bluuebunny/crossref_metadata_2025_split huggingface dataset:
FREE AND CONJUGATED CATECHOLAMINES IN HUMAN PLASMA DURING PHYSICAL EXERCISE
Authors: Ratge D. , Gehrke A. , Melzner I. , Wisser H. 
Published: June 2007

SUMMARY1. To investigate changes of free and sulfoconjugated catecholamines in response to alterations in sympatho‐adrenal activity, free and conjugated noradrenaline, adrenaline and dopamine were determined radioenzymatically in plasma of 49 subjects.2. During brief vigorous bicycle exercise (8 min, maximal heart rate: 177 beats/min) mean free noradrenaline and adrenaline values of 2.0 and 0.51 nmol/1 at rest, increased to 6.7 and 2 nmol/1 (P<0.001) respectively, at the maximal workload of 200 watt, whereas conjugated noradrenaline and adrenaline decreased from 3.4 and 0.8 nmol/1 to 2.1 and 0.4 nmol/1 (P<0.001) respectively. In the tenth min of the recovery period basal free and conjugated noradrenaline and adrenaline levels were measured.3. The moderate stress of a steam bath (20 min, maximal heart rate: 131 beats/min) doubled free noradrenaline and adrenaline levels. However, conjugated noradrenaline and adrenaline concentrations remained unchanged.4. The increase in free catecholamine values during an exhausting cross‐country march over 20 km was associated with an accumulation of sulfated catecholamines. After a rest of 30 min free noradrenaline and adrenaline reached basal values, whereas conjugated noradrenaline and adrenaline remained elevated by 64 and 70% respectively, compared to pre‐exercise concentrations.5. It was concluded that conjugated noradrenaline and adrenaline may be used as pools for free noradrenaline and adrenaline during brief vigorous exercise. In addition, they may also be indicators of chronic activation of the sympatho‐adrenal system.
THE CARDIOVASCULAR EFFECTS OF TRIMAZOSIN AND PRAZOSIN IN THE RABBIT
Authors: Vincent J. , Hamilton C. A. , Reid J. L. 
Published: June 2007

SUMMARY1. The cardiovascular effects of trimazosin, a quinazoline derivative similar in structure to prazosin, were investigated and compared with prazosin in the rabbit.2. Radioligand binding to cerebral membranes showed that trimazosin has roughly 100‐fold less affinity for the α1‐adrenoceptor. This was further supported by its lower pA2 derived from phenylephrine contractile responses in isolated thoracic aorta preparations.3. Trimazosin is less extensively distributed and has a lower clearance from whole blood than prazosin although their whole blood elimination half‐lives are comparable. In addition, although it is a less potent α1‐adrenoceptor antagonist in vivo, its peripheral vascular depressor effect tends to be greater than prazosin.4. Trimazosin at the dose used and under the conditions of study did not reverse the peripheral pressor effect of angiotensin II or B‐HT920 but at higher concentrations, unlike prazosin, it relaxed the K+ contracted thoracic aorta. In addition, following pharmacological autonomie blockade and treatment with prazosin in vivo, trimazosin caused a further depressor response. A similar though shorter lasting non‐α1‐receptor mediated action was also observed with prazosin.5. 1‐Hydroxytrimazosin (CP23445), the major metabolite of trimazosin in man, showed little affinity for either the α1‐ or α2‐adrenoceptor from radioligand binding studies.6. In addition to α1‐adrenoceptor antagonism, trimazosin may exert an additional direct vasodilator effect in rabbits.
PERSISTENT EFFECTS ON BLOOD PRESSURE AND RENAL HAEMODYNAMICS FOLLOWING CHRONIC ANGIOTENSIN CONVERTING ENZYME INHIBITION WITH PERINDOPRIL
Authors: Harrap Stephen B. , Nicolaci Joseph A. , Doyle Austin E. 
Published: June 2007

