bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stress‐Induced Elevation Of The St Segment In The Rat Electrocardiogram Is Normalized By An Adrenoceptor Blocker
Authors: Ueyama T , Yoshida K , Senba E 
Published: March 2003

SUMMARY1. Emotional stress is one of the aetiologies of cardiac accidents, but the precise mechanisms remain to be elucidated. In the present study we used the immobilization stress model in rats to investigate electrocardiographic (ECG) changes.2. A rapid elevation of the ST segment at the II, III, aVF and precordial leads in the ECG was found and this returned to prestress basal levels after removal of stress.3. This ECG change was normalized by combined blockade of α‐ and β‐adrenoceptors, but not by administration of a potent coronary vasodilator, such as a calcium channel blocker or nitroglycerin.4. These results suggest that direct activation of cardiac adrenoceptors by stress may result in angina‐like ECG changes.
Atrial Tachyarrhythmias Induced By Acetylcholine In Tilapia (Oreochromis SP.) Isolated Atria
Authors: Lin Tsai‐Chu , Hou Zone‐Yuan , Liu Hwan‐Wun , Wu Hui‐Sun , Lin Cheng‐I 
Published: March 2003

SUMMARY1. Effects of the parasympathetic neuromediator acetylcholine (ACh) on atrial tissues vary greatly depending on the species, the type of atrial cells and experimental conditions. The aim of the present study was to investigate, with microelectrode techniques, the arrhythmogenic effects of ACh in tilapia (Oreochromis sp.) isolated atria at room (22–25°C) and high temperature (37°C).2. Acetylcholine (1–10 μmol/L) shortened action potential duration (APD), depressed action potential plateau and decreased twitch force in tilapia atria, as it did in human atrial fibres. In addition, ACh induced premature responses and re‐entrant tachyarrhythmias (TA; frequency range from 7 to 25 Hz) in five of 19 and 14 of 22 tilapia atria tested at room and high temperature, respectively. The higher incidence of ACh‐induced TA at 37°C compared with room temperature was statistically significant.3. The ACh‐induced TA consisted of high‐frequency and uniform action potentials accompanied by tension oscillation and elevation of diastolic force (flutter). Acetylcholine‐induced TA could be readily abolished by atropine (1 μmol/L) and prevented by treatment with agents with local anaesthetic properties, such as 0.1 μmol/L tetrodotoxin or 3 μmol/L quinidine. The antagonistic action of quinidine occurred without significant prolongation of APD.4. The present findings suggest that pharmacological concentrations of the cholinergic muscarinic agonist ACh readily induce TA (mainly atrial flutter) in tilapia atria, presumably via sodium channel‐dependent re‐entrant excitation. The poikilothermic tilapia appears to be an appropriate animal model for the study of atrial TA.
Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin II
Authors: Hasser Eileen M , Cunningham J Thomas , Sullivan Margaret J , Curtis Kathleen S , Blaine Edward H , Hay Meredith 
Published: March 2003

SUMMARY1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume.2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation.3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by α2‐adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius.4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP‐dependent activation of neurons in the rostral ventrolateral medulla.
Centrally Produced Nitric Oxide And The Regulation Of Body Fluid And Blood Pressure Homeostases
Authors: Kadekaro Massako , Summy‐Long Joan Y 
Published: March 2003

SUMMARY1. Nitric oxide (NO) tonically inhibits the basal release of vasopressin and oxytocin into plasma.2. Nitric oxide inhibition on vasopressin secretion is removed, while that on oxytocin is enhanced, during water deprivation, hypovolaemia, moderate osmotic stimulation and angiotensin (Ang)II. This results in a preferential release of vasopressin over oxytocin that promotes conservation of water.3. Nitric oxide facilitates drinking behaviour stimulated by water deprivation, osmotic stimulation, haemorrhage and AngII. Together with the hormonal response, NO produces a positive water balance during reductions in intracellular and intravascular volumes.4. Nitric oxide produced within the central nervous system maintains resting arterial blood pressure partially by attenuating the pressor actions of AngII and prostaglandins.5. Central production of NO is enhanced during osmotic stimulation to counterbalance the salt‐induced pressor response.6. Paradoxically, central production of NO is also enhanced during haemorrhage, presumably to maintain peripheral vasodilation and blood flow to vital organs.
Anteroventral Third Ventricle Periventricular Tissue Contributes To Cardiac Baroreflex Responses
Authors: Bealer Steven L 
Published: March 2003

