bluuebunny/crossref_metadata_2025_split huggingface dataset:
CHRONIC STUDIES ON THE INTERACTION BETWEEN NITRIC OXIDE AND ENDOTHELIN IN CARDIOVASCULAR AND RENAL FUNCTION
Authors: Pollock David M 
Published: March 2003

1. Chronic inhibition of nitric oxide synthase (NOS) results in a persistent hypertension, while chronic blockade of endothelin ETA receptors has little effect on arterial pressure. These findings indicate that nitric oxide (NO) plays a more significant role than ET‐1 in the long‐term maintenance of arterial pressure.2. Although endothelin (ET) appears to contribute to the hypertension in the early stages of NOS inhibition, blockade of either ETA or both ETA and ETB receptors has only a minor effect on the hypertension beyond the initial 2 weeks of NOS inhibition.3. Endothelin may play a role in vascular lesion development associated with NOS inhibition, at least within the kidney, which may be related to angiotensin II activity.4. The processes involved in the hypertension associated with chronic NOS inhibition appear to be dynamic and may include an evolution of ET‐1 action. Variability in results from different laboratories may be related to genetic factors and choice of pharmacological agents.
ESTIMATION OF ARTERIAL MECHANICS IN CLINICAL PRACTICE AND AS A RESEARCH TECHNIQUE
Authors: Cameron James 
Published: March 2003

1. Large conduit artery pathophysiology is associated with considerable morbidity with even normal ageing, irrespective of concurrent influences, associated with impaired arterial function.2. Recent technical advances have enabled high‐resolution non‐invasive assessment of pulsatile arterial properties, but this has been largely confined to more muscular superficial arteries. There has been less study of arterial regions prone to disease that would, theoretically at least, benefit from pharmacological or other intervention to improve function.3. Based on studies in animal models and, in particular, human arterial segments, specific pharmacological agents have been proposed as improving arterial behaviour. If this is to become a therapeutic target, it behoves increased effort to understand and measure meaningful indices of arterial function and to find ways of assessing response and outcome.4. A number of different approaches to assessment and quantification of arterial mechanics are available in the literature. The present review compares and discusses some of these different techniques and looks at differences between arterial segments and evidence that appropriate intervention may beneficially modify arterial behaviour.5. For clinical or research usefulness, assessment of arterial mechanics must provide more information than currently derived from simple numerical measurement of brachial blood pressure. This is particularly true because epidemiological risk evidence is based on brachial rather than central blood pressure recordings. There has been an explosion of work in this field in recent years and the present review does not pretend to reference all relevant material; rather, it tries to provide a broad coverage of the topic and hopes to support the need for continued endeavours in the field of arterial mechanics.
EFFECTS OF MILD AEROBIC EXERCISE AND A MILD HYPOCALORIC DIET ON PLASMA LEPTIN IN SEDENTARY WOMEN
Authors: Okazaki Tetsuya , Himeno Etsuro , Nanri Hiroki , Ogata Hajime , Ikeda Masaharu 
Published: March 2003

