bluuebunny/crossref_metadata_2025_split huggingface dataset:
Blood Pressure and Heart Rate Responses to Centrally Administered Substance P Are Increased in Spontaneously Hypertensive Rats
Authors: Unger T. , Rockhold R. W. , Yukimura T. , Rettig R. , Ganten D. 
Published: August 2015

1. The cardiovascular effects after intracerebroventricular injections of substance P were investigated in normotensive Wistar-Kyoto and in spontaneously hypertensive rats.
2. Substance P increased blood pressure in both rat strains. Wistar-Kyoto rats responded with moderate, dose-dependent blood pressure increases, and heart rate decreased; spontaneously hypertensive rats showed two- to three-fold increased pressor effects and, concomitantly, marked heart rate increases to intracerebroventricular injections of substance P.
3. Sino-aortic baroreceptor denervation rendered Wistar-Kyoto rats supersensitive to intracerebroventricular substance P to a similar degree as unoperated spontaneously hypertensive rats. Sino-aortic denervation had no effect on the blood pressure responses to the peptide in spontaneously hypertensive rats.
4. The central pressor actions of substance P could be markedly attenuated. by intracerebroventricular pretreatment with the derivative of γ-aminobutyric acid, baclofen.
5. We conclude that the baroreceptor reflex is disturbed in spontaneously hypertensive rats. Substance P may contribute to the pathogenesis of hypertension. The effector pathways appear to be different from angiotensin.
Plasma Catecholamines and Plasma Renin Activity at Birth and during the First Days of Life
Authors: Leonetti G. , Bianchini C. , Picotti G. B. , Cesura A. , Caccamo Letizia , Marini A. 
Published: August 2015

1. Plasma noradrenaline and adrenaline concentrations and plasma renin activity were measured in 21 mothers at delivery and in their babies at birth (umbilical cord blood) and on days 1 and 5 of extrauterine life.
2. At birth plasma renin activity was significantly higher in the newborn than in mothers. Plasma renin activity increased further, but not significantly, on day 1 of life and significantly decreased on day 5. On day 5, 10 min head-up tilting caused no change in plasma renin activity.
3. Plasma noradrenaline in the newborn was higher than in mothers at birth and significantly decreased thereafter. Plasma adrenaline levels at birth were similar in the newborn and their mothers and significantly lower in the newborn in subsequent days. Tilting caused no increase in either plasma adrenaline or noradrenaline levels.
4. No correlation was found between plasma noradrenaline and adrenaline levels and plasma renin activity, or between noradrenaline, adrenaline or plasma renin activity and blood pressure.
Effects of Tonin on Vascular Smooth Muscle of the Hypertensive Rat and Normal Rabbit
Authors: Garcia R. , Schiffrin E. L. , Thibault G. , Boucher R. , Genest J. 
Published: August 2015

1. The response of arterial smooth muscle to noradrenaline was studied in one-clip hypertensive rats with or without the contralateral/kidney and in normotensive rabbits.
2. Strips of aorta from one-kidney, one-clip hypertensive animals were less responsive to noradrenaline than normotensive control rats. The contractile response of strips from two-kidney, one-clip hypertensive animals was not different from the control group. These results suggest that the mechanisms responsible for the lesser reactivity in the one-kidney hypertensive group are not a consequence of elevated blood pressure itself, but may be related to the intrinsic contractility of aortic smooth muscle.
3. Tonin potentiated the contraction induced by noradrenaline in aortic strips from hypertensive and normotensive rats. However, this effect was more important in the one-kidney, one-clip hypertensive animals. In the aortic and mesenteric strips from normal rabbits, tonin produced not only potentiation to noradrenaline but direct contraction.
4. The potentiation to noradrenaline and the direct effect of tonin were not affected by a variety of antagonists but were blocked by a calcium ion antagonist, verapamil, suggesting that tonin may act directly on vascular smooth muscle through mechanisms which might be mediated by calcium ions.
Haemodynamics of Stable Renal Transplant Recipients
Authors: Kim K. E. , Bates O. , Lyons P. , Pitone J. , Martinez E. W. , Valvo E. , Sabanayagam P. , Bower R. , Swartz C. , Onesti G. 
Published: August 2015

