bluuebunny/crossref_metadata_2025_split huggingface dataset:
ROLE OF PROSTAGLANDINS DURING REVERSAL OF ONE‐KIDNEY, ONE‐CLIP HYPERTENSION IN THE RAT
Authors: Vandongen Robert , O'Dwyer Julie , Barden Anne 
Published: June 2007

SUMMARY1. Unclipping the one‐kidney, one‐clip rat returned blood pressure to normotensive levels within 24 h and was associated with a substantial increase in urinary PGE2 and 6‐keto PGF1α excretion.2. Prior treatment with indomethacin (6.0 mg/kg) markedly reduced urinary prostaglandins after clip removal and attenuated the fall in blood pressure. Aspirin (100 mg/kg) treatment, which reduced 6‐keto PGFα to a lesser degree without altering PGE2 excretion, had no significant effect on the blood pressure fall.3. It is suggested that in the one‐kidney, one‐clip rat prostaglandins are released as the result of exposing the unclipped kidney to elevated arterial pressure, and that these contribute to the subsequent fall in blood pressure.
LOCALIZATION OF ANGIOTENSIN CONVERTING ENZYME IN RAT FOREBRAIN AND OTHER TISSUES BY IN VITRO AUTORADIOGRAPHY USING 125‐I‐LABELLED MK351A
Authors: Mendelsohn F. A. O. 
Published: June 2007

SUMMARY1. The potent angiotensin converting enzyme inhibitor, MK351A, was radioiodinated and found to show saturable, high affinity, reversible binding to membrane fractions of rat lung. At 20°C the labelled inhibitor bound to lung membranes with a T½ of ≏ 2–3 min and reached a plateau at 15 min; the complex dissociated with a T½, ≏ 65 min on addition of excess unlabelled MK521.2. The potency of a series of converting enzyme inhibitors in displacing the radioactive ligand closely paralleled their anticatalytic potency, strongly suggesting that the ligand labels the active site of converting enzyme.3. This ligand has the desired properties as a probe for autoradiographic localization of converting enzyme since it exhibits high affinity, stable binding to the enzyme with very low non‐specific binding (< 2% of total).4. In vitro autoradiographic analysis using 125I‐MK351A revealed a very high density of converting enzyme in lung, small bowel mucosa, adrenal zona glomerulosa and medulla and renal cortex. In rat forebrain a very high density of binding was found in the choroid plexus, subfornical organ and caudate‐putamen.5. This technique provides a promising method for the quantitative localization of angiotensin converting enzyme in tissues.
DEVELOPMENT OF ANGIOTENSIN CONVERTING ENZYME IN FETAL LUNG AND PLACENTA OF THE RAT AND HUMAN
Authors: Sim M. K. , Seng K. M. 
Published: June 2007

SUMMARY1. Angiotensin converting enzyme (ACE) activity in fetal lung and placenta was determined by the method of Cushman and Cheung (1971) during the second trimester of human pregnancy and throughout the rat gestation. The enzyme activity in the neonatal rat lung was also determined during the first 19 days of life.2. The enzyme activity in both tissues of both species increased with gestation. The activity in human fetal lung at the end of the second trimester was already 70% of that present in the adult human lung while rat fetal lung enzyme activity at term was only 15% of the adult value. The activity in the term placenta of the human and rat was respectively 13% and 5% that of the adult lung value. Developmental increases in enzyme activity continued in the neonatal rat lung till adult value at about 19 days postpartum.3. The pattern of fetal lung enzyme development in the rat resembled that of the rabbit fetal lung as determined by other investigators using different techniques but was different from that of the human.4. The findings support the suggestion that ACE in the lung and placenta play important roles in the maintenance of circulatory homeostasis during the latter part of gestation, at birth and early postpartum, albeit at a different extent in different species.
ALTERATIONS IN CEREBROSPINAL FLUID SODIUM AND OSMOLALITY IN RATS DURING ONE‐KIDNEY, ONE‐WRAP RENAL HYPERTENSION
Authors: Haywood J. R. , Buggy J. , Fink G. D. , DiBona G. F. , Johnson A. K. , Brody M. J. 
Published: June 2007