1. The present study was conducted to investigate whether mild aerobic exercise and a mild hypocaloric diet, instead of severe restrictions on caloric intake, would affect weight reduction and plasma leptin concentrations.2. Forty‐one middle‐aged sedentary women (15 obese and 26 non‐obese) participated in a 12 week lifestyle‐modification programme to reduce cardiovascular risk factors. Bodyweight, body composition, plasma leptin concentrations, serum lipid profiles, fasting plasma glucose and fasting plasma insulin were measured before and after the 12 week intervention. The intervention consisted of aerobic exercise, corresponding to approximately 50% of maximal oxygen consumption, and personal diet counselling.3. Bodyweight decreased by (mean±SD) 3.9±3.4 kg in the obese group (P < 0.05) and by 1.7±1.8 kg in the non‐obese group (P < 0.05). The plasma leptin concentration decreased significantly from 14.7±5.3 to 8.9±3.6 ng/mL in the obese group (P < 0.001) and from 7.6±3.9 to 5.6±2.2 ng/mL in the non‐obese group (P < 0.01).4. Overall, for all subjects, both pre‐ and postintervention, the plasma leptin concentration was significantly correlated with body mass index (BMI; pre‐intervention: r = 0.73, P < 0.0001; postintervention: r = 0.67, P < 0.0001), fat mass (FM; pre‐ intervention: r = 0.74, P < 0.0001; postintervention: r = 0.63, P < 0.0001) and fasting plasma insulin (pre‐intervention: r = 0.66, P < 0.001; postintervention: r = 0.45, P < 0.01). The change in plasma leptin concentration was significantly correlated with the respective changes in BMI (r = 0.64, P < 0.0001), FM (r = 0.48, P < 0.01) and fasting plasma insulin (r = 0.58, P < 0.0001). Interestingly, the ratio of plasma leptin concentration to BMI or FM diminished significantly after intervention. In addition, we found that the plasma leptin concentration decreased in participants whose FM did not decrease. These results suggest that the production of leptin per unit FM decreased after intervention.5. Mild aerobic exercise and a mild hypocaloric intake decreased body mass and the plasma leptin level in Japanese middle‐aged sedentary women. This decrease in plasma leptin levels was likely to be associated with weight reduction plus some unknown factor(s).
LEFT VENTRICULAR MASS AND MICROALBUMINURIA: RELATION TO AMBULATORY BLOOD PRESSURE
Authors: Gatzka Christoph D , Reid Chris M , Lux Alan , Dart Anthony M , Jennings Garry L 
Published: March 2003

1. Both microalbuminuria and left ventricular hypertrophy may reflect target organ damage in essential hypertension. Both are related to the prevailing level of blood pressure and both are associated with an increase in morbidity and mortality.2. The database of the Hypertension Diagnostic Service, a multicentre secondary referral clinic for patients with essential hypertension, was analysed in order to clarify the level of association between microalbuminuria and left ventricular hypertrophy, which might explain the observed increase in morbidity and mortality in patients with microalbuminuria. Microalbuminuria was measured semiquantitatively by urine dip‐stix. After the exclusion of patients with potential secondary hypertension, renal disease and diabetes mellitus, patients with complete data for microalbuminuria, left ventricular mass (LVM) and 24 h blood pressure monitoring were selected.3. Data were complete for 704 patients (47% male, age 51±12 years) and 42% tested positive for microalbuminuria. Microalbuminuria was positively related to 24 h systolic blood pressure and weight and was negatively related to age. Left ventricular mass was higher in patients with microalbuminuria (men, 265±69 g; women, 207±61 g) than in those without (men, 250±64 g, P < 0.05; women, 185±50 g, P < 0.001). After correction for the effects of gender, body mass index and 24 h systolic blood pressure, the presence of microalbuminuria was associated with an increase in LVM of 10 g (P < 0.05, 95% confidence interval, 2–19 g).4. Microalbuminuria as measured by urine dip‐stix is associated with an increase in LVM in patients with essential hypertension, independent of other known determinants.
HYPERTENSION AND INSULIN RESISTANCE: ROLE OF PEROXISOME PROLIFERATOR‐ACTIVATED RECEPTOR γ
Authors: Itoh Hiroshi , Doi Kentaro , Tanaka Tokuji , Fukunaga Yasutomo , Hosoda Kiminori , Inoue Gen , Nishimura Haruhiko , Yoshimasa Yasunao , Yamori Yukio , Nakao Kazuwa 
Published: March 2003

