bluuebunny/crossref_metadata_2025_split huggingface dataset:
FUNCTION, CHARACTERIZATION AND AUTORADIOGRAPHIC LOCALIZATION AND QUANTITATION OF β‐ADRENOCEPTORS IN CARDIAC TISSUES
Authors: Molenaar Peter , Russell Fraser D. , Shimada Tatsuo , Summers Roger J. 
Published: June 2007

SUMMARY1. This paper demonstrates the use of organ bath, radioligand binding and autoradiography to detect β1‐ and β2‐adrenoceptors in human and guinea‐pig cardiac tissues.2. In organ bath experiments, non‐selective and β1‐ and β2‐adrenoceptor selective agonists produced concentration‐dependent inotropic responses in human right atrial appendage. Both subtypes mediate inotropic responses. In guinea‐pig right atria chronotropic responses were mediated predominantly through β1‐adrenoceptors.3. Receptor binding studies using (—)[125I]‐cyanopindolol (CYP) and β1‐ and β2‐adrenoceptor selective antagonists showed that β2‐adrenoceptors comprised 25% of the total population of β‐adrenoceptors in guinea‐pig right atria. In human right atria the proportion is higher (40%).4. Quantitative autoradiography was used to determine the location and densities of β1‐ and β2‐adrenoceptors in guinea‐pig heart. Both β2‐ and β2‐adrenoceptors were distributed on myocardium. The atrioventricular conducting system had a higher density of β2‐adrenoceptors compared with myocardium.
OPIATE RECEPTORS: LIGANDS AND METHODS OF STUDY
Authors: Olley Jean E. 
Published: June 2007

SUMMARY1. An introduction to the current knowledge of the μ‐, k‐ and δ‐opioid receptors will be given.2. The many problems associated with opiate ligands with respect to selectivity, potency, slow receptor kinetics, instability and poor access to the central nervous system will be discussed.3. Current systems for analysis of the receptor profile of opiate ligand activity will be given.4. The properties of opioid ligands will be discussed in the context of the identified problems.
METHOD OF MEASURING LIQUID JUNCTION POTENTIALS IN SMALL (NANOLITRE) DROPLETS OF BIOLOGICAL FLUIDS
Authors: Sugo E. , Györy A. Z. 
Published: June 2007

SUMMARY1. A method is described which allows the determination of liquid junction potentials between biological fluid samples of less than 1 nL with a reproducibility of 10%. This was achieved by use of a micro‐method and the use of 3% agarose added to the electrolyte in the measuring electrodes.2. Validation was performed with a modified flowing boundary method and the system was also tested using a solution containing divalent ions. Liquid junction potential between surface fluid from rat kidneys and harvested renal proximal tubular fluids was‐0.62 ± 0.11 mV (mean ± s.d., n= 66).
ACTIONS OF SOME AUTACOIDS AND PEPTIDES, INCLUDING RELAXIN, ON COSTO‐UTERINE MUSCLE FROM RATS
Authors: Fox D. , Handberg G. M. , Hartley M. L. , Monagle J. , Pennefather J. N. 
Published: June 2007