SUMMARY1. The studies reviewed in the present paper demonstrate that the anteroventral third ventricle (AV3V) region contains tissue that can modify cardiac baroreflex sensitivity in response to circulating angiotensin (Ang)II and hyperosmolality.2. The response to hyperosmolality appears to be mediated by noradrenergic receptors. Although the role of noradrenergic receptors in the AV3V region in modification of baroreflex‐induced responses to AngII has not been directly tested, this neurotransmitter is a good candidate for control of heart rate because noradrenaline in the AV3V region is critical for mediating other responses to AngII.3. Results from studies indicate that the AV3V region is part of a central nervous system circuit involved in modulation of cardiac baroreflex sensitivity by circulating substances, possibly acting at the organum vasculosum lamina terminalis.4. The findings extend the role of the AV3V periventricular tissue as a central site integrating autonomic nervous system function by demonstrating that this brain area contributes to cardiac function, in addition to its well‐characterized role in sympathetic nervous system regulation of blood pressure and mechanisms of fluid and electrolyte regulation.
Enalapril Prevents Aortic Hyperreactivity And Remodelling In One‐Kidney, One‐Clip Hypertensive Rats Without Reducing Arterial Pressure
Authors: Cunha Valdeci , Salgado Helio C , Salgado Maria Cristina O 
Published: March 2003

SUMMARY1. The present study was designed to evaluate the blood pressure‐independent effects of angiotensin‐converting enzyme (ACE) inhibition on cardiovascular structure and function in one‐kidney, one‐clip (1K1C) hypertensive rats.2. The study was conducted in four groups of rats: (i) uninephrectomized normotensive rats (1K); (ii) 1K1C hypertensive rats; (iii) 1K rats treated with enalapril; and (iv) 1K1C rats treated with enalapril. Enalapril treatment (20 mg/kg per day, p.o.) was started after surgery to induce hypertension or nephrectomy and continued for 5 weeks.3. The increase in blood pressure of 1K1C rats was associated with activation of cardiac and aortic, but not plasma, ACE activity and with hypertrophy of both heart and aorta. No difference in cardiac output and in vitro systolic function was observed among the groups. Hypertrophied aorta isolated from 1K1C rats displayed increased sensitivity to phenylephrine (PE) and unaltered responses to both acetylcholine (ACh) and sodium nitroprusside compared with the 1K group.4. Enalapril treatment effectively inhibited plasma and tissue ACE activity in 1K1C and 1K rats. Enalapril did not prevent the development of hypertension and cardiac hypertrophy nor did it change haemodynamic parameters in 1K1C rats. However, enalapril prevented the increase in aortic media thickness and cross‐sectional area and restored the hypersensitivity to PE in aortic rings of 1K1C rats. The endothelium‐dependent response to ACh was enhanced by enalapril in the aorta of 1K but not 1K1C rats.5. These results suggest a role for activated local angiotensin II generation in aortic but not cardiac hypertrophy secondary to 1K1C hypertension.
Neuronal Response To Physical Injury And Its Relationship To The Pathology Of Alzheimer’s Disease
Authors: King Ce , Adlard Pa , Dickson Tc , Vickers Jc 
Published: March 2003

SUMMARY1. Central nerve cells undergo a stereotyped regenerative response following physical injury.2. This reaction involves adaptive changes within the axon and cell body of origin, directed at sprouting and synaptogenesis.3. Intimately associated with the regenerative response are specific alterations to cytoskeletal proteins, including the neurofilament (NF) triplet.4. The morphological and neurochemical alterations to NF within axons following injury are reminiscent of plaque‐ associated dystrophic neurites (DN) in early Alzheimer’s disease (AD).5. Associated changes in perikaryal NF resemble Alzheimer neurofibrillary tangle pathology, while growth‐associated sprouting markers are localized to the abnormal neurites of AD.6. The present review postulates that β‐amyloid plaques in AD cause physical damage to local nerve cell processes and it is the chronic stimulation of the stereotyped response to injury that results in the end‐stage pathology and neurodegeneration associated with AD.
Bedside Perspectives On The Use Of Opioids: Transferring Results Of Clinical Research Into Practice
Authors: Ravenscroft Peter , Schneider Jennifer 
Published: March 2003