1. Haemodynamics, blood volume, plasma renin concentration and creatinine clearance were evaluated in 24 stable renal transplant recipients.
2. The mean cardiac index of the transplant recipients was not different from that of the normal subjects.
3. The transplant recipients comprised eight hypertensive and 16 normotensive patients. The mean cardiac index was the same in eight hypertensive and 16 normotensive patients. Thus the hypertension of stable renal transplant recipients is sustained by a high total peripheral resistance.
4. The mean blood volume, plasma renin concentration and creatinine clearance were similar in eight hypertensive and 16 normotensive patients. Therefore the hypertension of stable renal transplant recipients is not related to blood volume expansion, elevated peripheral renin or low creatinine clearance. The cause of the elevated total peripheral resistance in hypertension in stable renal transplant recipients remains to be elucidated.
Haemodynamic Changes Associatedc with Obesity and High Blood Pressure in Crats with Ventromedial Hypothalamic Lesions
Authors: Reisin E. , Suarez D. H. , Frohlich E. D. 
Published: August 2015

1. The haemodynamic and plasma volume changes associated with obesity and high blood pressure were studied in nine male rats with electrolytic ventromedial hypothalamic lesions and their paired sham-operated controls. Body weight and arterial pressure were greater in the rats with ventromedial hypothalamic lesions (565 ± 16 vs 462 ± 14 g, P&lt;0.001; 128 ± 3 vs 118 ± 3 mmHg, P&lt;0.05, respectively). Cardiac output was slightly elevated, and that portion of cardiac output distributed to the kidneys was reduced (P&lt;0.001). Plasma volume was contracted in the rats with ventromedial hypothalamic lesions (21.0 ± 0.1 vs 2.8 ± 0.1 ml/100 g, P&lt;0.001).
2. The haemodynamic characteristics of rats in which obesity and mild hypertension have been induced by electrolytic ventromedial hypothalamic lesion are similar to mild obesity essential hypertension in men.
Abnormal Left Ventricular Relaxation in Hypertensive Patients
Authors: Fouad F. M. , Tarazi R. C. , Gallagher J. H. , MacIntyre W. J. , Cook S. A. 
Published: August 2015

1. The maximum rates of left ventricular ejection and filling were derived (Fourier analysis) from the left ventricular volume curve (99mtechnetium-human serum albumin gated blood pool studies) in 12 normotensive subjects and 15 hypertensive patients of matched age groups.
2. Average values of cardiac output, ejection fraction, heart rate and left ventricular ejection rate were not significantly different in the two groups.
3. Hypertensive patients had a slower rate of left ventricular filling (P&lt;0.05), suggesting diminished left ventricular compliance in hypertension.
Effect of β-Receptor-Blocking Agents on Cardiovascular Structural Changes in Spontaneous and Noradrenaline-Induced Hypertension in Rats
Authors: Yamori Yukio , Tarazi R. C. , Ooshima Akira 
Published: August 2015

1. Continuous intravenous noradrenaline infusion for 1 week into rats by osmotic minipumps significantly increased blood pressure and left ventricular weight.
2. Concomitant α-receptor-blockade infusion significantly lowered blood pressure and the aortic weight without significant reduction in left ventricular weight.
3. Two β-receptor-blocking agents in noradrenaline-infused rats normalized left ventricular weight and significantly reduced the aortic weight, although blood pressure was still higher than control non-infused rats.
4. In 7-week-old spontaneously hypertensive rats, propranolol (perorally for 2 weeks) did not lower blood pressure but reduced significantly cardiovascular protein synthesis ([14C]lysine and [3H]uridine incorporation into non-collagen protein and RNA respectively) in both left ventricle and aorta. This effect was in contrast to hydrallazine, which normalized blood pressure but did not reduce cardiovascular protein synthesis.
5. Results suggest that β-receptors play a modulating role in the structural cardiovascular response to blood pressure.
Renal Blood Flow and Noradrenaline Secretion during Treatment with Propranolol
Authors: De Leeuw P. W. , Punt R. , Birkenhager W. H. 
Published: August 2015

1. Fifty-five patients with uncomplicated essential hypertension were admitted to hospital, where 25 of them were treated with propranolol (average daily dose 240 mg) and 30 were left untreated.
2. In all of them renal arteriography was carried out, after which procedure renal plasma flow ([123I]hippuran clearance), cortical blood flow (xenon washout) and renal noradrenaline release were measured.
3. Compared with the untreated hypertensive patients, responders to propranolol (mean blood pressure ≤ 110 mmHg) during treatment showed enhanced cortical blood flow and reduced noradrenaline secretion. Non-responders had reduced cortical flow rates, but increased noradrenaline secretion.
4. Both in the untreated group and in the propranolol-treated group an inverse relationship between arterial noradrenaline concentration and cortical blood flow was found.
5. The results indicate that sympathetic activity may be an important determinant of renal blood flow in hypertension. The effectiveness of propranolol seems to depend upon a reduction in α-adrenergic tone.
Transluminal Balloon Dilatation of Renal Artery Stenosis Causing Hypertension: 18 Months' Experience
Authors: Yune H. Y. , Klatte E. C. , Grim C. E. , Weinberger M. H. 
Published: August 2015