SUMMARY1. The actions of angiotensin II, bradykinin, oxytocin, arginine vasopressin, relaxin, serotonin and the prostaglandins E2 and F2α were examined on preparations of costo‐uterine muscle from stilboestrol‐treated rats.2. All the agonists, except relaxin, when used in concentrations which contract the rat uterus, also produced contractions of costo‐uterine muscles. Concentration‐response curves were steep and maximal responses to the agonists were comparable. The negative log molar EC50 values were: serotonin, 6.5; angiotensin II, 8.8; bradykinin, 8.4; PGE2, 8.3; PGF2α, 7.1. The EC50 values (units/L) for oxytocin and vasopressin were 4.4 and 2.7 respectively.3. Indomethacin (2.8 or 5 μmol/L) did not decrease the contractile effects of the peptides or serotonin. The effects of serotonin were reduced, but not reversed, by methysergide (0.94 μmol/L).4. Porcine relaxin inhibited field stimulation‐induced contractions of costouterine muscle and uterine horns from immature rats pretreated with oestradiol cypionate and from stilboestrol‐treated mature rats. It was much less potent, and its effects were less clearly concentration‐related, on costo‐uterine muscle.5. The inhibitory effects of relaxin on the uterus were unaffected by propranolol (1 μmol/L), confirming that on this tissue relaxin acts independently of the release of catecholamines. Progesterone (30 μmol/L) was also without effect on the action of relaxin on the uterus.6. These results taken together indicate that the costo‐uterine muscle of the rat: (i) contracts in response to serotonin and the peptides angiotensin II, arginine vasopressin, bradykinin and oxytocin independently of the release of the contractile prostaglandins F2α and E2; and (ii) in contrast to the uterus, may lack a significant population of receptors for relaxin. These differences from the whole uterine horn of this species may reflect the absence of endometrial tissue, and/or of sensitivity of the smooth muscle cells of the costo‐uterine muscle to oestrogen.
RENAL HYPER‐RESPONSIVENESS TO BLOOD VOLUME EXPANSION IN BRATTLEBORO RATS IS NOT RELATED TO PLASMA ANF IMMUNOREACTIVITY
Authors: Palluk Rainer , Veress Anthony T. , Sonnenberg Harald 
Published: June 2007

SUMMARY1. Anaesthetized homozygous Brattleboro (DI) rats were used to study the renal response to iso‐oncotic blood volume expansion.2. With the same degree of hypervolaemia DI rats had exaggerated diuresis, natriuresis, and chloriuresis, but not kaliuresis, compared with heterozygous control rats. This increased excretion resulted in negative water balance by the end of the experiment in DI rats, whereas the controls showed restoration of normal balance. The control rats retained significant amounts of sodium and chloride, the Brattleboro rats, however, did not.3. The lithium clearance method was used to localize the defect in sodium reabsorption. As judged from this method, there was a significantly lower sodium reabsorption in the proximal tubules as well as in the distal parts of the nephron of DI rats.4. Plasma immunoreactivity of atrial natriuretic factor (ANF) was not different between groups before volume expansion. ANF levels rose and fell similarly in both groups during and after the iso‐oncotic infusion.5. Our results demonstrate that DI rats respond to acute hypervolaemia with an exaggerated diuresis and saluresis. The mechanism of the increased salt excretion may involve inhibition of sodium transport in the proximal tubules as well as in the distal parts of the nephron. These transport defects are not dependent on differing plasma ANF levels.
WHOLE BLOOD AGGREGATION AND PLASMA LYSO‐PAF RELATED TO SMOKING AND ATHEROSCLEROSIS
Authors: Sturm Marian J. , Strophair Julie M. , Kendrew Phillip J. , Vandongen Robert , Beilin Lawrence J. , Taylor Roger R. 
Published: June 2007

SUMMARY1. Aggregation of diluted whole blood (impedance method) and thromboxane B2 production during aggregation were measured in cigarette smokers and non‐smokers, aged 41–68 years, with (n= 14) and without (n= 15) major symptomatic peripheral vascular disease. The plasma level of the lyso derivative of platelet activating factor (lyso‐PAF) was also measured using a bioassay with 14C‐serotonin labelled rabbit platelets, after extraction and acetylation to active PAF.2. Aggregation to ADP and collagen was significantly less in non‐smokers without vascular disease (n= 8) than in the other three groups (P < 0.01; ANOVA). Thromboxane B2 production was not significantly different between the groups. There was no significant difference in plasma lyso‐PAF between groups. No change was found in any variable after smokers smoked two cigarettes.3. In these older age subjects, both vascular disease and the smoking habit were associated with greater whole blood aggregation. However, current smoking and the smoking of two cigarettes did not affect aggregation in subjects with vascular disease and plasma lyso‐PAF levels were not consistently related to either smoking or vascular disease.
EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na+,K+‐ATPase
Authors: Hegde Sharath S. , DeFeo Maria L. , Jandhyala Bhagavan S. 
Published: June 2007

