bluuebunny/crossref_metadata_2025_split huggingface dataset:
REPRODUCIBILITY OF ARTERIAL COMPLIANCE AND CAROTID WALL THICKNESS MEASUREMENTS IN NORMAL SUBJECTS
Authors: Liang Yu‐Lu , Cameron James D. , Teede Helena , Kotsopoulos Dimitra , McGrath Barry P. 
Published: June 2007

SUMMARY1. Non‐invasive techniques to measure indices of arterial function and wall thickness are frequently used as surrogate markers of cardiovascular disease. Reproducibility of measurements of arterial compliance has been infrequently reported and little is known about the interrelationships of the various indices in vivo.2. The present study was designed to assess reproducibility and interrelationships of indices of systemic arterial compliance, pulse wave velocity, carotid compliance and intima‐media thickness (IMT).3. Fifty healthy volunteers (20 male and 30 female; aged 20‐70 years, mean 46.5 years), participated in the present study. Each subject was studied on two occasions by the same investigators, using an identical protocol at an interval of 1‐5 weeks (mean 2.5 weeks) without lifestyle change.4. There were no significant differences between visits for any recorded general data, except resting blood pressure, which was lower on the second occasion. There were no systematic differences within each pair over the range of measurements for any of the variables. Bland‐Altman plots of repeatability of changes in indices showed that the mean values between visits were not significantly different. All indices of central arterial compliance were significantly related to age and IMT.5. Thus, under controlled experimental conditions, there was satisfactory repeatability of measurements of indices of both intrinsic and functional arterial mechanical properties (central and carotid arterial compliance and IMT). This type of information will permit the construction of sample size tables for clinical trials using these indices.6. Central arterial compliance may be an important determinant of IMT.
PITUITARY‐ADRENAL RESPONSES TO COMBINED ORAL D‐FENFLURAMINE AND INTRAVENOUS NALOXONE IN HUMANS
Authors: Grice Jeffrey E. , Torpy David J. , Hockings Gregory I. , Walters Margaret M. , Crosbie Georgina V. , Jackson Richard V. 
Published: June 2007

SUMMARY1. Fenfluramine is an optically active 5‐hydroxytryptamine (5‐HT) releaser and re‐uptake inhibitor. Increased brain 5‐HT mediates appetite suppression, the d enantiomer being more active than l‐ or dl‐fenfluramine. Fenfluramine also stimulates the hypothalamic‐pituitary‐adrenal (HPA) axis, leading to suggestions that this could act as a marker for its biological actions. However, the d enantiomer appears less active than a comparable dl racemate dose in animals, while effects of D‐fenfluramine on the human HPA axis remain unproven. The aim of the present study was to clarify this.2. Seven healthy human volunteers (three male, four female; 18‐58 years) received 30 mg oral D ‐fenfluramine or placebo, followed by 125 p‐g/kg, i.v. naloxone or placebo, in randomized, double‐blinded, placebo‐controlled afternoon studies. We measured plasma adrenocorticotropic hormone (ACTH) and Cortisol levels in samples taken at intervals throughout the study period.3. In contrast to previous results with dl‐fenfluramine, we found no dynamic responses to d ‐fenfluramine alone and no augmentation of responses to naloxone.4. Central pathways to HPA axis activation are apparently not stimulated by d ‐fenfluramine at this dose in humans, in contrast with dl‐fenfluramine, where the l enantiomer may be more selective for proposed corticotropin‐releasing hormone‐mediated, post‐synaptic 5‐HT2 or noradrenergic mechanisms. As previously reported, d‐fenfluramine significantly blunted the circadian fall in basal plasma Cortisol, providing in vivo evidence for serotonergic involvement in circadian regulation.
AMYLIN: PHYSIOLOGICAL ROLES IN THE KIDNEY AND A HYPOTHESIS FOR ITS ROLE IN HYPERTENSION
Authors: Wookey Peter J. , Cooper Mark E. 
Published: June 2007