SUMMARY1. Measurements of plasma and cerebrospinal fluid (CSF) sodium and osmolality were made throughout the course of one‐kidney, one‐wrap Grollman renal hypertension.2. Although the plasma sodium and osmolality did not rise after 28 days, CSF sodium and osmolality was increased significantly at 3 days postwrap.3. As a result, the CSF to plasma ratio for both sodium and osmolality was significantly elevated during the initial postwrap period.4. These observations suggest that an increase in CSF sodium may provide an initiating stimulus for an elevated arterial pressure in one‐kidney, one‐wrap renal hypertension.
THE MEASUREMENT OF PLASMA THROMBOXANE B2 AND THE EFFECT OF SMOKING
Authors: Sturm M. , Barden A. , Beilin L. J. , Taylor R. R. 
Published: June 2007

SUMMARY1. Plasma thromboxane B2 (TxB2) was measured by radioimmunoassay using an iodinated ligand following extraction and further purification by thin layer chromatography. Venous blood was sampled into a syringe containing the cyclooxygenase inhibitor meclofenamate.2. Normal levels, 15 pg/ml (s.d. = 8, n= 21), were lower than usually reported and measured values increased several fold over 20 min sampling from an indwelling needle.3. With appropriate sampling there was a statistically insignificant increase in plasma TxB2 after subjects smoked two cigarettes (n= 11). An average decrease occurred in a control group (n= 10) and the difference between groups was of borderline significance (P<0.05). Smoking did not change TxB2 production associated with platelet aggregation induced in vitro by collagen, whereas plasma adrenaline increased significantly.4. The results emphasize the importance of the technique of sampling and assay in the measurement of plasma TxB2.
A COMPARISON OF THE EFFECTS OF SALBUTAMOL, ETILEFRINE AND DEXTRAN DURING HYPOTENSION AND LOW CARDIAC OUTPUT STATES IN RABBIT
Authors: Adigun S. A. , Fentem P. H. 
Published: June 2007

SUMMARY1. The effects of salbutamol (25 and 50 μg/kg), etilefrine (50 and 200 μg/kg) and dextran (8 ml/kg) on cardiovascular function have been studied in the rabbit.2. The three drugs raised the resting cardiac output (with salbutamol producing Δ max 52%, P<0.001, n=5) and right heart filling pressure (RHFP, Δ max from dextran 3.5 cmH2O; P<0.001, n=6) and lowered total peripheral resistance (TPR, Δ max from salbutamol 46%, P<0.001, n=5). However, TPR rose with the 200 μg/kg etilefrine (P<0.05, n=5). Pulse pressure rose with salbutamol (P<0.001, n=6) and etilefrine (P<0.05, n=6). Etilefrine raised resting BP (Δ max, P<0.001, n=6); salbutamol lowered resting BP (Δ max, P<0.001, n=6) while dextran (n=6) had little effect on resting BP.3. The actions of salbutamol are mediated mainly through β2‐adrenoceptors although the drug also has some minor β1‐adrenoceptor action. With etilefrine, the increase in cardiac output and the reduction in TPR are mediated through (β‐adrenoceptors while the increases in RHFP, blood pressure and TPR are a direct action on the α‐adrenoceptors.4. However, during haemorrhage the fall in diastolic pressure produced by salbutamol was considerably reduced while the reduction in mean BP and systolic pressure (which sometimes rose) was abolished. Dextran raised BP during hypotension produced by either sympathectomy or haemorrahge but not during normotension.5. The reflex recovery in RHFP and the reflex tachycardia were slightly attenuated during lower body negative pressure (LBNP) after salbutamol or dextran. The reflex recovery in blood pressure was complete and the pressure sometimes exceeded the resting level by up to 10 mmHg during LBNP after salbutamol, etilefrine (50 μg/kg only) and dextran.6. The reduced TPR (presumably due to vasodilation) and the increases in cardiac output and RHFP at an adequately maintained blood pressure produced by suitable doses of the three drugs may be useful in the management of circulatory shock and related states.
INTERACTION OF CHOLINE WITH NICOTINIC AND MUSCARINIC CHOLINERGIC RECEPTORS IN THE RAT BRAIN IN VITRO
Authors: Costa Lucio G. , Murphy Sheldon D. 
Published: June 2007