SUMMARY1. These studies were conducted to determine whether preservation of the functional integrity of the membrane, Na+,K+‐stimulated ATPase is essential for the atrial natriuretic factor (r‐ANF‐8–33) to enhance guanosine 3′,5′‐monophosphate (cGMP) content in the rat aortic smooth muscle. In freshly dissected rat aortic tissues, levels of cGMP were estimated using radioimmunoassay.2. ANF (0.1 μmol/L in Krebs‐Henseleit media) produced significant elevation in cGMP levels in the aortic smooth muscle when compared with that incubated in the control media, whereas suppression of Na+‐pump with ouabain (1.0 mmol/L) and/or K+‐free media did not produce any significant changes in the basal cGMP level; these two experimental manoeuvres did not prevent enhancement of cGMP by ANF.3. Incubation of the tissues in the media containing ouabain plus vasoconstrictor concentrations of norepinephrine (0.3 μmol/L) also did not alter basal cGMP levels and did not prevent the ability of ANF to elevate cGMP.4. These studies demonstrate that the antagonism by ouabain, of vasorelaxant effects of ANF (as reported in the literature) are not due to the prevention of the ability of ANF to enhance cGMP levels in the arterial smooth muscle. It is proposed that such an antagonism may be related to the actions of ouabain and ANF on diverse, and perhaps independent, mechanisms which affect Ca2+‐fluxes across the cell membrane.
COMPARISON OF THE VASCULAR AND GLOMERULAR CHANGES IN AORTIC‐LIGATURE AND DOCA‐SALT HYPERTENSION
Authors: Hewitson Tim , Kamitsuji Hidekazu , Whitworth Judith A. , Kincaid‐Smith Priscilla 
Published: June 2007

SUMMARY1. Animals and histology from two previous investigations were used to test the hypothesis that a similar elevation in blood pressure may result in a different sequence of pathological changes in different experimental models of hypertension, DOCA‐salt and aortic‐ligature hypertension.2. To assess differences in morphological parameters, individual animals in the two groups were paired (n= 12) for the same level of blood pressure at sacrifice.3. Vascular damage was significantly less in the DOCA‐salt group (P < 0.01). Glomerular lesions however were more severe in the DOCA‐salt group. In rats with aortic‐ligature hypertension significantly fewer glomeruli had fibrinoid and/or crescents than in DOCA‐salt rats (P < 0.001). There were fewer glomeruli with epithelial cell droplets (ECD) and fewer ECD per glomerulus in aortic‐ligature when compared with DOCA‐salt hypertension (P < 0.001, P < 0.001, respectively).4. This study highlights the significance of factors other than blood pressure per se in producing vessel and glomerular lesions in experimental hypertension.
A METHOD FOR EXAMINING TURNOVER AND SYNTHESIS OF PALMITATE‐CONTAINING BRAIN LIPIDS IN VIVO
Authors: Robinson Peter J. , Rapoport Stanley I. 
Published: June 2007

SUMMARY1. A theoretical three compartment model is presented which gives the rate of incorporation of plasma palmitate into brain, Jpalm, in terms of turnover and synthesis of palmitate‐containing lipids, de novo synthesis of palmitate from acetate, and recycling of palmitate within lipids.2. Jpalm equals 4 h brain radioactivity following intravenous injection of [U‐14C]‐palmitate (determined with quantitative autoradiography), divided by integrated plasma specific activity of palmitate. Jpalm follows the time course of brain lipid synthesis during development of the rat, but is age‐invariant in the adult.3. At 1–7 days after 5 min of bilateral carotid occlusion in the awake gerbil, intravascular [14C]‐palmitate incorporation is reduced in the CA1 pyramidal layer of the hippocampus, consistent with delayed neuronal death, but is elevated in the CA3 and CA4 pyramidal layers and dentate gyrus, suggesting synthesis of new membrane during recovery from the ischaemic insult.4. Several weeks after unilateral destruction of the cochlea in 11 day old rats, incorporation of [14C]‐palmitate from plasma into appropriate central auditory regions is reduced, corresponding to reduced cell size and altered morphology.5. [14C]‐palmitate incorporation into the left hypoglossal nucleus is increased during and following axonal regeneration (up to 23% compared with control side) following transection of the left hypoglossal nerve in Fischer‐344 rats, whereas incorporation is decreased 6–7% when regeneration is prevented. Time courses of incorporation in both cases correspond to histological changes.6. The results show that the palmitate method can be used to examine regional turnover and synthesis of brain lipids following injury, sensory deprivation, development, regeneration and ageing.
NIFEDIPINE IN CORTICOSTEROID‐DEPENDENT ASTHMA: PRELIMINARY STUDY
Authors: Al‐Waili Noori S. 
Published: June 2007

