bluuebunny/crossref_metadata_2025_split huggingface dataset:
A STRUCTURAL ANALYSIS OF HUMAN RENIN
Authors: Morris Brian J. , Guss J. Mitchell , Hunter William N. , Catanzaro Daniel F. 
Published: June 2007

SUMMARY1. A three‐dimensional model of human renin has been used to define amino acid residues involved in interaction with substrate.2. The structure revealed proteolytic cleavage sites on the surface of the molecule that may help explain numerous experimental observations concerning prorenin and its activation and forms of renin differing in size.
ACUTE HAEMODYNAMIC RESPONSES TO UNILATERAL RENAL ARTERY STENOSIS IN CONSCIOUS DOGS
Authors: Anderson Warwick P. , Woods Robyn L. , Kline Robert L. , Korner Paul I. 
Published: June 2007

SUMMARY1. The acute responses to renal artery stenosis were studied in chronically instrumented, unanaesthetized dogs.2. Stenosis of one renal artery produced a rise in arterial pressure and a fall in total peripheral conductance, but no change in cardiac output.3. The resistance to blood flow of the stenotic kidney 1 h after stenosis was 25% greater than before stenosis. This rise in resistance was due to the resistance of the renal artery stenosis itself.4. Blood flow to the contralateral kidney fell by 13% (s.e.m. =3) at 1 h and resistance rose by 39% (s.e.m. = 5).5. Plasma renin activity was elevated approximately 10 fold.6. Calculations of changes in peripheral conductances following stenosis showed that the stenotic kidney was responsible for 14% of the fall in total peripheral conductance at 1 h, and the contralateral kidney for 18%.7. Thus acute renal artery stenosis produced a prompt rise in arterial pressure due to reduced peripheral conductance, of which the two kidneys (stenotic and contralateral) were responsible for one‐third.
THE MEDIATORS OF ALLERGIC CONTRACTION OF HUMAN AIRWAY SMOOTH MUSCLE: A COMPARISON OF BRONCHIAL AND LUNG PARENCHYMAL STRIP PREPARATIONS
Authors: Creese B. R. , Temple Diana M. 
Published: June 2007

SUMMARY1. Antigen‐induced contractions of passively sensitized preparations of human bronchi and lung parenchymal strips were studied.2. Mepyramine did not affect the magnitude or time course of the contractile responses of either preparation.3. Indomethacin potentiated the responses of lung parenchymal strips, but inhibited those of bronchial preparations.4. Responses of both tissues were inhibited by the leukotriene antagonist FPL 55712, by the lipoxygenase inhibitor BW 755C, and by the anti‐allergic compound disodium cromoglycate5. Disodium cromoglycate and BW 755C inhibited histamine release from lung parenchymal strips.6. The results indicate an important role for leukotrienes in allergic contraction of both large and small human airways, while histamine is of little importance. Broncho‐constrictor prostaglandins may also contribute to the response of large airways.
INFLUENCE OF MONENSIN ON FERTILITY IN RATS
Authors: Atef Mohamed , Shalaby Moustafa A. , El‐Sayed Mossad G. A. , El‐Din Salah , Youssef A. H. , El‐Sayed Mohamed A. I. 
Published: June 2007