SUMMARY1. Spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats aged 4 and 16 weeks were given an acute oral dose of either Perindopril (3 mg/kg) or vehicle. Direct blood pressure (BP), glomerular filtration rate (GFR) and renal blood flow (RBF) were measured, and renal vascular resistance (RVR) calculated. GFR and RBF were lower in vehicle‐treated SHR than WKY at 4 weeks of age, but were not different at 16 weeks. Acute Perindopril increased GFR and RBF and reduced RVR in both strains at both 4 and 16 weeks.2. Total body sodium, sodium intake and blood pressure were measured in SHR and WKY from 1 to 28 weeks of age. Rats of both strains were treated daily between 4 and 16 weeks of age with either Perindopril (3 mg/kg per day) or vehicle. Chronic Perindopril treatment prevented the development of hypertension in the SHR. From 16 to 28 weeks of age, after stopping Perindopril, BP rose slowly in SHR, but remained lower than vehicle‐treated SHR. No changes in total body sodium occurred during Perindopril treatment.3. GFR and RBF were measured in SHR and WKY chronically treated with either Perindopril or vehicle, 3 days or 12 weeks after stopping treatment. In WKY, GFR and RBF were not different between Perindopril‐treated and untreated rats at either measurement. In SHR, GFR and RBF remained significantly higher in rats previously treated with Perindopril at both ages.4. These findings suggest that renal haemodynamic abnormalities may be important in the initiation of hypertension in the SHR. These renal circulatory abnormalities and the hypertension of the SHR depend, at least in part, on intact converting enzyme activity, yet appear to be independent of abnormalities of total body sodium. At a later age, hypertension seems to develop independently of renal vascular abnormalities.
INFLUENCE OF ETHANOL TREATMENT ON THE PLASMA CONCENTRATIONS OF PROLACTIN AND LEUTINIZING HORMONE IN TURKEYS (MELEAGRIS GALLOPAVO)
Authors: Ali B. H. , Czarnecki Caroline M. , EL Halawani M. E. 
Published: June 2007

SUMMARY1. The effect of ethanol consumption on the plasma concentrations of prolactin (PRL) and leutinizing hormone (LH) was investigated in turkey poults.2. Ethanol (4–5% v/v in drinking water for 42 days) significantly increased the concentration of PRL, and tended to decrease that of LH.3. It is suggested that the hyperprolactinaemia produced by ethanol might be due to its stressor action on the birds.
NALOXONE ATTENUATES AUGMENTATION OF cAMP LEVELS AND ARRHYTHMIAS FOLLOWING MYOCARDIAL ISCHAEMIA AND REPERFUSION IN THE ISOLATED PERFUSED RAT HEART
Authors: Lee A. Y. S. , Wong T. M. 
Published: June 2007

SUMMARY1. The effects of myocardial ischaemia and reperfusion on arrhythmias and cAMP levels were studied using the Langendoff isolated perfused rat heart preparation.2. Myocardial ischaemia and reperfusion caused arrhythmias and augmentation of cAMP levels concurrently, supporting the suggestion that myocardial cAMP is related to arrhythmias.3. Pretreatment with naloxone attenuated both arrhythmias and augmentation of cAMP levels to a similar extent. The results suggest that the anti‐arrhythmic effect of naloxone may involve myocardial cAMP.
THE EFFECTS OF 4‐METHYL‐2‐THIOURACIL ON FIBRE TYPE AND CROSS‐SECTIONAL AREA IN THE SOLEUS MUSCLE OF THE RAT
Authors: Rajikin Mohd Hamim , Merican Zainuddin , Morat Paden 
Published: June 2007

