August 2015

1. The complement 3 (C3) phenotype distribution in 112 patients with essential hypertension was compared with the distributtion in 316 normotensive control subjects.
2. A significant increased frequency of the C3F-gene was found among the patients (0.2637 vs 0.1721, P = 0.0031), indicating an association between the C3F-gene and essential hypertension.
3. The relative risk of essential hypertension was calculated to be 1.90 for C3F-positive individuals.
4. The association between the C3F-gene and essential hypertension was stronger among the untreated patients, where a relative risk of 3.89 was found for C3F-positive subjects.
5. A significant negative correlation was found between the C3F-positivity and the severity of the hypertensive disease estimated by eye ground changes. This might be in accordance with a negative natural selection of C3F-positive hypertensive patients.
6. The study supports the hypothesis that immunogenetic factors may be of pathogenetic importance in essential hypertension.
Anger, Anxiety, Guilt and Increased Basal and Stress-Induced Neurogenic Tone: Causes or Effects in Primary Hypertension?
Authors: Sullivan P. A. , Procci W. R. , DeQuattro V. , Schoentgen Sarah , Levine D. , Van Der Meulen J. , Bornheimer J. F. 
Published: August 2015

1. Basal plasma and spinal fluid noradrenaline were increased in patients with primary hypertension and phaeochromocytoma compared with normotensive patients (P &lt; 0.01).
2. Patients with primary hypertension had more anger (P &lt; 0.01), anxiety (P &lt; 0.01) and guilt (P &lt; 0.05) than normotensive patients or patients with phaeochromocytoma.
3. The responses of noradrenaline and adrenaline concentrations were similar after mental and isometric stress in primary hypertensive and normotensive subjects.
4. However, after mental stress and isometric exercise there were increased responses of plasma noradrenaline and systolic blood pressure respectively, in patients with high anxiety and anger compared with those below the 50th percentile (P &lt; 0.05).
5. Increased central and peripheral neurogenic tone at rest and after stress in association with increased anxiety and suppressed anger appear to be pathogenic factors in some patients with primary hypertension and may not be a result of the blood pressure elevation.
Response of Patients with Renal Involvement by Progressive Systemic Sclerosis to Antihypertensive Therapy
Authors: Traub Y. M. , Shapiro A. P. , Osial T. A. , Rodnan G. P. , Medsger T. A. , Leb D. E. , Christy W. C. 
Published: August 2015

1. Renal involvement in progressive systemic sclerosis is characterized by hypertension, grade III or IV hypertensive retinopathy, rapidly progressive renal failure and enhanced plasma renin activity.
2. Of 70 patients with progressive systemic sclerosis involving the kidneys seen since 1955, 48 died within less than 3 months and 16 are alive or survived longer than 1 year.
3. Aggressive antihypertensive therapy was the principal factor that prevented early death in the 16 survivors.
4. Angiotensin converting enzyme inhibition with captopril appears to be the treatment of choice at present, but methyldopa or minoxidil may be successful in certain patients whose response to captopril is not satisfactory.
The Hypotensive Effect of Propranolol in Captopril-Treated Patients Does Not Involve the Plasma Renin—Angiotensin—Aldosterone System
Authors: Staessen J. , Fagard R. , Lijnen P. , Verschueren L. J. , Amery A. 
Published: August 2015

1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril—placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg.
2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration.
3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in the plasma aldosterone concentration or in the urinary aldosterone excretion.
The Effect of Oral Prazosin on Blood Pressure and Plasma Concentrations of Renin and Angiotensin II in Man
Authors: McAreavey D. , Cumming A. M. M. , Sood V. P. , Leckie B. J. , Morton J. J. , Murray G. D. , Robertson J. I. S. 
Published: August 2015

1. We studied the effect of oral prazosin on blood pressure, plasma active renin and angiotensin II in 16 recumbent hypertensive patients between 09.00 and 12.00 hours.
2. In untreated patients there were no significant changes in blood pressure, plasma active renin or angiotensin II during the 3 h period.
3. After an initial dose of prazosin (2 mg) there was a significant fall in recumbent blood pressure with progressive increases in plasma active renin and angiotensin II concentrations.
4. After 3–4 weeks' treatment with oral prazosin only, recumbent blood pressure at 09.00 hours, 15 h after the last dose of prazosin, was significantly lower than before treatment, but plasma active renin and angiotensin II were not significantly different from untreated values.
5. After the usual morning dose of prazosin, blood pressure did not change, but there were significant rises in plasma active renin and angiotensin II, less marked than after the first dose of prazosin.
6. Prazosin therefore stimulates the renin—angiotensin system acutely, both after the initial dose and during long-term therapy; however, no effect on renin and angiotensin II is apparent 15 h after the last dose of prazosin.
Fibrin Deposition in the Kidney and Renal Blood Flow during Intravascular Coagulation in the Rat: Influence of the Renin–Angiotensin System
Authors: Ståhl E. , Karlberg B. E. , Rammer L. 
Published: August 2015