SUMMARY1. Monensin was given orally to female rats at two dose levels (1.75 and 3.50 mg/kg body weight) over the period of 9‐17 days of pregnancy where organogenesis of fetuses occur. The dams were killed on the nineteenth day of gestation and their fetuses were subjected to morphological, visceral and skeletal examination. The small dose of monensin increased the number of resorbed and dead fetuses and induced marked retardation in growth of viable fetuses, but visceral or skeletal defects in these fetuses were not seen. Large doses produced fetal resorption in all dams and no viable fetuses were delivered.2. Prolonged oral administration of monensin in male rats for 60 successive days at two dose levels, decreased the conception rate in non‐treated females (mated with treated males) to 33.3% and 0% for the small and large doses, respectively. Both doses markedly decreased the weights of testicles, epididymides and seminal vesicles. The small dose of monensin caused oligospermia, whereas the large dose induced azospermia. Both doses decreased the activity of spermatogenic epithelium and caused degeneration in germ cells after histopathological examination of the testicles.3. It is concluded that monensin given during pregnancy to female rats is fetotoxic and when administered chronically to male rats, causes damage to the reproductive organs. The delayed effects of this drug are especially prominent.
HAEMORRHAGE‐INDUCED SECRETION OF ACTIVE AND INACTIVE RENIN IN CONSCIOUS AND PENTOBARBITONE‐ANAESTHETIZED SHEEP
Authors: Mzail A. H. K. , Noble A. R. 
Published: June 2007

SUMMARY1. The response of plasma levels of active and inactive renin to haemorrhage was investigated in sheep with indwelling artery and vein catheters.2. In conscious animals, loss of 10% of estimated blood volume over a 5 min period increased plasma active renin by a mean of 59%, a surprisingly small change. Plasma inactive renin also increased, but only by 86%. Maximum increases in both forms of renin occurred within 1 h of the haemorrhage.3. The effects of an equivalent blood loss were investigated in pentobarbitone‐anaesthetized sheep maintained in an upright posture using padded slings. Anaesthesia per se had no effect on plasma active or inactive renin. In anaesthetized sheep, 3 h after haemorrhage, plasma active renin had increased by 403% and inactive renin by 299% above control values, but a plateau (maximum) response was not reached during this time.4. In both conscious and anaesthetized animals the haemorrhage‐induced increases in active and inactive renin occurred in parallel.5. It appears that haemorrhage of this intensity is a comparatively mild stimulus to increase plasma renin concentration in conscious sheep but is much more effective in anaesthetized animals. This may be linked to anaesthetic‐induced increases in prostaglandin synthesis within the kidney.
ALLOGENEIC TRANSFUSION OF MACROPHAGES IN ACUTE URINARY TRACT INFECTION
Authors: AL‐Waili Noori S. , AL‐Ani Miqdad A. 
Published: June 2007

SUMMARY1. Three patients with acute urinary tract infections that failed to respond to antibiotics were treated by allogeneic peritoneal macrophage transfusions.2. No harmful effects were observed following macrophage transfusions and the urinary infections were eradicated in treated patients.3. It could be concluded that allogeneic macrophage transfusion is feasible between unrelated individuals and can combat severe resistant urinary infections.
THE EFFECT OF NALOXONE ON PRESSOR RESPONSES TO ANGIOTENSIN II IN ANAESTHETIZED GREYHOUNDS
Authors: Wilkinson Dean L. , Scroop Garry C. 
Published: June 2007

SUMMARY1. In greyhounds anaesthetized with morphine and chloralose, vertebral artery infusions of angiotensin II resulted in a similar pressor response but smaller tachycardia than in greyhounds anaesthetized with chloralose alone. The pressor responses to intravenous infusions of angiotensin II were significantly larger in the morphine premedicated greyhounds.2. In greyhounds anaesthetized with morphine and chloralose, pressor responses to vertebral artery angiotensin II were potentiated following the administration of naloxone via either a vertebral artery or intravenously although the effect was more consistent with the former route. No such effect was seen in greyhounds anaesthetized with chloralose alone. Naloxone had no effect on the pressor responses to intravenous angiotensin II or carotid artery occlusion.3. The heart rate responses to vertebral artery angiotensin II in greyhounds anaesthetized with morphine and chloralose were potentiated by naloxone such that they were not significantly different from the responses obtained in greyhounds anaesthetized with chloralose alone before naloxone. As was observed with the pressor responses, the potentiation was more apparent with the vertebral artery route of administration of naloxone. There was no potentiation of the heart rate responses in the chloralose group of greyhounds.4. It is suggested that morphine premedication may repress the vagal withdrawal mechanism while potentiating the sympathetic vasomotor mechanism mediating the central cardiovascular actions of angiotensin II.
DEVELOPMENT OF HYPERTENSION AND PROTEINURIA WITH AGE IN FAWN‐HOODED RATS
Authors: Kuijpers Marga H. M. , Provoost Abraham P. , de Jong Wybren 
Published: June 2007