SUMMARY1. There are high‐affinity binding sites for amylin in the renal cortex associated with proximal tubules. These appear to represent seven transmembrane (heptatopic) receptors that are known to form ternary complexes with G‐proteins and activate second messenger systems.2.Amylin stimulates sodium/water reabsorption from the basolateral side of the proximal tubules and plays a role in sodium homeostasis.3. The transient expression of amylin‐like mRNA has been detected perinatally, using in situ hybridization, in the sub‐nephrogenic zone of the metanephros and is associated with proximal tubules of the developing nephron. There it is thought to play a role as a growth factor for brush border epithelial cells in the developing kidney and in renal regrowth in the adult kidney.4. In two models of hypertension, the spontaneously hypertensive rat (SHR) and one created surgically by subtotal nephrectomy, renal amylin receptors are activated. In the SHR, activation precedes the rise in blood pressure and suggests that activation of the amylin system may be an important event in the development of hypertension.
ROLE OF THE MESOLIMBIC DOPAMINE SYSTEM IN CARDIOVASCULAR HOMEOSTASIS. STIMULATION OF THE VENTRAL TEGMENTAL AREA MODULATES THE EFFECT OF VASOPRESSIN ON BLOOD PRESSURE IN CONSCIOUS RATS
Authors: van den Buuse Maarten 
Published: June 2007

SUMMARY1. The possible role of the ventral tegmental area (VTA) and its dopaminergic projections in cardiovascular regulation is reviewed.2. Our own work has shown that stimulation of the VTA by local microinjection of the substance P analogue DiMe‐C7 caused an increase in blood pressure. The mechanism of the pressor response was an interaction of central dopaminergic activation, most likely at the level of the baroreflex, with the circulatory actions of vasopressin.3. These findings are important for a possible role of the mesolimbic dopamine system in cardiovascular homeostasis. Several studies reviewed here show that neuronal activity of the VTA and its mesolimbic projections is altered by changes in blood pressure, salt and electrolyte balance, stress and food and water intake.4. The VTA and mesolimbic dopamine system, while playing a widely accepted role in locomotor activity, cognition and reward mechanisms, may also be involved in the integration of sensory and behavioural information with cardiovascular homeostasis.
DOPAMINE RELEASES ENDOTHELIUM‐DERIVED RELAXING FACTOR VIA α2‐ADRENOCEPTORS IN CANINE VESSELS: COMPARISONS BETWEEN FEMORAL ARTERIES AND VEINS
Authors: Segawa Tomonori , Ito Hiroyasu , Inoue Kiyoaki , Wada Hisayasu , Minatoguchi Shinya , Fujiwara Hisayoshi 
Published: June 2007

SUMMARY1. We investigated the role of vascular smooth muscle α‐adrenoceptor subtypes in the vasoconstrictor response of femoral arteries and veins to dopamine and whether the vasoconstriction is modified by endothelium‐dependent relaxation mediated via the activation of α2‐adrenoceptors in ring preparations of femoral arteries and veins from mongrel dogs.2. Dopamine contracted both arteries and veins in a dose‐dependent manner and this contraction was inhibited by pre‐treatment with phentolamine or prazosin. Pretreatment with yohimbine shifted the dose‐response curve for dopamine to the right in femoral veins, but not in arteries.3. Phenylephrine contracted femoral arteries and veins in a dose‐dependent manner and this contraction was inhibited by pretreatment with prazosin.4. Clonidine produced a bell‐shaped dose‐response curve in femoral veins and this curve was shifted upwards by pretreatment with NG‐nitro‐l‐arginine (l‐NNA). In contrast, femoral arteries were not affected by clonidine. NG‐Nitro‐l ‐arginine potentiated contractile responses to dopamine in both veins and arteries. This potentiation was inhibited by yohimbine or by the removal of the endothelium in both arteries and veins.5. These results suggest that dopamine contracts femoral arteries via stimulation of α1‐adrenoceptors and contracts femoral veins via stimulation of both α1‐ and α2‐adrenoceptors and that these contractions are attenuated by the vasodilator action of dopamine via α2‐adrenoceptor‐mediated release of endothelium‐derived relaxing factor.
FUNCTIONAL ASSESSMENT OF α1‐ADRENOCEPTOR SUBTYPES IN PORCINE CORONARY ARTERY
Authors: Yan Ming , Zhang Youyi , Du Xiao‐Jun , Han Chide 
Published: June 2007