SUMMARY1. The ability of choline to interact with nicotinic receptors was investigated by measuring its ability to inhibit the specific binding of [3H]‐nicotine in rat brain.2. Choline, with an IC50 of 241 μmol/l, was three times more potent than its analogue deanol and almost 1000‐fold less potent than acetylcholine.3. Choline also inhibited the binding of the antagonist [3H]‐quinuclidinyl benzilate (IC50=2.5 mmol/l) and of the agonist [3H]‐oxotremorine‐M (IC50=165 μmol/l) to muscarinic cholinergic receptors.4. These results indicate that choline is able to interact directly, in vitro with brain cholinergic receptors of both the nicotinic and muscarinic type.
PARADOXICAL CARDIOVASCULAR RESPONSE TO VISCERAL AFFERENT STIMULATION IN THE ESTABLISHED SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Koyama Shozo , Manning John W. 
Published: June 2007

SUMMARY1. Afferent splanchnic nerve stimulation with different frequencies in Wistar Kyoto rats caused depressor and pressor responses depending on the frequency employed.2. Similar visceral afferent activation in spontaneously hypertensive rats caused depressor responses at all frequencies of stimulation.3. It is suggested that the central integrated mechanisms for activating a cardiovascular state change as evoked by visceral afferents may differ in the established hypertensive rat from that of the normotensive.
FURTHER STUDIES ON THE EFFECTS OF ADRENAL STEROIDS IN THE ACTIVE TRANSPORT OF SEROTONIN INTO RAT PLATELETS
Authors: Lee P. H. K. , Chan Mo‐Yin 
Published: June 2007

SUMMARY1. Male rats were treated with a fixed dose of aminoglutethimide (50 mg/kg s.c.) or with progressively increasing doses (50‐100 mg/kg s.c.) for 3 days. Corticosterone levels were found to be decreased in the latter group. Platelet uptake of serotonin as well as the apparent Vmax were decreased, whereas the Km of uptake were increased when compared with that of the control group.2. Addition of ACTH (10 iu/dl) to control rat platelet and corticosterone (10‐80 μg/dl) or triamcinolone (0.5‐5.0 μg/dl) to adrenalectomized rat platelet suspension in vitro did not increase the serotonin uptake of the preparation.3. Administration of exogenous dexamethasone (0.05‐0.2 mg/kg i.m.) or triamcinolone (0.05‐5.0 mg/kg i.m.) to adrenalectomized rats, caused a dose related increase in active uptake of serotonin by the platelets. Deoxycorticosterone (0.1‐1.0 mg/kg i.m.) did not have this effect.4. The time course of response to, and the maximum percentage increase in platelet serotonin uptake by, exogenous corticosteroids are related to their glucocorticoid potency.5. The possible role of glucocorticoids on platelet serotonin uptake process is discussed.
CHOLINERGIC NEUROMODULATION BY ATP, ADENOSINE AND ITS N6‐SUBSTITUTED ANALOGUES IN GUINEA‐PIG ILEUM
Authors: Katsuragi T. , Furuta K. , Harada T. , Furukawa T. 
Published: June 2007