SUMMARYBlood pressure and urinary protein excretion were monitored in male fawn hooded rats (FH rats) from 8 until 46 weeks of age. Mild hypertension was already observed at 8 weeks of age. Between the age of 5 and 7 months the blood pressure rose steeply to a plateau of about 200 mmHg. Then it stabilized and the level was different for animals of different litters but similar for littermates. Concomitantly with the increase in blood pressure, proteinuria increased with age. Examination of renal tissue at 6.5 and 9 months of age revealed the presence of focal and segmentai glomerulosclerosis. The renal changes were not accompanied by gross alterations in renal function. In animals with severe hypertension pronounced proteinuria occurred, and they appeared to form a distinct class. In some of the animals intermittent haematuria occurred. Persistent haematuria, however, had a bad prognosis. There was no glucosuria. Water intake of the animals with severe hypertension was increased. Water intake of young FH rats was found to be of value for predicting the severity of the hypertension in these animals at a later age. It is concluded that the FH rat is an example of a non‐inbred rat strain showing spontaneous hypertension. This hypertension may result from an aberrant renal water handling and/or volume regulation.
AUTORADIOGRAPHIC ANALYSIS OF (‐)‐[125I]‐CYP BINDING IN MOUSE KIDNEY
Authors: Lew Robert , Summers Roger J. 
Published: June 2007

SUMMARY1. The distribution and binding characteristics of the radioligand (‐)‐[125I]‐cyanopindolol (CYP) have been examined in slide mounted mouse kidney sections, using the technique of in vitro labelling and autoradiography.2. (‐)‐[125I]‐CYP binding to sections was of high affinity (KD=55.8 pmol/l, s.e.m. = 8. 1, n= 4) to a single population of non‐interacting sites (nH = 0. 95, s.e.m. = 0. 01, Bmax= 0.74 fmol/section, s.e.m. = 0. 12, n= 4) and stereoselective with respect to the (‐)‐ and (+)‐isomers of both propranolol and pindolol.3. Autoradiographic studies showed that (‐)‐[125I]‐CYP binding was localized to areas in the renal cortex and medulla. Both cortical and medullary binding were abolished by the inclusion of (‐)‐propranolol (1 μmol/l) in the incubation medium, whereas (‐)‐isoprenaline (200 μmol/l) selectively abolished cortical binding.4. Medullary binding could be prevented by the inclusion of the lipophilic compounds cinanserin (10 μmol/l), haloperidol (10 μmol/l) or phentolamine (10 μmol/l), either alone or together or by washing at 37°C. These results suggest that medullary binding sites are lipid rather than receptor‐related.5. In conclusion, in mouse kidney sections, (‐)‐[125I]‐CYP binds to discrete areas in the cortex and medulla. Cortical binding sites have the molecular characteristics of β‐adrenoceptors while medullary binding sites are lipid‐related. Caution should therefore be exercised when defining non‐specific binding of lipophilic radioligands. The autoradiographic technique is useful for discriminating between receptor and non‐receptor binding sites.
ECHOCARDIOGRAPHIC MEASUREMENT OF LEFT VENTRICULAR HYPERTROPHY IN UNTREATED ESSENTIAL HYPERTENSION
Authors: Laufer E. , Jennings G. , Dewar E. , McKenzie A. , Korner P. 
Published: June 2007