SUMMARY1. The effects of 4‐methyl‐2‐thiouracil (MTU, 0.1% in drinking water) on the composition and cross‐sectional area of muscle fibres of the rat soleus muscle were studied.2. The percentage of fast twitch‐oxidative‐glycolytic (FOG) fibres fell after 2 weeks of treatment with MTU to zero at 8 weeks. In contrast the percentage of FOG fibres in untreated animals fell to 19.2±2.1% during this period.3. The mean cross‐sectional area of FOG and slow twitch‐oxidative (SO) fibres were respectively 39.9% and 23.8% smaller than those of their respective controls 6 weeks after treatment. At 8 weeks the percentage reduction of SO fibre area was 26.8% of the control value.4. This study indicates that MTU treatment causes atrophy and redistribution of fibre type in the soleus muscle.
BLOCKADE OF ANGIOTENSIN CONVERTING ENZYME IN CIRCUMVENTRICULAR ORGANS OF THE BRAIN AFTER ORAL LISINOPRIL ADMINISTRATION DEMONSTRATED BY QUANTITATIVE IN VITRO AUTORADIOGRAPHY
Authors: Sakaguchi Keiji , Chai Siew Yeen , Jackson Bruce , Johnston Colin I. , Mendelsohn Frederick A. O. 
Published: June 2007

SUMMARY1. To elucidate the central effect of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor, ACE localization and levels were followed in the brain of Sprague‐Dawley rats by quantitative in vitro autoradiography after administration of the drug.2. Following acute lisinopril (10 mg/kg p.o.) treatment, serum ACE activity was acutely reduced, but returned to normal by 24 h.3. Levels of ACE in most parts of the brain, including the basal ganglia and choroid plexus of all ventricles were not affected by lisinopril. Lisinopril inhibited brain ACE in the subfornical organ and organum vasculosum of the lamina terminalis, circumventricular organs, where the blood brain barrier is deficient. These regions are rich in ACE and angiotensin II receptors, and are known targets for angiotensin II‐induced effects on fluid, electrolyte and blood pressure homeostasis.4. These observations indicate that quantitative in vitro autoradiography is a powerful method to study the access of drugs to the central nervous system.5. This study shows that blood brain barrier plays an important role in limiting the penetration of lisinopril into the central nervous system. The circumventricular organs may be important targets for ACE inhibitors.
EFFECT OF GRADED LOW‐DOSE NORADRENALINE INFUSIONS ON NORADRENALINE CLEARANCE IN NORMALS AND ESSENTIAL HYPERTENSIVES
Authors: Gordon Richard D. , Bachmann Anthony W. , Gueizelar Brenda , Dai Yung 
Published: June 2007

SUMMARY1. In normal subjects and essential hypertensives, plasma noradrenaline (NA) levels, and NA clearance (3H‐NA constant infusion), were measured during graded infusion of NA.2. Plasma levels of NA were similar in both groups, with parallel increases to levels approximately three times basal, but still in the upper normal range.3. Clearance did not increase in either group with increasing plasma NA levels. There was no correlation between plasma NA achieved and NA clearance, which was similar in hypertensives and normotensives.5. Insofar as plasma clearance reflects tissue clearance, these studies provide no support for the contention that altered NA metabolism might predispose to elevated NA levels in essential hypertension.
EFFECT OF ATRIAL NATRIURETIC PEPTIDE ON COLLECTING DUCT FUNCTION EVALUATED BY STOP‐FLOW IN RABBITS
Authors: Fitzgibbon Wayne , Morgan Trefor 
Published: June 2007

SUMMARY1. The effect of a low dose of a synthetic atrial natriuretic peptide (ANP), rat atriopeptin II (23 amino acids), on stop‐flow sodium concentrations was examined in rabbits in water diuresis.2. Atrial natriuretic peptide (2 μg/kg body weight) was injected intravenously as a bolus either before or after the commencement of stop‐flow.3. Atrial natriuretic peptide induced a significant natriuresis within 2 min of injection. This natriuresis was associated with smaller increases in urine volume and potassium excretion. Atrial natriuretic peptide did not alter blood pressure.4. Atrial natriuretic peptide did not significantly alter stop‐flow sodium concentrations.5. These findings indicate that ANP does not directly alter sodium transport across medullary collecting ducts.6. It is proposed that ANP acts via a mediator to alter sodium movement across terminal segments of the nephron.
ALDOSTERONE‐PRODUCING ADENOMAS RESPONSIVE TO ANGIOTENSIN POSE PROBLEMS IN DIAGNOSIS
Authors: Gordon R. D. , Hamlet S. M. , Tunny T. J. , Klemm S. A. 
Published: June 2007