SUMMARY1. To test whether nifedipine reduces corticosteroid requirements of patients with asthma, a 16‐week double‐blind crossover trial comparing nifedipine with placebo was performed.2. Eight females and seven males with corticosteroid‐dependent asthma were studied, ranging in age between 20 and 65 years (mean = 45 years).3. Results showed that in 12 of 15 patients, nifedipine caused significant reduction in corticosteroid requirements when compared with placebo (P < 0.01). No side‐effects were reported apart from mild headache and leg oedema observed in a few patients receiving nifedipine.4. It could be concluded that nifedipine has a steroid‐sparing effect in steroid‐dependent asthma.
INTERRELATIONSHIP BETWEEN CORTISOL AND ATRIAL NATRIURETIC FACTOR IN THE IMMATURE OVINE FETUS
Authors: Wintour E. Marelyn , Cooper Elizabeth , McDougall John G. , Shine Peter F. , Towstoless Michelle K. 
Published: June 2007

SUMMARY1. In chronically cannulated ovine fetuses (100–130 days of gestation) the infusion of cortisol (86.7 ± 15 μg/h for 4 h) or human atrial natriuretic factor (ANF; 4.4 μg for 2 h) resulted in highly significant increases in the excretion of sodium, chloride, potassium and water.2. Cortisol had no significant effect on fetal plasma ANF concentrations. All values are mean and s.e.m. Plasma immunoreactive ANF was 53 ± 5 and 67.3 ± 13 pmol/L in the 4 h saline infused fetuses, and 51.3 ± 14.3 and 74 ± 13.3 pmol/L in cortisol‐infused fetuses (n= 7). A separate group of fetuses received 2 h infusions of saline or hANF (4.4 ug/h), and plasma IR‐ANF values were measured (n= 3). The values, at 0, 60, 90 and 120 min were, respectively, 19.7 ± 3, 17.3 ± 0.7, 18.7 ± 3.7 and 20.7 ± 3.7 pmol/L in the saline infused group, and 25.3 ± 5.3, 80.7 ± 32.3, 123.3 ± 4.3 and 100 ± 15 pmol/L in the ANF‐infused fetuses.3. Blood cortisol concentrations, in fetuses infused for 4 h with 0.9% NaCl, were 3.1 ± 0.8 nmol/L (n= 7); in fetuses infused with 0.9% NaCl for 2 h were 3.6 ± 1 nmol/L (n= 3); in fetuses infused for 4 h with cortisol were 19.9 ± 1.9 nmol/L (n= 7); and in fetuses infused with hANF for 2 h were 6.0 ± 3.0 nmol/L (n= 5).4. There was no effect of fetal hANF infusion on maternal or fetal blood aldosterone concentrations.5. The conclusion of this study was that cortisol and ANF cause natriuresis and diuresis in the immature ovine kidneys by independent mechanisms.
STUDY OF THE INHIBITORY EFFECT OF LEAD ACETATE ON DUODENAL CONTRACTILITY IN RAT
Authors: Karmakar N. , Anand S. 
Published: June 2007