SUMMARY1. The prevalence of left ventricular hypertrophy (LVH) in human essential hypertension is uncertain. Echocardiography was used to calculate left ventriuclar wall thickness (WT), relative wall thickness (t/r) and left ventricular mass (LVM) in 52 normal subjects, 30 patients with borderline hypertension and 33 untreated patients with essential hypertension.2. In 52 normal subjects WT was independent of age, sex, BSA, BP or habitual physical activity, but LVM was significantly related to BSA and age.3. After correction of LVM for age and BSA, 88% of 33 patients with untreated essential hypertension had LVM greater than predicted which identified a larger proportion of hypertensives with LVH than previous studies suggest.4. Wall thickness measurement alone also indicated that about 80% of newly diagnosed hypertensives have LVH.
CAPTOPRIL ANTAGONIZES THE HYPOTENSIVE ACTION OF ATRIAL NATRIURETIC PEPTIDE IN THE ANAESTHETIZED RAT
Authors: Nicolantonio Robert Di , Stevens Janine , Weaver Debbie , Morgan Trefor O. 
Published: June 2007

SUMMARY1. Atrial natriuretic peptide (8‐33; ANP) caused a prolonged hypotensive response following intravenous injection in anaesthetized rats.2. This response was abolished by captopril treatment and restored by concomitant angiotensin II infusion.3. These results suggest that ANP exerts its hypotensive action in the anaesthetized rat by the antagonism of the vasoconstrictor action of endogenous angiotensin II.
ENDOTHELIUM‐DEPENDENT VASODILATATION IN BOVINE CORONARY ARTERIES: CALCIUM DEPENDENCE AND INHIBITION BY PROADIFEN
Authors: Macdonald P. S. , Dubbin P. N. , Dusting G. J. 
Published: June 2007

SUMMARY1. Vasodilator responses were examined in bovine coronary artery rings pre‐constricted with the thromboxane‐mimetic, U46619.2. A23187 produced endothelium‐dependent vasodilatation that was abolished in calcium‐free solution. In contrast, endothelium‐dependent vasodilatation produced by arachidonic acid was not altered in calcium‐free solution.3. In calcium‐free solution, indomethacin (10 μmol/1) did not affect arachidonate‐induced relaxations whereas BW755C (100 μmol/1) reduced relaxations to low concentrations of arachidonate, and proadifen (SKF‐525A, 1 mmol/1) abolished them at all concentrations.4. Endothelium‐independent relaxations produced by glyceryl trinitrate were not affected by proadifen (1 mmol/1).5. It is clear that arachidonic acid bypasses a calcium‐dependent step in the release of endothelium‐derived relaxing factor, perhaps acting as an intermediate precursor. The data support the hypothesis that a cytochrome P‐450 mono‐oxygenase may also be involved.
PLASMA LEVELS OF ATRIAL NATRIURETIC PEPTIDE IN MAN IN PRIMARY ALDOSTERONISM, IN GORDON'S SYNDROME AND IN BARTTER'S SYNDROME
Authors: Tunny T. J. , Higgins B. A. , Gordon R. D. 
Published: June 2007

SUMMARY1. Plasma levels of ANP were measured in normal subjects and in three conditions associated with disturbed volume homeostasis.2. Levels of ANP were appropriately raised in seven patients with primary aldosteronism, and fell to normal following removal of an aldosterone‐producing adenoma in six and dexamethasone treatment in one patient with glucocorticoid‐suppressible hyperaldosteronism.3. The level of ANP in one patient with Gordon's syndrome (a condition associated with plasma volume expansion) was lower than in the patients with primary aldosteronism, both before and after saline infusion. This is consistent with reduced ANP responsiveness in this condition.4. Levels of ANP were inappropriately elevated in three patients with Bartter's syndrome (a condition with plasma volume contraction) and rose further during saline infusion. This is consistent with primary hypersecretion of ANP.
PRESSOR RESPONSIVENESS IN STEROID‐INDUCED HYPERTENSION IN MAN
Authors: Whitworth Judith A. , Connell J. M. C. , Lever A. F. , Fraser R. 
Published: June 2007