SUMMARY1. A subgroup of patients with aldosterone‐producing adenoma (APA) have been identified who lack many of the biochemical features regarded as characteristic of APA and used to distinguish APA from bilateral adrenal hyperplasia.2. In these patients, aldosterone is responsive to infused angiotensin II (angiotensin‐responsive APA), which explains their uncharacteristic responses to upright posture, saline infusion and fludrocortisone acetate administration.3. The angiotensin‐responsiveness of these patients may derive from the contra‐lateral adrenal gland, since renin levels are less completely suppressed in angiotensin‐responsive APA than in angiotensin‐unresponsive APA.4. However, while the excretion of 18‐oxo‐cortisol was consistently increased in angiotensin‐unresponsive APA, it was normal in angiotensin‐responsive APA, consistent with biochemical and biosynthetic distinctiveness residing in the tumours.5. Angiotensin‐responsive APA should always be considered as an alternative diagnosis to bilateral hyperplasia causing primary aldosteronism.
INTERACTION OF VASOPRESSIN, ANGIOTENSIN AND α‐ADRENERGIC SYSTEM IN SODIUM DEPLETION IN THE RAT
Authors: Jover Bernard F. , McGrath Barry P. 
Published: June 2007

SUMMARY1. The role of vasopressin in cardiovascular adaptation to sodium depletion was examined in rats after 6 days on a low sodium diet. Studies were performed after selective or combined blockade with d(CH2)5 Tyr(Me)AVP (AVPA), enalaprilat (CEI) and phentolamine (PHENTOL). AVPA alone had no effect on systemic haemodynamics or regional blood flow distribution. After CEI or PHENTOL pretreatment, AVPA led to significant falls in peripheral resistance and increases in cardiac output and renal blood flow. In sodium depletion, endogenous vasopressin acts as a vasoconstrictor hormone, particularly in the kidney, when either the renin‐angiotensin or α‐adrenergic system is inhibited.
REGULATION OF SODIUM INFLUX AND SODIUM, POTASSIUM PUMP ACTIVITY BY A SODIUM‐HYDROGEN ANTIPORT IN RAT VASCULAR SMOOTH MUSCLE
Authors: Bobik Alex , Weissberg Peter L. , Little Peter J. 
Published: June 2007

SUMMARY1. The effects of Na‐H antiport inhibitors on sodium influx, intracellular pH and Na, K‐pump activity were examined in vascular smooth muscle from rats.2. Amiloride and 5‐(N‐ethyl‐N‐isopropyl)amiloride inhibited Na accumulation following inhibition of the Na, K‐pump.3. Inhibition of Na influx was associated with a reduction in basal Na, K‐pump activity and intracellular pH.4. It is concluded that a Na‐H antiport system in vascular smooth muscle regulates Na influx rate, contributes to intracellular pH regulation and influences basal levels of Na, K‐pump activity.
ADRENALINE INFUSION AND ADRENOCORTICOTROPHIN (ACTH) AND CORTISOL RELEASE IN NORMOTENSIVE AND HYPERTENSIVE MAN
Authors: Jackson R. V. , Jackson A. J. , Grice J. E. , Penfold P. J. , Armour M. B. , Bachmann A. W. 
Published: June 2007

SUMMARY1. Adrenaline causes ACTH release from cultured rat pituitary corticotrophs (Vale et al. 1983) and there is evidence that it causes ACTH release in rats in vivo (Plotsky et al. 1985).2. The present study examined the effects of intravenous adrenaline infusion with and without simultaneous administration of the known ACTH secretagog, arginine vasopressin, in normotensive and mild essential hypertensive men on their plasma ACTH and cortisol levels.3. Low dose adrenaline infusion (0.013 μg/kg per min) does not cause ACTH or cortisol release, but appears to blunt the ACTH and cortisol rise caused by arginine vasopressin (0.14 pressor units/kg, i.m.).
EFFECTS OF ANGIOTENSIN AND NORADRENALINE ON ATRIAL NATRIURETIC PEPTIDE LEVELS IN MAN
Authors: Tunny T. J. , Klemm S. A. , Gordon R. D. 
Published: June 2007