1. We have treated 25 patients with renovascular hypertension with balloon catheter dilatation.
2. In 17 patients, surgical treatment was thought to be either risky or difficult due to the presence of a serious medical condition or because of the peripheral location of the lesion.
3. Seventeen patients had atherosclerotic lesions, six patients had fibromuscular dysplasia and one patient had neurofibromatosis and one had stricture of an aorto-renal bypass graft.
4. Of the total group, six in the atherosclerotic group, three patients with fibromuscular dysplasia and the one with neurofibromatosis are normotensive without medications.
5. Five patients with atherosclerosis, two patients with fibromuscular dysplasia and the patient with aorto-renal bypass graft are either normotensive or have reasonable control of blood pressure with medication.
6. Four technical and treatment failures and three major medical complications were encountered. Recurrence of stenosis occurred in eight patients but none of these was in the fibromuscular dysplasia group.
Impaired Lipoprotein Lipase Activation by Uraemic and Post-Transplant Sera
Authors: Crawford G. A. , Mahony J. F. , Stewart J. H. 
Published: August 2015

1. Lipoprotein lipase was separated from normal human post-heparin plasma by affinity chromatography and assayed with a 14C-labelled triolein emulsion. No enzyme activity was detected unless whole serum was included in the assay as a source of cofactor, apolipoprotein C-II.
2. After a 10 h fast, serum obtained from 46 normal subjects, eight patients with hypertriglyceridaemia but normal renal function, patients with chronic renal failure (24 undialysed, 20 haemodialysed) and 14 recipients of renal allografts, was added to incubation medium for the assay of lipoprotein lipase to determine the maximum activation of the enzyme.
3. When serum was obtained from normal subjects, maximum activation of the enzyme correlated positively with the concentration of triacylglycerol in the sample. Neither sex nor age had a significant effect on the maximum activation achieved by serum from control subjects.
4. The maximum lipoprotein lipase-activating capacity of serum from uraemic and transplant patients was significantly reduced when compared with serum from healthy controls or from the non-uraemic hypertriglyceridaemic patients.
5. Maximum enzyme activation correlated positively with high-density lipoprotein cholesterol in serum from undialysed patients, but did not correlate positively with total serum triacylglycerols in any of the patient groups. Only in transplant recipients was there a significant inverse relationship between serum creatinine concentrations and maximum enzyme activation.
6. Although lipoprotein lipase activation was impaired in uraemic subjects and renal transplant recipients, this appeared to be due more to the presence of an inhibitor than to cofactor deficiency.
Portal Vein Prostacyclin Activity in Experimental Portal Hypertension in Rats
Authors: Hamilton G. , Rosza I. , Hutton R. , Chow F. P. R. , Dandona P. , Hobbs K. E. F. 
Published: August 2015

1. Portal hypertension was produced experimentally in rats by partial ligation of the portal vein.
2. One week later portal veins of these animals were shown to release significantly greater amounts of prostacyclin than control animals.
3. It is postulated that if this response occurs in man, local vasodilatation and inhibition of platelet aggregation may be exacerbatory factors in the severity of haemorrhage from oesophageal varices that complicate portal hypertension.
Identification of N-Monoacetylcystine in Uraemic Plasma
Authors: Gejyo F. , Ito G. , Kinoshita Y. 
Published: August 2015

1. An unidentified ninhydrin-positive substance of an acidic nature was detected in the plasma of uraemic patients. This substance was isolated from haemodialysate by ion-exchange chromatography and gel filtration, and identified as a sulphur-containing amino acid: N-monoacetylcystine.
2. The quantitative determination of sulphur amino acids in plasma revealed that the plasma levels of cysteic acid, homocysteic acid, taurine, cystine and cystathionine as well as N-monoacetylcystine in uraemic patients were markedly higher than in normal subjects (P &lt; 0.001 for each). However, the plasma levels of methionine in uraemic patients were within normal limits.
Human Parathyroid Gland Adenylate Cyclase Activity: Inhibition by 24,25-Dihydroxycholecalciferol in vitro
Authors: Cloix J. F. , Ulmann A. , Monet J. D. , Funck-Brentano J. L. 
Published: August 2015