SUMMARY1. Abdominal colic and constipation are symptoms of lead poisoning in man, but mechanisms of these effects are not yet fully understood. In this study the effect of lead acetate on contractility of rat duodenum was determined in vivo in 70 rats.2. Rats were orally dosed with 44 mg/kg per day lead as 53 mmol/L lead acetate, for 4 weeks. Motility of the duodenum was recorded with an electrical impedance probe.3. A significant decrease in the amplitude of contraction waves in case of treated rats was observed compared with controls which received an equal volume of saline. The number of contractions increased from 26 per min in controls to 33 per min in treated rats. Gastrointestinal transit rate decreased by 64% and 69% after 9 and 15 days of lead exposure, respectively.
EFFECT OF SOME DRUGS ACTING AT THE CENTRAL‐TYPE BENZODIAZEPINE RECEPTORS ON BLOOD GLUCOSE IN MICE
Authors: Najim Rafid A. , Al‐Essa Luay Y. , Al‐Jawad Faruk H. 
Published: June 2007

SUMMARY1. The effects of some drugs acting at the central‐type benzodiazepines receptors on blood glucose levels in mice were studied.2. Clonazepam, injected intraperitoneally in doses of 0.625–5 mg, produced a dose‐dependent increase in blood glucose 30 min after administration.3. The hyperglycaemic effect of clonazepam (2.5 mg/kg, i.p.) was dose‐dependently reduced by Ro 15–1788 (10–40 mg/kg, i.v.), a benzodiazepine antagonist.4. Ro 5–3663, a GABA antagonist which may act at the picrotoxinin site, produced a significant increase in blood glucose (5 or 10 mg/kg, i.p.); however, when given together with clonazepam (2.5 mg/kg, i.p.) attenuation of the hyperglycaemic effect was observed.5. Pk 8165, a partial agonist, lacked an effect on blood glucose over the dose range of 5–20 mg/kg, i.p. but caused a slight increase in blood glucose in a dose of 40 mg/kg, i.p.
FACILITATION OF NORADRENALINE RELEASE BY ISOPRENALINE IN RAT ISOLATED ATRIA DOES NOT INVOLVE ANGIOTENSIN II FORMATION
Authors: Mian M. A. , Majewski H. , Rand M. J. 
Published: June 2007

SUMMARY1. Rat isolated atria were incubated with 3H‐noradrenaline and the intramural sympathetic nerves were stimulated at 2 Hz for 60 s. The stimulation‐induced (SI) efflux of radioactivity was used as an index of release of transmitter noradrenaline.2. Isoprenaline (0.1 μmol/L) alone did not increase noradrenaline release. Cocaine (30 μmol/L) produced a 73% increase in the stimulation‐induced release of noradrenaline. In the presence of cocaine, isoprenaline enhanced noradrenaline release by 22%.3. In the presence of cocaine, both angiotensin I (0.3 μmol/L) and angiotensin II (0.3. μmol/L) produced almost two‐fold enhancements in the SI release of noradrenaline.4. Captopril (5 μmol/L) blocked the facilitatory effect of angiotensin I on nor‐adrenaline release but did not alter that of isoprenaline.5. Saralasin (0.1 μmol/L) reduced the facilitatory effect of angiotensin II on noradrenaline release but did not alter that of isoprenaline.6. The findings indicate that the facilitation of noradrenaline release by isoprenaline in rat atria is not mediated by local formation of angiotensin II.
ELIMINATION OF DIFLUNISAL AS ITS ACYL GLUCURONIDE, PHENOLIC GLUCURONIDE AND SULFATE CONJUGATES IN BILE‐EXTERIORIZED AND INTACT RATS
Authors: Dickinson Ronald G. , King Andrew R. , Verbeeck Roger K. 
Published: June 2007