SUMMARY1. A significant positive correlation was found between changes in circulating noradrenaline (NA) levels and changes in atrial natriuretic peptide (ANP) levels during NA infusion and clonidine administration.2. A significant positive correlation was also found between changes in arterial blood pressure and changes in ANP level during infusion of angiotensin II and of NA.3. Two patients with very high circulating NA levels due to phaeochromocytoma, but receiving α‐and β‐blockade, did not have clearly elevated ANP. A third not receiving medications and aged 73 years had elevated levels.4. Atrial natriuretic peptide response to NA and angiotensin II may be mediated by changes in blood pressure levels or increased noradrenergic and angiotensinergic receptor activity in the atria or both. Atrial natriuretic peptide may have a role in blood pressure regulation in both normotensive and hypertensive man.
RENIN SECRETION FROM MALIGNANT PULMONARY METASTATIC TUMOUR CELLS OF VASCULAR ORIGIN
Authors: Morris B. J. , Pinet F. , Michel J.‐B. , Soubrier F. , Corvol P. 
Published: June 2007

SUMMARY1. A pulmonary chemodectoma/glomangiosarcoma that had metastasized from the thigh was studied after removal from a 22 year old Algerian patient with hypertension, high plasma prorenin and signs of secondary aldosteronism.2. Renin and renin mRNA were localized in sections of the tumour tissue using monoclonal anti‐human renin antibody and human renin cDNA probe, respectively.3. The cells grew prolifically in culture, but, even though their renin content was similar to that of transfected human juxtaglomerular cell tumour cells (∼1 pg/μg DNA), their rate of secretion of renin was much lower (0.05–0.15 cf. 0.5–1.5 pg/h per μg DNA).4. Forskolin (10 μmol/l for 24 h) increased secretion of renin from 1.9 ± 0.36 to 4.1 ± 0.64 pg/ml per h of culture (P< 0.001, n= 11), consistent with cAMP being a second messenger in the secretory mechanism.5. The cells should provide valuable information about intracellular mechanisms for the regulation of renin synthesis and secretion.
ACTIVATION BY PUFF ADDER VENOM OF INACTIVE RENIN IN NORMAL AND HYPERTENSIVE RAT PLASMA
Authors: Morris Brian J. , Taylor Jane E. 
Published: June 2007

SUMMARY1. Inactive renin has been studied extensively in human plasma, but in animal plasma its accurate quantification has proved more difficult, due partly to higher activity of plasma protease inhibitors. Such activity in human plasma can be conveniently destroyed by a metalloprotease in Bitis arietans venom, with concommitant release of endogenous enzyme activities, such as plasma kallikrein, that then activate inactive renin. It was therefore of interest to look for inactive renin in rat and rabbit plasma using this approach, so providing, in addition, a comparison for the disparate data of other groups who have used trypsin or acid for activation.2. In both rat and rabbit plasma the proportion of inactive renin was 62% of total renin, whereas human plasma contained more inactive renin and a higher proportion, 82%. A higher concentration of venom was required for rat (33 ug venom/ml plasma) and rabbit (4 μg/ml) than needed for activation, at a similar rate, in human plasma (1 μg/ml).3. When applied to studies of rats made hypertensive and hyper‐reninaemic by aortic ligation for 5 days, higher total (active + inactive) renin was observed. The proportion of inactive renin, as a percentage of total renin in plasma collected at this time, was, however, found to diminish significantly.4. In conclusion, puff adder venom activates inactive renin in rat and rabbit plasma and can be used to study physiological changes in inactive renin in such animal plasma.
VINBLASTINE BUT NOT OTHER MICROTUBULE INHIBITORS BLOCK TRANSFERRIN ENDOCYTOSIS AND IRON UPTAKE BY RETICULOCYTES
Authors: Morgan Evan H. , Iacopetta Barry J. 
Published: June 2007