SUMMARY1. Transference of research findings to clinical practice has been a challenge for those managing chronic pain. Generally, pain is not well controlled in hospitals and steps need to be taken to make pain control more effective.2. Clinical trials of opioids have shown that pain can be controlled in the great majority of patients. Apart from the use of the World Health Organization Analgesic Ladder, a ‘pain diagnosis’ should be made and a comprehensive view of pain needs to be considered by the clinician. This would include pain and other physical symptoms, psychological issues and social and spiritual stresses.3. Respiratory depression and tolerance for opioids are often seen as negative aspects of opioids and, therefore, may lead to inadequate control of pain. The evidence cited suggests that, in the long‐term treatment of cancer pain, respiratory depression almost never occurs. The only situation that warrants caution is when an anaesthetic block or similar procedure relieves pain treated by opioids, when that patient has been receiving large doses of opioids. Long‐term studies with opioids show that tolerance may occur, but is not a clinical problem and should not impair their use in adequate doses to relieve the patient’s pain.4. The active morphine metabolites, morphine‐3‐glucuronide (M3G) and morphine‐6‐glucuronide (M6G) do need to be considered when administering morphine. There seems to be considerable interindividual variation in the production and elimination of metabolites. In cases of renal failure or in the elderly, the ratios of M3G and M6G to morphine accumulate exponentially, making opioid toxicity more likely. Even different routes of administration seem to be associated with different ratios of metabolites. A knowledge of these sources of pharmacokinetic variability may lead to more effective use of the opioids in clinical practice.
A New Method For Simultaneous Measurements Of Mast Cell Proteases In Human Vascular Tissue
Authors: Takai Shinji , Sakaguchi Masato , Jin Denan , Miyazaki Mizuo 
Published: March 2003

SUMMARY1. Human mast cells contain carboxypeptidase A, chymase and tryptase. In the present study, in order to analyse the mast cell proteases simultaneously, we investigated a method for the measurement of carboxypeptidase A, chymase and tryptase in human vascular tissues.2. Human vascular tissues were homogenized in 10 mmol/L phosphate buffer containing 0.2, 0.4, 0.6, 0.8, 1.0, 1.2, 1.4, 1.6 or 1.8 mol/L KCl and 0.1% non‐idet P‐40 and samples were then extracted. Because carboxypeptidase A and chymase convert angiotensin (Ang)I to Ang‐(1–9) and AngII, respectively, the extracts were incubated with AngI in the presence of an angiotensin‐converting enzyme (ACE) inhibitor. The extract prepared in buffer with over 0.8 mol/L KCl converted AngI to Ang‐(1–9) and AngII. Formation of Ang‐(1–9) and AngII plateaued in extracts with 1.0 and 1.2 mol/L KCl, respectively.3. The formation of Ang‐(1–9) and AngII in the extract with 1.2 mol/L KCl was inhibited by inhibitors of carboxypeptidase A and chymase, respectively, suggesting that Ang‐(1–9) and AngII were generated from AngI by carboxypeptidase A and chymase, respectively.4. Using a specific tryptase substrate, tryptase activity was detected in extract in buffer with over 0.8 mol/L KCl and reached a plateau at concentrations of KCl over 1.0 mol/L.5. These findings show that the maximum activity of carboxypeptidase A, chymase and tryptase was detected in extracts of human homogenized vascular tissues in buffer at 1.2 mol/L KCl. The present study demonstrates a new method for the simultaneous measurement of proteases derived from mast cells in humans.
Activity Of The Na+/H+ Exchanger Contributes To Cardiac Damage Following Ischaemia And Reperfusion
Authors: Allen Dg , Xiao X‐H 
Published: March 2003

SUMMARY1. The present review considers the evidence that Na+–H+ exchange activity contributes to cardiac damage following ischaemia and reperfusion. The basic mechanism involved is that protons are produced during ischaemia and leave the myocytes on the Na+/H+ exchanger during either ischaemia and/or reperfusion. The resulting elevation of [Na+]i causes Ca2+ loading through the Na+/Ca2+ exchanger and the elevated [Ca2+]i is thought to lead to myocardial damage.2. Inhibition of the Na+/H+ exchanger during ischaemia and/or reperfusion produces a substantial cardioprotective effect by blocking the damage caused by the coupled exchanger mechanism described above. Preconditioning also produces a cardioprotective effect and the evidence that this also involves the Na+/H+ exchanger is reviewed.3. The intracellular mechanisms associated with ischaemic damage and preconditioning are of great interest because they may provide targets for potential therapeutic interventions. The intracellular regulation of the Na+/H+ exchanger appears to be an important component of these pathways and may become a focus for therapeutic approaches.
Role For Capillaries In Coupling Blood Flow With Metabolism
Authors: Sarelius Ingrid H , Cohen Kenneth D , Murrant Coral L 
Published: March 2003