SUMMARY1.α1‐Adrenoceptors are known to play an important role in vasoconstriction in response to adrenergic stimulation. However, the functional importance of α1‐adrenoceptor subtypes at the epicardial coronary artery remains unclear. We examined α‐adrenoceptor subtypes by comparing functional affinities for α‐adrenoceptor antagonists on noradrenaline (NA)‐induced vasoconstriction in porcine denuded right coronary arteries.2. Noradrenaline induced a dose‐dependent vasoconstriction in incubated vessel rings. Prazosin and phentolamine were potent and competitive antagonists for NA‐induced contraction (pA2 10.27 and 9.03, respectively). In contrast, the selective α2‐adrenoceptor antagonist yohimbine had a low affinity (pA2 6.13). Two selective α1A‐adrenoceptor antagonists, WB 4101 and 5‐methyl urapidil, were potent and competitive antagonists of α1‐adrenoceptor‐induced contraction (pA2 10.67 and 8.90, respectively) and the selective α1D‐adrenoceptor antagonist BMY 7378 had a low affinity (pA2 6.06). Noradrenaline‐induced contraction was insensitive to the alkylating effects of chlorethyl‐clonidine. These observations indicate that the vasoconstriction is predominantly mediated by the α1A‐adrenoceptor subtype. This was also supported by a good correlation between pA2 values from the present study and reported binding affinities (pKi) of various α‐adrenoceptor antagonists with cloned human α1A‐adrenoceptors (r= 0.98), but not for α1B‐ or α1D‐adreno‐ceptor subtypes (r= 0.77 and 0.41, respectively).3. Our results indicate that the α1A‐adrenoceptor is the main functional receptor subtype in porcine denuded coronary arteries.
METABOLIC EFFECTS OF THIOCTIC ACID IN RODENT MODELS OF INSULIN RESISTANCE AND DIABETES
Authors: Black Kelly , Qu Xianqin , Seale J Paul , Donnelly Richard 
Published: June 2007

SUMMARY1. The antioxidant thioctic acid (TA) has been used in the treatment of diabetic neuropathy and recent studies have suggested that TA also has pancreatic and peripheral effects that improve glucose transport and metabolism. In the present study, the metabolic effects of TA were evaluated in rodent models of insulin resistance (fructose‐fed Sprague‐Dawley rat) and insulin deficiency (streptozotocin (STZ)‐induced diabetic rat). Oral and intravenous glucose tolerance tests (OGTT and IVGTT, respectively) were performed in conscious rats after treatment with 50 mg/kg per day TA or vehicle for 5 days.2. Fructose feeding for 7 days induced insulin resistance and impaired glucose tolerance and hypertriglycerideaemia. Treatment of fructose‐fed rats with TA had no significant effect on fasting or stimulated glucose levels or on fasting triglyceride concentrations (e.g. the area under the curve for glucose (AUCglu) following OGTT was 1233 ± 67 and 1284 ± 59 in fructose‐fed rats treated with either TA (n= 12) or vehicle (n= 12), respectively). Similarly, TA had no significant effect on IVGTT profiles in fructose‐induced insulin resistance.3. Low‐dose STZ (80 mg/kg, i.p, over 2 days) induced hyper‐glycaemia, but TA had no significant glucose‐lowering effects in STZ‐diabetic rats (AUCglu (OGTT) following oral administration was 5507 ± 27 and 5450 ± 27 in TA (n= 12) and vehicle‐treated (n= 12) rats, respectively). Nor did pretreatment with TA affect the diabetogenic response to STZ.4. In contrast with previous in vitro studies reporting favourable metabolic effects of TA, the present study shows that after short‐term oral therapy there are no significant improvements in glucose tolerance in rodent models of insulin resistance and insulin deficiency. Thioctic acid is unlikely to be of therapeutic benefit as an anti‐diabetic drug in clinical practice.
EVOLUTION OF SURFACE ACTIVITY RELATED FUNCTIONS OF VERTEBRATE PULMONARY SURFACTANT
Authors: Daniels Christopher B. , Lopatko Olga V. , Orgeig Sandra 
Published: June 2007