1. Intravascular coagulation in the kidneys of rats was induced by intravenous infusion of thrombin and by inhibition of fibrinolysis with tranexamic acid under α-chloralose anaesthesia. The amount of fibrin in the kidneys was measured with radioactively labelled fibrinogen. Chronic saline loading and inhibition of angiotensin II (ANG II) with saralasin reduced the fibrin deposition in the kidneys. Infusion of ANG II had the opposite effect.
2. Renal and aortic blood flows were measured by injection of radioactively labelled microspheres. After thrombin infusion the renal and aortic blood flows were reduced to about one-third of the pre-infusion values. Chronic saline loading diminished these changes, but saralasin had no effect.
3. Plasma renin activity (PRA), measured by radioimmunoassay, decreased by about 50% after thrombin infusion.
4. The reduction in PRA and the lack of effect of saralasin indicate that the renin—angiotensin system is not the mediator of the observed decrease in the renal blood flow. As saralasin reduced the amount of fibrin the mechanism regulating fibrin deposition appears to be independent of the mechanism that reduces the renal blood flow.
Effect of Noise on Blood Pressure and ‘Stress’ Hormones
Authors: Andrén L. , Lindstedt G. , Björkman M. , Borg K. O. , Hansson L. 
Published: August 2015

1. Noise stimulation (95 dBA) for 20 min caused a significant increase in diastolic (12%, P &lt; 0.001) and mean arterial pressure (7%, P &lt; 0.001) in 15 healthy normotensive male subjects.
2. There was no significant change in systolic blood pressure or heart rate during exposure to noise.
3. Adrenaline, noradrenaline, prolactin, cortisol and growth hormone concentrations in venous plasma were not affected during noise stimulation.
Sulphydryl Oxidation in the Mechanism of Molecular-Weight Conversion of Renin in Dog Kidney
Authors: Ikemoto Fumihiko , Takaori Kazuo , Iwao Hiroshi , Yamamoto Kenjiro 
Published: August 2015

1. A high-molecular-weight renin (Mr 60 000) was formed by the reaction of a low-molecular-weight renin (Mr 40 000) with a renin-binding substance in canine renal cortical extract in the presence of the sulphydryl (SH) group oxidizing agent potassium tetrathionate; thus the reaction required SH oxidation.
2. Renin extracted from isolated renin granules was adsorbed on to thiopropyl Sepharose 6B, and then liberated with dithiothreitol (50 mmol/l), indicating that it possessed on SH moiety(s).
3. However, the renin was capable of reaction with the renin-binding substance even after its SH moiety (or moieties) was protected with 5,5′-dithiobis-(2-nitrobenzoic acid).
4. The high-molecular-weight renin was converted into the low-molecular-weight renin by incubation (37°C, 15 min) with cytosol (soluble fraction) of renal cortex and liver. Such converting ability was diminished after the cytosol was treated with perchloric acid or potassium tetrathionate.
5. These results suggest that the reaction of renin with the renin-binding substance does not require disulphide bond(s) and that an enzymelike substance which is sensitive to SH oxidation is involved in the conversion from the high-molecular-weight renin into the low-molecular weight renin.
Diagnostic Enzymology of a-L-Iduronidase with Special Reference to a Sulphated Disaccharide Derived from Heparin
Authors: Hopwood J. J. , Muller Vivienne 
Published: August 2015

1. Iduronosyl anhydro[1-3H]mannitol 6-sulphate (IMs), iduronosyl anhydro[1-3H]mannitol, phenyl iduronide (PhI) and 4-methylumbelliferyl iduronide have been compared as substrates for the diagnostic estimation of α-l-iduronidase activity present in human leucocyte and cultured skin fibroblast homogenates. The pH profile of leucocyte and fibroblast iduronidase activity was dependent on substrate structure and concentration, the ionic strength and the nature of the buffer ion used in the assay mixture.
2. NaCl, KBr and Na2SO4 were shown to be parabolic competitive inhibitors of IMs activity, the K1 with fibroblast homogenates being 34, 13.4 and 0.22 mmol/l respectively. NaCl and KBr were shown to have a primary salt effect on the interaction between enzyme and substrate but Na2SO4 appeared to have a specific ion effect at a cationic binding site.
3. NaCl inhibited the hydrolysis of IMs at all pH values studied, whereas NaCl concentrations of 0.2 mol/l inhibited the hydrolysis of PhI at pH values below 3.8 but activated the enzyme at higher incubation pH values.
4. Cu2+ was shown to be a potent non-competitive inhibitor of IMs enzyme activity with an apparent Kl, of approximately 0.02 mmol/l. The enzyme activity was inhibited by Fe2+ (Kl 4 mmol/l), Hg2+ and Ag+, but has not significantly been affected by other univalent or bivalent cations.
5. The presence of solvent and salt effects on apparent Km but not the Vmax. suggest that the binding of IMs to the enzyme involved charge neutralization, and it is inferred that two cationic binding sites are present at the active site. It is postulated that one site specifically binds to the iduronic acid carboxyl group, the other to the 6-sulphate of the anhydromannitol moiety.
Factors Influencing Hepatic Glutathione Concentrations: A Study in Surgical Patients
Authors: Shi E. C. P. , Fisher R. , McEvoy Maeve , Vantol Rebecca , Rose Margaret , Ham J. M. 
Published: August 2015

1. Hepatic total glutathione (reduced plus oxidized) and oxidized glutathione levels were measured in operative wedge liver biopsy specimens obtained from 70 patients.
2. The effects on hepatic reduced glutathione (GSH) level of four potential risk factors (abnormal liver histology, abnormal preoperative tests of liver function, drug ingestion and protein malnutrition) were examined.
3. Each of the four risk factors was associated with a significant reduction in hepatic GSH. Multivariate analysis indicated that only three of these risk factors (abnormal liver histology, drug ingestion and protein malnutrition) had independent effects in reducing hepatic GSH.
4. Twenty-five of the 70 patients studied did not have any of the four risk factors. The mean hepatic GSH level in these patients was 3.92 μmol/g of liver wet weight (sd 0.62), giving a 95% reference range of 2.71–5.14 μmol/g of liver wet weight.