SUMMARY1. Skeletal muscle blood flow is coupled with metabolism; for this coupling to be effective in matching blood flow to capillary exchange, control of capillary blood flow and recruitment must reside at the capillary level.2. Capillaries are, indeed, capable of sensing and responding to vasoactive stimuli. We report studies that indicate that contraction of skeletal muscle fibres underneath capillaries is capable of increasing blood flow in those capillaries.3. This presumed metabolically related signal initiates remote dilations in arterioles upstream of the stimulated capillaries. Our findings indicate that the vasodilatory signal is transmitted along the blood vessel wall.4. Although we present evidence supporting a role for gap junctionally mediated communication of this vasodilatory signal, it appears unlikely to be primarily electrotonic spread of membrane potential changes.5. Our studies further indicate that the transmitted signal is not dependent on changes in endothelial cell calcium.
Glomerular Expression Of Endothelial Nitric Oxide Synthase In Deoxycorticosterone Acetate‐ Salt‐Treated Rats
Authors: Tsuchiya Ken , Naruse Mitsuhide , Nihei Hiroshi 
Published: March 2003

SUMMARY1. In the present study, we investigated the relationship between chronic volume loading and glomerular endothelial nitric oxide synthase (eNOS) expression. Immunohistochemical expression of eNOS in glomeruli was semiquantified by graded scores of staining intensity. Each glomerulus was isolated by microdissection and mRNA expression was detected by reverse transcription–polymerase chain reaction (RT‐PCR) in desoxycorticosterone acetate (DOCA)‐salt‐treated rats.2. Glomerular expansion and dilatation of tubules were the main histological findings and glomerular and vascular injury scores were significantly higher in the DOCA‐salt‐treated group than in the control group. Endothelial NOS staining in glomeruli in DOCA‐salt‐treated animals was 81.4% lower than in control animals. Endothelial NOS mRNA was also detected at a very low rate in the kidney of treated rats compared with control rats (22/80 vs 74/80 glomeruli, respectively).3. These results suggest that eNOS protein and mRNA expression in glomeruli was reduced by DOCA‐salt loading. Chronic volume loading may damage the glomerulus and this may be mediated, at least in part, by disruption of eNOS.
Ischaemic Preconditioning Ameliorates Functional Disturbance And Impaired Renal Perfusion In Rat Ischaemia–Reperfused Kidneys
Authors: Ogawa Toshihisa , Mimura Yoshikazu , Hiki Naoki , Kanauchi Hajime , Kaminishi Michio 
Published: March 2003

SUMMARY1. The effects of ischaemic preconditioning (IP) on renal function, haemodynamics and lipid peroxidation in the rat ischaemia–reperfused kidney model were examined.2. In Wistar male rats, application of a single or three periods of 5 min bilateral renal ischaemia was performed prior to 30 min bilateral ischaemia and 90 min reperfusion (IR). The glomerular filtration rate (GFR) was estimated in terms of inulin clearance. Fractional excretion of sodium (FENa) and lithium (FELi), indicating total and proximal tubular sodium handling, respectively, was also measured and renal blood flow was monitored throughout the experiment. In addition, renal lipid peroxidation (LPO) levels in reperfused kidneys were evaluated.3. A 2.8‐fold increase in recovery of GFR (P < 0.005), a 50% reduction in FENa (P < 0.005) and a 40% decrease in FELi (P < 0.05) after IR resulted from the single period of 5 min IP. Renal blood flow was also higher than that in the control group (P < 0.01). No change of LPO levels was observed.4. We conclude that IP may have an ability to ameliorate reperfused renal function and haemodynamics with a suitable period of preconditioned ischaemia, although this effect is independent of LPO.
Neural Regulation Of Renal Blood Flow: A Re‐Examination
Authors: Malpas Simon C , Leonard Bridget L 
Published: March 2003