SUMMARY1. Pulmonary surfactant is a mixture of lipids and proteins that lines the air‐liquid interface of the lungs of all vertebrates. In mammals, it functions to reduce and vary surface tension, which helps to decrease the work of breathing, provide alveolar stability and prevent alveolar oedema. The present review examines the evolution and relative importance of these surface activity related functions in the lungs of vertebrates.2. The surface activity of surfactant from fish, amphibians, birds and most reptiles is generally very low, correlating with a low body temperature and a low disaturated phospholipid content of their surfactant. In contrast, the surfactant of those reptiles with a higher preferred body temperature, as well as that of birds and mammals, has a much higher surface activity.3. The two main functions of surfactant in mammals are to provide alveolar stability and to increase compliance of the relatively stiff bronchoalveolar lung. As the respiratory units of most non‐mammalian vertebrates are up to 1000‐fold larger and up to 100‐fold more compliant, surfactant is not required for these functions.4. In non‐mammals, surfactant appears to act as an anti‐glue preventing the adhesion of respiratory surfaces that may occur when the lungs collapse (e.g. during diving, swallowing of prey or on expiration). Surfactant also controls lung fluid balance. These functions can be fulfilled by a surfactant with relatively low surface activity and may represent the primitive functions of surface active material in vertebrate lungs.
EVOLUTION OF THYROID HORMONE DISTRIBUTION
Authors: Schreiber Gerhard , Prapunpoj Porntip , Chang Linus , Richardson Samantha J. , Aldred Angela R. , Munro Sharon L. 
Published: June 2007

SUMMARY1. Appropriate distribution of thyroxine between the lipid‐soluble compartments of cells and tissues and the extracellular aqueous space is established by binding to extracellular proteins. Among these proteins, transthyretin is of particular interest because it is the only one synthesized in the brain.2. The evolutionary onset of transthyretin synthesis in cells of the blood‐brain barrier precedes that in the liver, with the exception of a very short period of transthyretin synthesis in the liver of tadpoles, just prior to the climax of metamorphosis. In adult liver, transthyretin is only synthesized in endothermic vertebrates.3. The affinity of transthyretin for thyroxine increases and that for 3,5,3′‐triiodothyronine decreases during the evolution of eutherians from reptile/bird‐like common ancestors.4. A systematic change of the N‐terminal region of transthyretin occurred during evolution, leading to shorter and more hydrophilic transthyretin N termini in eutherians compared with those in reptiles and birds.5. The molecular mechanism of the evolution of the transthyretin N termini is a stepwise shift of the splice site at the intron 1/exon 2 border in the 3’ direction. The most probable cause for this shift is a series of single base mutations.6. As the N termini are located on the surface of transthyretin near the entrance to its central channel leading to the thyroxine binding sites, it is possible that a change in the structure of this region could influence the access of thyroxine to the binding sites. The increase in affinity for thyroxine could then be a driving force in the natural selection during evolution of transthyretins with shorter and more hydrophilic N termini.
PARATHYROID HORMONE‐RELATED PROTEIN IN LOWER VERTEBRATES
Authors: Danks JA , Trivett MK , Power DM , Canario AVM , Martin TJ , Ingleton PM 
Published: June 2007