SUMMARY1. The effects of ATP, adenosine and N6‐substituted adenosines, adenosine receptor agonists, on the twitch contraction of guinea‐pig ileum evoked by transmural stimulation were evaluated.2. Adenosine and ATP produced an immediate and concentration dependent inhibition of the twitch, IC50 being 1.1 × 10−5 mol/l and 1.2 × 10−5 mol/l, respectively.3. N6‐l‐phenylisopropyl adenosine (L‐PIA), N6‐cyclohexyl adenosine (CHA) and N6‐allyl adenosine also induced inhibitions which were gradual and persistent, IC50 being 2.6 × 10−8, 2.7 × 10−8 and 5.4 × 10−7 mol/l, respectively.4. Dipyridamole (10−7 mol/l), an adenosine uptake inhibitor, markedly augmented the inhibition evoked by adenosine and ATP, but not that by three N6‐substituted adenosines, while theophylline (10−4mol/l) almost completely antagonized the inhibitory effects of all purine compounds. IC50 value of adenosine in the presence of dipyridamole (5 × 10−7 mol/l) was shifted to the left about 50 times from the control, whereas that of L‐PIA was virtually unchanged.5. Tissue‐medium ratios indicating uptake of [H]adenosine, [3H]ATP and [3H]CHA into the segment were 3.23 (s.e.m. =0.59), 3.59 (s.e.m. =0.78) and 0.41 (s.e.m. =0.04), respectively.6. These results suggest that not only adenosine and ATP but also these N6‐substituted adenosines are potent agonists for the PI receptor, implying a similarity between PI and A, receptor in a functional role and these purine compounds may thereby modulate cholinergic neurotransmission by altering adenylate cyclase activity.
REGIONAL O2 SUPPLY/CONSUMPTION IN NORMAL AND ISCHAEMIC RABBIT MYOCARDIUM: EFFECT OF NIFEDIPINE
Authors: Eliades Diane , Talafih Khalid , Weiss Harvey R. 
Published: June 2007

SUMMARY1. The effect of nifedipine infusion on myocardial O2 supply and consumption in flow‐restricted and normal regions of the left ventricle was tested in anaesthetized open‐chest rabbits after ligation of the left anterior descending coronary artery for one hour.2. Ten min after occlusion, nifedipine‐treated animals were given either a low or high dose of the drug: a 5 μg/kg bolus followed by 1 μg/kg per min infusion or a 10 μg/kg bolus and 10 μg/kg per min infusion, respectively. Regional blood flow was measured before and after occlusion using radioactive microspheres and O2 saturation was measured microspectrophotometrically; the Fick Principle was then employed to determine regional O2 consumption.3. After a 60 min occlusion, blood flow was reduced overall to 51% of pre‐ligation flows in the occluded region, and treatment with nifedipine or vehicle did not significantly alter this flow reduction.4. Blood flow in nonoccluded regions increased 1.6‐fold only with the high dose of nifedipine and was unchanged in all other groups.5. Microspectrophotometric analysis of low dose nifedipine and control hearts showed that O2 extraction was greater in occluded than in normal myocardium (9.0, s.d. = 0.9, ml O2/100 ml blood vs 7.2, s.d. = 0.7, respectively) and that subendocardial extraction exceeded subepicardial.6. These data suggest that nifedipine administration at this dose had no apparent beneficial effect on O2 supply or O2 consumption in normal or flow‐restricted regions of the left ventricle during 1 h of coronary artery occlusion.
THE EFFECTS OF NIFEDIPINE ON THE SYSTEMIC AND CORONARY VASCULAR BEDS OF THE SHEEP: A POTENTIAL METHOD FOR INDUCTION OF ISCHAEMIA
Authors: Fu W. K. , Yong A. C. , Gangell P. , Roberts M. S. , Kilpatrick D. 
Published: June 2007

SUMMARY1. Nifedipine has been reported to aggravate symptoms of ischaemic heart disease in some patients. To investigate the possible reasons for this, vascular resistance changes in the systemic and coronary beds of sheep were compared with and without coronary artery stenoses.2. In six anaesthetized sheep, the dose‐response curve comparing vascular resistance to nifedipine dose showed greater sensitivity than that reported for either dogs or humans. The coronary vascular bed was more reactive than the systemic vascular bed but this difference did not reach a level of statistical significance.3. With fixed non‐elastic proximal coronary artery stenoses, the relationship of both coronary flow and coronary resistance to a standard dose of nifedipine (5 μg/kg) was indirectly related to the degree of stenosis. With stenosis reducing flow at rest by 50% or more, nifedipine usually produced a reduction in coronary flow in the stenosed artery and associated ST elevation, consistent with severe ischaemia in the distribution of the coronary. This effect is related to the reduction in perfusion pressure.
AN INVESTIGATION OF THE RECEPTORS INVOLVED IN THE CORONARY VASODILATORY EFFECT OF ADENOSINE ANALOGUES
Authors: Leung Edward , Johnston Colin I. , Woodcock Elizabeth A. 
Published: June 2007