SUMMARY1. The disposition of diflunisal (DF) was investigated in both bile‐exteriorized and intact rats given 10 and 100 mg/kg doses intravenously (i.v.).2. In addition to the phenolic glucuronide (DPG) and acyl glucuronide (DAG) conjugates, the sulfate conjugate (DS) was found to be a major metabolite. The glucuronides were excreted preferentially in bile, whereas DS was excreted almost exclusively in urine.3. In bile‐exteriorized animals, recoveries of DPG, DAG and DS in bile were 12.2%, 23.8%, 0.4%, respectively, and in urine, 10.3%, 5.6% and 15.2%, respectively, at the 10 mg/kg dose; and in bile, 11.3%, 41.6% and 1.0% respectively, and urine 2.9%, 1.1% and 17.0%, respectively, at the 100 mg/kg dose.4. Total plasma clearance of DF and formation clearance of DF to DPG were reduced at the higher dose, suggesting saturation of this glucuronidation pathway. Formation clearances of DF to DAG and DS were little affected by the dose change.5. Considerable enterohepatic recirculation of DF was apparent from the prolongation of DF and its conjugates in plasma of rats with an intact bile flow into the gut. The net metabolic effect of such cycling was enhancement of overall DS formation, from 15.6% and 18.0% of the 10 and 100 mg/kg doses, respectively, in bile‐exteriorized rats to 28.5% and 42.1% of the doses respectively, in the intact animals.
REGIONAL DISTRIBUTION OF THE CARDIAC OUTPUT AND RENAL RESPONSES TO ATRIAL ATRIURETIC PEPTIDE INFUSION IN RABBITS WITH CONGESTIVE HEART FAILURE
Authors: Langton David , Jover Bernard F. , Trigg Lisbeth , Fullerton Meryl , Blake Duncan W. , McGrath Barry P. 
Published: June 2007

SUMMARY1. A biventricular, low‐output congestive cardiomyopathy was induced in 19 rabbits by administering adriamycin (16 mg/kg). The effects of SaL‐rat atrial natriuretic peptide (ANP) infused at 0.1, 0.2 and 0.4 μg/kg per min, were then examined in terms of (i) central haemodynamics (ii) regional blood flow (iii) renal function and (iv) plasma norepinephrine and plasma renin.2. In this dose range, ANP produced progressive and significant falls in stroke volume, cardiac output and mean arterial pressure, owing to a fall in venous return. The heart rate response to this was blunted.3. Using radiolabelled microspheres, significant falls in the perfusion of cutaneous, gastrointestinal and musculoskeletal tissues were observed, due to reduced vascular conductances in these beds. These changes were accompanied by activation of the sympathetic nervous system as evidenced by a progressive rise in plasma norepinephrine. A significant increase in plasma renin was only observed with the highest infusion of ANP.4. Renal blood flow was maintained in the face of a falling mean arterial pressure and cardiac output, but diuretic and natriuretic effects were absent.5. It was concluded that the dominant influence of ANP infusion in this model of heart failure appeared to be a reduction in cardiac preload with detrimental overall haemodynamic consequences.
EFFECTS OF NEUROPEPTIDE Y ON BAROREFLEX CONTROL OF HEART RATE AND MYOCARDIAL CONTRACTILITY IN CONSCIOUS RABBITS
Authors: Minson R. B. , McRitchie R. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. The effects of intravenous (i.v.) neuropeptide Y (NPY, 10 μg/kg bolus) on the stimulus‐response curves relating changes in heart period (HP) and in peak left ventricular (LV) dP/dt to acute changes in mean arterial pressure (MAP) were determined in conscious, normotensive rabbits.2. The relationship between increases and decreases in MAP and the subsequent changes in HP were represented by a sigmoid‐shaped curve described by a logistic function. Following NPY administration there was a baroreflex‐dependent increase in the maximum slope (sensitivity) at the midpoint of this MAP‐HP curve from 7.0 ± 0.5 to 10.6 ± 1.3 ms/mmHg (P<0.05). NPY caused an upward shift in the whole curve which reflected the NPY‐induced bradycardia and was independent of baroreflexes.3. The relationship between increases in MAP and decreases in peak LV dP/dt was determined during fixed‐rate atrial pacing to prevent the effects of the accompanying bradycardia. Increases in MAP and the corresponding reductions in peak LV dP/dt were represented by an exponential function.The slope of the curve, measured at its origin 5–15 min after NPY administration, was reduced from −0.9 ± 0.2 to −0.4 ± 0.1 units (P<0.05).4. The effects of NPY are consistent with an action on efferent connections of the arterial baroreceptor reflex, mediated through a reduction in cardiac β‐adrenergic tone. They would also be explained through actions on the afferent or central neural connections of the baroreflex.