1. Plasma membranes were prepared from parathyroid adenomas in patients with primary hyperparathyroidism and from hyperplastic glands obtained from patients with chronic renal insufficiency. The basal and isoproterenol- or sodium fluoride-stimulated adenylate cyclase activities were measured in membranes in the presence of several vitamin D3 metabolites.
2. 24,25-Dihydroxycholecalciferol (10 and 1000 pmol/l) decreased isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in membranes prepared from parathyroid glands. 1,25-Dihydroxycholecalciferol (1000 pmol/l) inhibited the isoproterenol-stimulated adenylate cyclase activity. 25-Hydroxycholecalciferol and vitamin D3 had no effect on adenylate cyclase activities. Basal adenylate cyclase activity was not affected by any of the vitamin D3 metabolites tested.
3. These results indicate that 24,25-dihydroxycholecalciferol inhibits the isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in parathyroid tissues. Such an inhibition could explain the very rapid decrease in parathyroid hormone secretion after 24,25-dihydroxycholecalciferol administration that has been previously reported.
The Role of Histamine Receptors in Asthma
Authors: Eiser Noemi M. , Mills Jane , Snashall P. D. , Guz A. 
Published: August 2015

1. Eighteen non-asthmatic and 18 asthmatic subjects underwent challenge with increasing doses of histamine from a dosimeter—nebulizer system. Half the subjects in each group were atopic and half non-atopic. Bronchial response was monitored with serial measurements of specific airways conductance (sGaw) and a dose-response curve was constructed for each challenge. In addition, the nine atopic asthmatic patients underwent antigen challenges with a similar technique. In each subject the challenges were repeated, on separate days, after intravenous injections of either sodium chloride solution (150 mmol/l: saline) placebo, chlorpheniramine (an H1-receptor antagonist), cimetidine (an H2-receptor antagonist) or after both antagonists together. Baseline bronchial tone was always comparable within subjects immediately before challenge.
2. Cimetidine had no significant effect on baseline sGaw in any group, whereas chlorpheniramine raised baseline sGaw in the asthmatic subjects. Placebo did not alter the mean dose-response curves for histamine or antigen. However, there was a small, but significant, shift of the curves to the right after cimetidine and a much larger shift to the right with chlorpheniramine, whether given alone or with cimetidine. The effect of the histamine antagonists on histamine and antigen responses was very similar and there was no difference in the pattern of response among normal subjects as compared with asthmatics or among atopic as compared with non-atopic subjects.
3. In conclusion, the same pattern of histamine receptors exists in the airways of asthmatic and normal subjects. Histamine-induced bronchoconstriction is mediated predominantly via the H1-receptors, with little, if any, contribution from the H2-receptors. Histamine appears to be an important mediator in the immediate allergic response in airways since this response is blocked by an H1-receptor antagonist.
Cardiac Function in Chronic Bronchitis: Effects of Pacing and Plasma Expansion
Authors: Valette H. , Raffestin B. , Lockhart A. 
Published: August 2015

1. We have investigated left ventricular function in 25 selected patients with chronic bronchitis by use of atrial pacing and plasma volume expansion. Nine subjects had a past history of acute respiratory failure. None had either clinical or electrocardiographic signs of coronary heart disease. Paradoxical pulse was absent, since the difference between the highest and lowest systolic arterial pressure throughout the respiratory cycle was 5.4 ± 1.5 mmHg.
2. During atrial pacing, at a mean rate of 145 ±15, about 80% of the predicted maximal rate, none of the patients showed anginal pain or ventricular repolarization abnormality. Cardiac output remained unchanged compared with control values.
3. Plasma volume expansion was achieved by intravenous injection of 1 litre of gelatin over 30 min. Cardiac output, pulmonary wedge pressure and right atrial pressure rose as reported in literature for normal subjects. In four patients cardiac output did not increase although wedge pressure and right atrial pressure did; two of these four patients also had an overshoot in pulmonary wedge pressure just after atrial pacing, suggesting left ventricular dysfunction. Three out of 25 patients had high control right atrial pressures, probably in relation to impaired right ventricular function. No paradoxical pulse occurred during plasma volume expansion. Therefore competition for space in the pericardium between ventricles was unlikely.
4. Our data suggest that left ventricular dysfunction is rare in patients with chronic obstructuve pulmonary disease. There was no significant difference between subjects with and without a past history of acute respiratory failure.
Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions
Authors: Fagard R. , Amery A. , Lijnen P. 
Published: August 2015