SUMMARY1. Parathyroid hormone‐related protein (PTHrP) is an important mediator of humoral hypercalcaemia of malignancy in humans. Normal human subjects have very low levels of PTHrP in their circulation.2. Parathyroid hormone‐related protein has recently been demonstrated in high levels in the circulation and tissues of the sea bream and the dogfish, leading to the hypothesis that PTHrP may be a ‘classical’ hormone in fish.3. Immunohistochemistry and in situ hybridization were performed to investigate the evolutionary history of PTHrP. Tissues were examined from a number of lower vertebrates, including lungfish, lamprey and several species of bony and cartilaginous fish. Parathyroid hormone‐related protein was localized to the skin and to kidney tubules in all animals studied. In the developing lungfish, PTHrP was observed in the notochord, developing brain and skeletal muscle layers. These results suggest that PTHrP is of ancient origin and has a basic and fundamental function in vertebrates.
CHAOTIC CHARACTERISTICS OF RENAL NERVE PEAK INTERVAL SEQUENCE IN NORMOTENSIVE AND HYPERTENSIVE RATS
Authors: Zhang Tao , Johns Edward J 
Published: June 2007

SUMMARY1. The use of non‐linear dynamic analysis for the measurement of control processes in low‐dimensional signals, for example, blood pressure and heart rate variability, are well established and accepted. However, the application of these analytical techniques to a high‐dimensional signal, such as renal sympathetic nerve activity (RSNA), has not been validated.2. The present study set out to develop an approach whereby the high‐dimensional signal of RSNA was reduced to a low‐dimensional one by extracting the peak interval sequence (PIS), using Cluster analysis, in order to allow the use of non‐linear dynamics analysis. Brachial nerves were electrically stimulated (1.6 Hz, 0.2 ms, 15 V) to elicit a sympatho‐excitation in groups of anaesthetized normotensive Wistar and stroke‐sprone spontaneously hypertensive rats (SHRSP).3. It was found that, under basal conditions, the correlation dimension, D2, was stable over a range of embedding dimensions from 12 to 25. Moreover, the largest Lyapunov exponent had a small positive value that was also stable over these embedding dimensions. These values showed that the signal was of low dimensionality and that chaos was present.4. In Wistar rats, brachial nerve stimulation significantly (P<0.05‐0.001) increased blood pressure (by 25%), heart rate (by 5%) and RSNA (by 200%), which was associated with significant (P<0.05) reductions in the correlation dimension D2 and the largest Lyapunov exponent of the PIS generated from the renal nerve signal. In contrast, in SHRSP, there were similar increases in blood pressure, heart rate and RSNA in response to brachial nerve stimulation, but neither the correlation dimension nor largest Lyapunov exponent was altered.5. These findings demonstrate that by extracting the PIS from the renal sympathetic nerve signal, the application of non‐linear chaos analysis makes it possible to distinguish differences in the pattern of refiexly induced excitation in sympathetic traffic to the kidney in the pathophysiological state of hypertension. Whether this applies to sympathetic outflow to other organs and tissues remains to be investigated.
OXYGEN RADICALS AND NITRIC OXIDE IN RAT MESENTERIC ISCHAEMIA‐REPERFUSION: MODULATION BY L‐ARGININE AND NG‐NITRO‐L‐ARGININE METHYL ESTER
Authors: Haklar G , Ulukaya‐Durakbaś Ç , Yüksel M , Dagh T , Yalçin AS 
Published: June 2007