SUMMARY1. The coronary vasodilatory effect of stable adenosine analogues is mediated by adenosine A2 receptors.2. These coronary receptors differ from A2 receptors found in other tissues.
ACTIONS OF THE SLOW CHANNEL ACTIVATOR, BAY‐K‐8644, ON THE ELECTRICAL ACTIVITY OF 3‐DAY‐OLD EMBRYONIC CHICK HEARTS
Authors: Sada H. , Sada S. , Sperelakis N. 
Published: June 2007

SUMMARY1. In order to assess the effects of Bay‐K‐8644 on electrical activities of young embryonic chick hearts in which the rising phase of the action potential (AP) depends on tetrodotoxin‐insensitive slow Na+ currents, slow AP were recorded in spontaneously beating 3‐day‐old embryonic chick hearts.2. Bay‐K‐8644(10‐6 mol/l) caused increases in the maximum rate of rise, amplitude, and duration of the slow AP; there was a slow increase in the spontaneous firing rate.3. Thus, Bay‐K‐8644 stimulates Na+ influx through TTX‐insensitive slow channels.
EFFECTS OF HISTAMINE RECEPTOR ANTAGONISM ON ADRENALINE‐INDUCED CHANGES IN BLOOD PRESSURE IN INTACT DOGS
Authors: Johnson Michael D. , Williams J. Lynn 
Published: June 2007

SUMMARY1. This study was designed to test the hypothesis that histamine may contribute to the vasodepressor response which occurs in response to physiologic increments in adrenaline concentration in intact animals. Accordingly, following a control period of 30 min, adrenaline was infused intravenously for 45 min at a rate of 250 ng/kg per min in 14 anaesthetized dogs (Group 1).2. A second group of eight dogs received an identical adrenaline infusion following complete H1 and H2‐histamine receptor antagonism with tripelennamine plus cimetidine (Group II).3. A time control group of experiments, in which no drugs were infused, as well as groups receiving adrenaline plus either tripelennamine or cimetidine, were also performed.4. In Group I, adrenaline infusion increased heart rate and reduced mean arterial blood pressure by 10 mmHg (P <0.01).5. Following combined H1 and H2‐histamine receptor antagonism (Group II), adrenaline infusion failed to reduce mean arterial blood pressure.6. However, mean arterial blood pressure was reduced significantly in the groups receiving adrenaline plus only one of the histamine receptor blocking agents.7. Since only the combined histamine receptor blockade completely eliminated the vasodepressor response to adrenaline, the data suggest that histamine may play a physiological role in the vasodepressor response to circulating adrenaline in the intact animal, and that both H1‐ and H2‐histamine receptors may be involved.
THE EFFECT OF THE 'HYPERTENSINOGENIC STEROID, 9α‐FLUORO‐CORTISOL ON BLOOD PRESSURE IN SHEEP WITH ACTH‐INDUCED HYPERTENSION
Authors: Mills Eric H. , Coghlan John P. , Denton Derek A. , Nelson Mark A. , Spence Campbell D. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. The effect of treatment with 9α‐fluorocortisol (9aFF), a steroid which causes hypertension in sheep, was examined in sheep with ACTH‐induced hypertension.2. ACTH treatment alone increased mean arterial pressure (MAP), plasma Na concentration, water intake and urine volume and decreased plasma K concentration.3. 9αFF treatment, for 3 days during continuing ACTH administration, did not change blood pressure but increased heart rate, water intake and urine volume and decreased urinary K excretion.4. As 9αFF did not cause a further increment in blood pressure in sheep with ACTH‐induced hypertension it is possible that both ACTH and 9αFF may produce hypertension by similar mechanisms.
THE EFFECT OF ALTHESIN, KETAMINE OR PENTOTHAL ON RENAL FUNCTION IN SALINE LOADED RATS
Authors: Chen C. F. , Chapman B. J. , Munday K. A. 
Published: June 2007