SUMMARY1. The importance of renal sympathetic nerve activity (RSNA) in the regulation of renal function is well established. However, it is less clear how the renal vasculature responds to the different mean levels and patterns of RSNA. While many studies have indicated that small to moderate changes in RSNA preferentially regulate renin secretion or sodium excretion and only large changes in RSNA regulate renal blood flow (RBF), other experimental evidence suggests that small changes in RSNA can influence RBF2. When RSNA has been directly measured in conjunction with RBF, it appears that a range of afferent stimuli can induce reflex changes in RBF. However, many studies in a variety of species have measured RBF only during stimuli designed to reflexly increase or decrease sympathetic activity, but have not recorded RSNA. While this approach can be informative, it is not definitive because the ability of the vasculature to respond to RSNA may, in part, reflect the resting level of RSNA and, therefore, the vasoconstrictive state of the vasculature under the control conditions.3. Further understanding of the control of RBF by RSNA has come from studies that have analysed the underlying rhythms in sympathetic nerve activity and their effect on the cardiovascular system. These studies show that the frequency–response characteristic of the renal vasculature is such that higher frequency oscillations in RSNA (above 0.6 Hz) contribute to setting the mean level of RBF. In comparison, lower frequency oscillations in RSNA can induce cyclic vasoconstriction and dilation in the renal vasculature, thus inducing oscillations in RBF.4. In summary, the present review discusses the neural control of RBF, summarizing evidence in support of the hypothesis that RBF is under the influence of RSNA across the full range of RSNA.
Experimental Biology 2000 Symposium on Differential Control of Sympathetic Outflow A DEFENCE‐LIKE REACTION: AN EMERGENT PROPERTY OF A SYSTEM OF COUPLED NON‐LINEAR OSCILLATORS
Authors: Gebber Gerard L 
Published: March 2003

SUMMARY1. The present paper deals with the central mechanisms responsible for the defence‐like differential pattern of spinal sympathetic outflow elicited by electrical activation of the mid‐brain periaqueductal grey (PAG) in urethane‐anaesthetized, baroreceptor‐denervated cats. The pattern is characterized by increases in the 10 Hz discharges of the inferior cardiac (CN) and renal (RN) sympathetic nerves and a decrease in 10 Hz activity of the vertebral sympathetic nerve (VN) that supplies vasoconstrictor outflow to the forelimb.2. The model used to explain this pattern is based on the self‐organizing properties of a system of coupled brainstem oscillators rather than the activation of point‐to‐point hard‐wired connections leading to increases in sympathetic outflow to some targets and decreases to others.3. The fact that VN 10 Hz activity was inhibited by PAG stimulus frequencies equal to or just above, but not just below, that of the free‐running (control) rhythm argues against a ‘hard‐wired’ model.4. The evidence supporting the hypothesis that the defence‐like pattern is an emergent property of a system of coupled oscillators includes changes in the phase lag of VN 10 Hz activity relative to that in the CN, temporal correlation of the changes in phase angle and 10 Hz powers and the direct relationship between the magnitude of the change in phase angle and the degree to which PAG stimulation reciprocally affected the 10 Hz discharges of the CN and VN.5. It is proposed that changes in phase angle reflect the reorganization of the coupling of 10 Hz oscillators and that such changes in state lead to differential patterns of spinal sympathetic outflow.
Proceedings of the Australian Physiological and Pharmacological Society Symposium: Ion Channels GENETICS, AN ALTERNATIVE WAY TO DISCOVER, CHARACTERIZE AND UNDERSTAND ION CHANNELS
Authors: Schofield Peter R 
Published: March 2003

SUMMARY1. The conventional approach to understanding the structure and properties of ion channels has been to use physiological characterization.2. Purification and molecular cloning of ion channel genes has enabled more detailed structure–function analyses to be undertaken.3. An alternative approach to the identification of genes of pathophysiological importance has been the use of genetic linkage approaches and positional cloning or positional candidate analysis of ion channel genes.4. Using genetic approaches, mutations have been described that cause inherited neurological disorders of neurons (e.g. epilepsy, migraine, deafness, ataxia and startle disease), skeletal muscle (myotonia, malignant hyperthermia, periodic paralysis and myasthenia) and cardiac muscle (long QT syndrome and ventricular fibrillation).5. For each disease, gene structure–function analyses of the mutant alleles have provided further insights into the biology of ion channels.6. The present brief review examines the methods used in genetic linkage studies and positional cloning of disease genes. Understanding how ion channel gene mutations give rise to dysfunctional channels will be important in defining and treating the episodic and chronic channelopathies.