SUMMARY1. Pressor responsiveness to angiotensin II (AII) and phenylephrine (PE) was examined before and after 5 days of ACTH (1 mg, i.m., daily) or hydrocortisone (200 mg, orally, daily) in six normotensive men.2. Pulse pressure was higher prior to PE than AII infusion, presumably due to feeding.3. Systolic blood pressure (SBP) was increased by both ACTH and hydrocortisone treatment, but more by ACTH.4. There were no significant changes in AII pressor responsiveness with either ACTH or hydrocortisone.5. ACTH increased pressor responsiveness to PE at 1.35 and 2 μg/kg per min, and hydrocortisone at 0.6‐2 μg/kg per min, with falls in pulse rate at 0.3‐0.9 μg/kg per min.6. Changes in pressor responsiveness do not explain ACTH hypertension.
THYROIDAL RESPONSE TO AN INCREASE OR DECREASE OF ENDOGENOUS TSH IN PATIENTS WITH HYPERTHYROIDISM AND ITS CORRELATION WITH TSH BINDING INHIBITING IMMUNOGLOBULIN
Authors: Katakura M. , Koizumi Y. , Aizawa T. , Takasu N. , Yamada T. , Yukimura Y. , Nagata H. 
Published: June 2007

SUMMARY1. One hundred and twenty‐one patients with hyperthyroidism of Graves' disease were treated with antithyroid drugs for 3 years and thyroidal response to an increase or decrease of TSH and the serum thyroid stimulating immunoglobulin (TSI) activity were studied in relation to the presence or absence of TSH binding inhibiting immunoglobulin (TBII).2. TBII activity was positive in 83% of untreated patients but decreased gradually with time during antithyroid drug therapy. Thyroidal radioactive iodine uptake (RAIU) was suppressed by T3 in 86 of 121 treated patients but 16% of suppressible patients had TBII activity. Thyroidal RAIU was not suppressed by T3 in 35 treated patients, and 19 of 35 unsuppressible patients had TBII activity but other 16 patients did not. When suppressible and unsuppressible patients were combined, suppression of serum T4 and thyroidal RAIU by T3 tended to be less in the presence of TBII activity.3. TSI activity was detected in the sera of untreated patients but did not correlate with TBII activity. TSI activity was undetectable after treatment for 3 years irrespective of presence or absence of TBII activity and T3‐suppressibility.4. TSH, T4 and T3 elevation in response to 500 μg thyrotropin releasing hormone (TRH) was normal in all treated patients irrespective of presence or absence of TBII activity and T3‐suppressibility.5. It is suggested that in vivo thyroidal responsiveness to an increase or decrease of endogenous TSH did not correlate with the presence or absence of TBII activity after long‐term therapy with antithyroid drugs.
PLASMA NEUROPEPTIDE Y LEVELS RISE IN PATIENTS UNDERGOING EXERCISE TESTS FOR THE INVESTIGATION OF CHEST PAIN
Authors: Morris M. J. , Elliott J. M. , Cain M. D. , Kapoor V. , West M. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. Neuropeptide Y (NPY) is colocalised with noradrenaline in post‐ganglionic sympathetic neurons. In order to examine the possibility that activation of the sympathetic nervous system might cause release of NPY into the plasma NPY levels were measured in 16 patients undergoing exercise tests for investigation of chest pain.2. Plasma NPY concentrations rose in 14 out of the 16 patients, and the mean level of plasma NPY increased from 335 (s.e.m. = 37) to 455 (s.e.m. = 41) pg/ml.3. Plasma noradrenaline and adrenaline levels increased four‐ and two‐fold respectively.4. The increase in NPY correlated with the increase in noradrenaline, suggesting that NPY may be released with noradrenaline when sympathetic noradrenergic nerves are activated.
FRUSEMIDE INHIBITION OF SYMPATHETIC VASOCONSTRICTION IN THE RAT IN SITU BLOOD PERFUSED MESENTERY
Authors: Armsworth Stuart J. , Gerkens John F. , Smith Anthony J. 
Published: June 2007