SUMMARY1. Rats were prepared with chronic cannulae in the carotid artery, jugular vein and urinary bladder; they were then kept 2 days to allow recovery from surgery.2. A steady‐state continuous saline diuresis was established, then various anaesthetic agents were injected and changes in the urine flow, sodium and potassium excretion rates, GFR, ERPF, ERBF and blood pressure were measured.3. Five groups of rats were studied: (1) control animals given saline in place of any anaesthetic agent, all parameters measured remained constant; (2) althesin (1.2 mg/kg), all parameters remained constant except for the blood pressure which decreased slightly for 5 min; (3) althesin (12 mg/kg); (4) ketamine (50 mg/kg); (5) pentothal (50 mg/kg). The above anaesthetics altered all of the measured parameters except urine output.4. Various mechanisms for these anaesthetic agents are discussed.5. In althesin anaesthetized rats, all the retarded renal parameters recovered within 30 min. It is concluded that for the study of renal function, if a brief anaesthesia is needed, althesin is a more suitable anaesthetic agent.
EFFECTS OF OPIATES AND OPIOIDS ON INTRAOCULAR PRESSURE OF RABBITS AND HUMANS
Authors: Drago F. , Panissidi G. , Bellomio F. , Belle A. Dal , Aguglia E. , Gorgone G. 
Published: June 2007

SUMMARY1. Acute intraocular injection of morphine or D‐Ala‐met‐enkephalinamide (D‐Ala‐E) in rabbits caused a sustained decrease in intraocular pressure. Conjunctival instillation of naloxone solution prevented the lowering effect of morphine or D‐Ala‐E on intraocular pressure.2. Aqueous outflow facility appeared to be significantly higher in patients addicted to morphine or heroin than in healthy volunteers. Intraocular pressure was significantly lower in addicted patients than in control subjects. Conjunctival instillation of naloxone solution decreased aqueous outflow facility and increased intraocular pressure in addicted patients.3. Patients with chronic open angle glaucoma showed a significant decrease in intraocular pressure after conjunctival instillation of morphine solution.4. It is concluded that intraocular opiate receptors are involved in the regulation of intraocular pressure in animals and humans.
USE OF SYNTHETIC OLIGONUCLEOTIDE AND RECOMBINANT DNA PROBES TO STUDY RENIN GENE EXPRESSION
Authors: Darby Ian A. , Aldred G. Peter , Coghlan John P. , Fernley Ross T. , Penschow Jennifer D. , Ryan Graeme B. 
Published: June 2007

SUMMARY1. Using hybridization histochemistry renin gene expression has been localized in the juxtaglomerular apparatus (JGA) of the renal cortex in both mouse and sheep kidney.2. This technique also located renin gene expression in afferent arterioles and interlobular arteries distant from the glomerular tuft in lamb renal cortex.3. A short (30 mer) synthetic oligonucleotide probe, complementary to a region of the mouse submaxillary gland renin gene, specifically labelled mouse submaxillary gland and kidney.4. Hybridization histochemistry and Northern blot analysis using both the synthetic oligonucleotide (mouse) probe and a 700 base pair recombinant (sheep) probe showed differences in renin gene expression in the kidney in response to Na restriction in the mouse and Na depletion in the sheep.
BLOOD PRESSURE, SALT TASTE AND SODIUM EXCRETION IN RATS EXPOSED PRENATALLY TO HIGH SALT DIET
Authors: Myers J. B. , Smidt V. J. , Doig S. , Nicolantonio R. Di , Morgan T. O. 
Published: June 2007

SUMMARY1. Blood pressure, sodium excretion and salt taste were examined in Sprague Dawley (SD) and Munich Wistar (MW) rats exposed prenatally to either a high salt (2.3% NaCl w/w) or control diet.2. There was no significant difference in blood pressure at 2, 6 or 12 months between high salt and control groups in either strain. Similarly there was no significant difference in sodium excretion following a saline load by gavage (150 mmol/l, 1.5% BW).3. Munich Wistar rats which received high salt diet prenatally exhibited a reduced saline preference when offered a choice between water and 150 mmol/l NaCl as drinking fluid. There was no significant difference in saline preference between Sprague Dawley rats which received the high salt or control diet.4. Prenatal exposure to high salt diet failed to alter the blood pressure or excretion of a salt load in either SD or MW rats. In MW rats but not SD high salt diet prenatally resulted in a reduced saline preference at 3 months of age.