1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar1,Ala8]angiotensin II (saralasin) in man, saralasin was infused in subjects on a ‘normal’ sodium intake (group 1) and during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2), and in sodium-restricted subjects in whom plasma angiotensin II was suppressed by converting-enzyme inhibition with captopril (group 3).
2. The saralasin-induced increase of plasma aldosterone concentration in group 1 was different (P&lt;0.005) from the decrease in group 2, whereas saralasin produced a significant increase of plasma aldosterone in group 3. For the three groups combined the changes of plasma aldosterone were significantly related to control angiotensin II levels, but not to the 24 h urinary sodium excretion. The data suggest that it is the rise of angiotensin II in response to the sodium restriction and not the sodium restriction per se that is associated with the antagonistic action of saralasin on the adrenal receptors.
3. On average mean intra-arterial pressure at 30 min was not affected by saralasin in group 1, had decreased in group 2 and increased (P&lt;0.001) by 4.4 mmHg in group 3. Overall the changes of arterial pressure were significantly related to control angiotensin II, but not to the 24 h sodium excretion, suggesting that the angiotensin II levels predominantly determine the agonistic-antagonistic balance of saralasin's actions on arterial pressure.
4. Although saralasin did not affect plasma renin activity in group 1, plasma renin rose in group 2 and was reduced by 40% (P&lt;0.001) in group 3. For the three groups together the changes of plasma renin activity were significantly related to the changes of mean arterial pressure both on single and multiple regression analyses. The changes of pressure ‘explain’, however, only a fraction of the changes of plasma renin; it is suggested that saralasin has an agonistic effect on the renal receptors involved in the direct suppression of renin by angiotensin II in low-sodium, low-angiotensin conditions and that an antagonistic effect may contribute to the saralasin-induced rise of renin during sodium restriction with appropriate angiotensin II levels.
Effect of the Converting-Enzyme Inhibitor SQ 14 225 (captopril) in Early One-Kidney, One-Clip Hypertension in the Rat
Authors: Vandongen R. , Tunney Anne , Martinez Patricia 
Published: August 2015

1. Arterial plasma renin activity was significantly elevated in rats with one-kidney, one-clip hypertension of less than 3 weeks duration.
2. Intraperitoneal injection of the angiotensin-converting enzyme inhibitor SQ 14 225 (captopril) caused a dose-related decrease in systolic blood pressure in hypertensive rats. The lowest dose of captopril used (3.5 mg/kg) inhibited conversion of exogenous angiotensin I and maximally potentiated the depressor response to bradykinin, but failed to restore blood pressure to that of the normotensive controls.
3. Removal of the solitary clipped kidney also did not restore blood pressure to normal. Injection of captopril (3.5 mg/kg) 24 h after nephrectomy, when no circulating renin activity was detectable, lowered blood pressure further in hypertensive but not in similarly nephrectomized controls.
4. These results indicate that raised blood pressure in early one-kidney, one-clip hypertension in the rat cannot be entirely attributed to the renin-angioterisin system, even when plasma renin activity is significantly increased.
5. This study has also confirmed a hypotensive action of captopril in anephric rats when plasma renin activity is undetectable.
Inactive Renin in Rabbit Plasma: Effect of Frusemide
Authors: Richards H. K. , Lush D. J. , Noble A. R. , Munday K. A. 
Published: August 2015

1. An inactive form of renin exists in rabbit plasma. This can be activated, and therefore measured, after acidification (pH 2.8).
2. The effect of frusemide diuresis, with replacement of volume losses, on plasma levels of active and inactive renin was studied over a 3 1/2 h time course. Plasma active renin increased during frusemide diuresis but inactive renin disappeared from the circulation. The time courses for the changes in the two forms of renin were similar.
3. The peak of the frusemide-induced changes in renal function (urine flow, sodium and potassium excretion and creatinine clearance) preceded the maximum changes in the two forms of renin by 90 min.
4. The response of plasma levels of inactive renin to physiological stimuli depends on the nature of the stimulus, as well as its duration. Some form of sodium-sensitive mechanism may control the activation of inactive renin.