SUMMARY1. Mesenteric perfusion pressure was measured in the in situ blood‐perfused mesentery of anaesthetized rats. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation at 3, 6 and 10 Hz before and after the administration of frusemide 5 mg/kg intravenously (i.v.) or vehicle. Loss of volume due to diuresis was prevented by replacement with intravenous saline.2. Frusemide did not cause any changes in blood pressure or baseline perfusion pressure. Responses to electrical stimulation were inhibited by frusemide (P < 0.05) but unchanged by vehicle administration.3. Acute bilateral nephrectomy or treatment with indomethacin (2 mg/kg i.v.) prevented the inhibitory effect of frusemide on responses to sympathetic nerve stimulation.4. Responses to sympathetic nerve stimulation were potentiated by an infusion of angiotensin II (12 ng/min) into the mesenteric artery. This infusion did not alter either blood pressure or baseline perfusion pressure. Administration of frusemide 5 mg/kg i.v. attenuated the potentiating effect of angiotensin II on vasoconstrictor responses to electrical nerve stimulation.5. Frusemide may lead to the release of a prostanoid or prostanoid precursor which inhibits vascular constrictor responses.
TEMPORAL PROFILE OF TISSUE LEVELS OF DOPAMINE AND ITS METABOLITES, HVA AND DOPAC FOLLOWING FOCAL CEREBRAL ISCHAEMIA IN ANAESTHETIZED PRIMATES
Authors: Kuruvilla A. , Cherian R. , Theodore D. R. , Abraham J. 
Published: June 2007

SUMMARY1. Occlusion of the middle cerebral artery produced ischaemia and consequent changes in basal ganglia in the primate model of stroke within 0.5 h.2. Dopamine content was decreased in the right basal ganglia from 0.5 h up to 12 h after occlusion.3. Homovanillic acid content of the right basal ganglia increased initially at 0.5 h but, was decreased at 12 h.4. The DOPAC content was increased at 2 h after occlusion in the right basal ganglia, but was decreased significantly at 12 h.5. In the substantia nigra, there was a significant reduction in the DA content in the right side at 12 h.6. Minimal changes were observed in the DOPAC and HVA content in the right substantia nigra at 2 h and 4 h, respectively. At other time periods there was no significant change in the content of HVA and DOPAC in substantia nigra.
EFFECT OF ACUTE ADMINISTRATION OF PRAZOSIN ON BLOOD PRESSURE, HEART RATE AND PLASMA RENIN LEVEL IN THE CONSCIOUS NORMOTENSIVE RAT
Authors: Atkinson J. , Luthi P. , Sonnay M. , Boillat N. 
Published: June 2007

SUMMARY1. This study investigated whether the specific α‐antagonist, prazosin, stimulated basal plasma renin levels and heart rate. Furthermore the β‐adrenergic nervous system was also investigated to ascertain whether it was involved in this effect.2. Prazosin (0.1 or 1 mg/kg) was injected subcutaneously (s.c.) to conscious normotensive rats, either alone or in combination with the β‐adrenoceptor antagonist, dl‐propranolol (1 or 3 mg/kg). Rats bore chronically implanted dorsal aorta cannula for measurement of blood pressure and heart rate and blood sampling for renin determinations.3. Acute administration of prazosin (1 mg/kg, s.c.) produced a fall in mean arterial pressure accompanied by renin release and tachycardia. A tenfold lower dose of prazosin did not alter blood pressure or heart rate but did stimulate renin release.4. Acute administration of dl‐propranolol, (1 or 3 mg/kg, s.c.) produced falls in blood pressure and heart rate but did not affect plasma renin level.5. Combinations of prazosin with propranolol gave falls in blood pressure similar to those predicted on the basis of a simple addition of the effects of the two drugs given separately. Prazosin‐induced tachycardia and renin release were attenuated by propranolol.6. It appears that prazosin produces renin release and tachycardia via stimulation of the β‐adrenergic adrenoceptor.