SUMMARY1. The aims of the present study were to detect changes in superoxide anion (O2−), nitric oxide (NO) and other reactive oxygen species (ROS) directly by measurement of chemilumin‐escence (CL) and to investigate the role of L‐arginine, a nitric oxide synthase (NOS) substrate, and NG‐nitro‐L ‐arginine methyl ester (L‐NAME), a NOS inhibitor, together with their molecular enantiomers D‐arginine and D‐NAME, in a rat mesenteric ischaemia‐reperfusion (I/R) model.2. Seventy‐nine female Wistar albino rats were divided into eight groups. The first three groups underwent sham operation; group 1 was the control group, group 2 received L‐arginine and group 3 received L‐NAME. Ischaemia was produced in the remaining five groups by ligation of the superior mesenteric artery for 30 min followed by 60 min reperfusion. Group 4 rats were control I/R rats and groups 5‐8 received either L‐arginine, L‐NAME, D‐arginine or D‐NAME, respectively.3. Both luminol and lucigenin CL was significantly increased in I/R groups compared with sham‐operated groups. L‐Arginine significantly reduced CL measurements. D‐Arginine was also protective, but not as much as L‐arginine. Both L ‐ and D‐arginine had in vitro O2−‐scavenging potential, as tested by the xanthine‐xanthine oxidase system. NG‐Nitro‐L‐arginine methyl ester decreased lipid peroxidation values in addition to reducing CL measurements. Nitric oxide concentrations were significantly increased in I/R groups in comparison with sham‐operated groups. Peroxynitrite formation was increased by I/R. Treatment with L‐NAME was beneficial by reducing NO concentrations in the reperfused ileum.4. In our I/R model, O2−, NO and other ROS were increased. Although NOS inhibitors were effective in reducing oxidative damage, increasing NO concentrations with L‐arginine was also beneficial, presumably due to the ability of L‐arginine to inhibit phagocyte adherence and its radical scavenging potential. In fact, NO may have different effects in terms of tissue injury or protection depending on the concentration of oxygen and the haemodynamic state of the tissue.
TEMPERATURE‐DEPENDENT INOTROPIC EFFECTS OF LIGNOCAINE AND ETHANOL ON RAT HEART PAPILLARY MUSCLES
Authors: Schulz Carlos S , Salvatici Raul P , Standen Dolly J , Cabezas Mirtha E , Carpentier Robert G 
Published: June 2007

SUMMARY 1. The main objective of the present study was to investigate the temperature dependence of the cardiac inotropic effects of lignocaine and ethanol (EtOH). 2. We studied the in vitro inotropic actions and interactions of EtOH (2.4 g/L) and lignocaine (25 mg/L) on rat papillary muscles superfused with Tyrode's solution and stimulated at 1 Hz at either 37 or 30°C. Peak tension developed (PTD), maximum velocity of development of tension (VmaxT) and time to peak tension (TPT) were measured. 3. At 37°C, EtOH depressed PTD, while VmaxT and TPT remained unchanged. At 37°C, lignocaine alone or in combination with EtOH depressed all three parameters. 4. At 30°C, EtOH did not modify PTD or VmaxT, whereas TPT decreased. At 30°C, lignocaine decreased TPT, but VmaxT did not change and the effect of lignocaine on PTD was smaller at 30°C than at 37°C. Ethanol and lignocaine in combination decreased all three parameters at 30°C. However, the depression of VmaxT by the combination of lignocaine and EtOH was less at 30°C than at 37°C. 5. Hypothermia (30°C) protected the myocardium against the depressant actions of EtOH and lignocaine, alone or in combination. With EtOH alone, the protection resulted in no change in PTD. When lignocaine was involved, the protection resulted in a weaker action on PTD and VmaxT. The temperature dependence of the action of lignocaine may explain, at least in part, the development of ventricular failure in cardiac surgical patients exposed to lignocaine during hypothermia and rewarming.
EFFECT OF GRAPEFRUIT JUICE ON URINARY 6β‐HYDROXYCORTISOL/CORTISOL EXCRETION
Authors: Seidegård Janeric , Dahlström Kerstin , Kullberg Annika 
Published: June 2007

SUMMARY1. The aim of the present study was to evaluate the effect of grapefruit juice on urinary 6β‐hydroxycortisol and Cortisol excretion in healthy subjects.2. The ratio of 6β‐hydroxycortisol/cortisol was significantly decreased (P= 0.036) in the 0–4 h fraction of urine after ingestion of grapefruit juice, but not in the 4–24 h fraction (P= 0.218) or for the compiled data, fraction 0–24 h (P= 0.114).3. These results indicate that endogenous Cortisol metabolism may not only be of hepatic origin, but may also be dependent on the metabolic capacity of cytochrome P450IIIA (CYP3A) in the gut mucosa.4. This finding may cast further doubts of the usefulness of the 6β‐hydroxycortisol/cortisol ratio as an indicator of hepatic CYP3A activity.