SUMMARY1. The antimicrotubule reagents, colchicine, griseofulvin, nocodazole, podophyl‐lotoxin and taxol had no effect on transferrin endocytosis or iron uptake by rabbit or rat reticulocytes but were inhibitory when used at high concentrations with rat fetal liver erythroid cells. The results imply that microtubules do not have a role in endocytosis and iron uptake by reticulocytes but may have a permissive role in the fetal cells.2. The only reagent found to inhibit iron uptake by reticulocytes was vinblastine. It was shown to act by inhibiting the endocytosis of transferrin.3. It is concluded that this effect is not the result of an interaction with microtubules, but may result from a non‐specific action on the cell membrane or a more specific effect, such as inhibition of calmodulin.
COMPLEMENTARY CHANGES IN PLASMA ATRIAL NATRIURETIC PEPTIDE AND ANTIDIURETIC HORMONE CONCENTRATIONS IN RESPONSE TO VOLUME EXPANSION AND HAEMORRHAGE: STUDIES IN CONSCIOUS NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Morris Margaret , Cain Michael , Chalmers John 
Published: June 2007

SUMMARY1. Plasma concentrations of atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) were measured in conscious stroke‐prone spontaneously hypertensive (SPR), spontaneously hypertensive (SHR) and normotensive Wistar‐Kyoto (WKY) rats before and after acute volume expansion or haemorrhage.2. Plasma ANP concentration was reduced to one‐third of resting values 30 min after a 1.5% haemorrhage (1.5 ml of blood per 100 g bodyweight). Plasma ADH concentration rose immediately 50‐fold on haemorrhage and remained elevated at 30 min.3. Plasma ANP concentration increased 2.5‐fold relative to resting values 1 min after infusion of 2.0 ml per 100 g 5% dextrose; after 10 min plasma ANP remained elevated. Plasma ADH concentration tended to fall on volume expansion although no significant decrease was observed.4. There was no difference in the basal levels of ANP and ADH, or in the changes produced by alterations in blood volume, in hypertensive SPR and SHR compared with normotensive WKY.5. Thus, plasma ANP concentrations moved in opposite directions in response to two physiological stimuli: volume expansion and haemorrhage. Reciprocal changes were observed in plasma ADH.
BLASTOCYSTIS HOMINIS: EVIDENCE FOR HUMAN PATHOGENICITY AND EFFECTIVENESS OF METRONIDAZOLE THERAPY
Authors: Guirges Sami Y. , Al‐Waili Noori S. 
Published: June 2007

SUMMARY1. Clinical symptoms and oral treatment with metronidazole were studied in 103 patients with pure infections by Blastocystis hominis.2. The results showed that excessive flatulence is the chief gastrointestinal symptom associated occasionally with diarrhoea and abdominal cramps. All the patients showed good responses with treatment of metronidazole and 74 patients whose stools were reexamined 1–2 months after the treatment demonstrated no signs of infections.3. It is concluded that B. hominis is a pathogenic intestinal parasite and the infection could be eradicated successfully by oral metronidazole.
PHARMACOKINETICS OF ANGIOTENSIN CONVERTING ENZYME INHIBITION IN TISSUES FOLLOWING ORAL LISINOPRIL: STUDIES IN THE RAT USING QUANTITATIVE RADIOINHIBITOR BINDING
Authors: Jackson B. , Cubela R. , Sakaguchi K. , Johnston C I. 
Published: June 2007

SUMMARY1. The pharmacokinetics of angiotensin converting enzyme (ACE) inhibition in plasma and tissues were measured in the rat following 10 mg/kg lisinopril given by oral gavage.2. Specific binding of 125I‐351A to ACE was measured in plasma, and homogenates of lung, aorta, kidney, testis, epididymis and brain, and used as an index of ACE activity.3. Plasma ACE binding of 125I‐351A was reduced to 5% of that in untreated rats 2 h after treatment, and returned to normal by 48 h. Kidney ACE showed a similar time course. Angiotensin converting enzyme from lung, aorta and brain was inhibited at a slower rate, and to a lesser degree. No significant inhibition of ACE was detected in epididymis or testis.4. Individual tissues in the rat had differences in time course and degree of ACE inhibition after a single dose of lisinopril.