1. Insulin resistance has been highlighted as a common causal factor for hypertension, hyperlipidaemia, diabetes mellitus and obesity, all of which are recognized to occur simultaneously, and a distinct clinical entity is defined as ‘multiple risk factor syndrome’.2. Recently, a new class of antidiabetic agents, thiazolidinediones (TZD) has been developed and has been shown to improve insulin resistance by binding and activating a nuclear receptor, peroxisome proliferator‐activated receptor (PPAR)γ.3. cDNA of rat PPARγ1 and γ2 were cloned and gene regulation of PPARγ in rat mature adipocytes was examined. Hydrogen peroxide, an oxygen radical, which is recognized to be the common intracellular signal for multiple risk factors, potently down‐regulated PPARγ mRNA expression in rat mature adipocytes.4. Tumour necrosis factor (TNF)‐α, which is considered to play a role in obesity‐induced non‐insulin‐dependent diabetes mellitus and to augment oxidative stress, also suppressed PPARγ expression.5. Thiazolidinediones dose‐dependently recovered TNF‐α‐induced down‐regulation of PPARγ mRNA expression.6. The modulation of PPARγ expression by TZD can be one mechanism for the improvement of insulin resistance by TZD.7. Vascular tone and remodelling are controlled by several vasoactive autocrine/paracrine factors produced by endothelial cells in response to several vascular injury stimuli, including hypertension. The PPARγ gene transcript was detected in cultured endothelial cells.8. The administration of TZD stimulated the endothelial secretion of type‐C natriuretic peptide, which is one of the natriuretic peptide family and is demonstrated by us to act as a novel endothelium‐derived relaxing peptide.9. Concomitantly, TZD significantly suppressed the secretion of endothelin, a potent endothelium‐derived vasoconstricting peptide.10. Thiazolidinediones can affect vascular tone and growth by modulating the production of endothelium‐derived vasoactive substances to influence occurrence and progression of hypertension and atherosclerosis.
CIGARETTE SMOKE AND ITS EXTRACT DELAYS ULCER HEALING AND REDUCES NITRIC OXIDE SYNTHASE ACTIVITY AND ANGIOGENESIS IN RAT STOMACH
Authors: Ma L , Chow JYC , Liu ESL , Cho CH 
Published: March 2003

SUMMARY1. The purpose of the present study was to examine whether cigarette smoke and its extract could affect ulcer healing, angiogenesis and nitric oxide synthase (NOS) activity in the gastric mucosa.2. Ulcerated rats were either exposed to cigarette smoke or given smoke extract once daily for 3 days. Rats were killed and stomachs were removed for the measurement of ulcer size, angiogenesis and NOS activity.3. Angiogenesis and constitutive NOS activity were concomitantly and dose‐dependently reduced by cigarette smoke or its extract. The same treatments also delayed ulcer healing.4. These results indicate that cigarette smoke and its extract repress the processes of new blood vessel formation and NOS activity during tissue repair in the gastric mucosa. These could, in turn, retard the healing process in the gastric mucosa.
Effects Of Resistance Training On Bone Parameters In Young And Mature Rats
Authors: Bennell Kim , Page Carolyn , Khan Karim , Warmington Stuart , Plant David , Thomas David , Palamara Joseph , Williams David , Wark John D 
Published: March 2003

SUMMARY1. Osteoporosis is a major public health problem that is predicted to worsen over the next decade and preventative strategies that increase bone strength have become the focus of substantial research.2. Although mechanical load is a primary factor in the acquisition and maintenance of skeletal tissue, the type of exercise used and when in life it is most effectively prescribed remain inconclusive.3. The present study compared 10 weeks of resistance training in both young and mature female Sprague‐Dawley rats and measured bone density and body composition by dual energy X‐ray absorptiometry and biomechanical properties by three point bending tests of the tibia and femur.4. No significant differences were observed for any of the bone parameters when comparing exercise and control groups at either age. This was despite using a comparable training protocol to that in humans and using loads of approximately 150% bodyweight.5. The present study concludes that more intensive work programmes of resistance training or different outcome measures are required when using animal models for skeletal research.
Skeletal Muscle Metabolism During Exercise In Humans
Authors: Hargreaves Mark 
Published: March 2003

SUMMARY1. Contracting skeletal muscle is able to use a number of intra‐ and extramuscular substrates to generate ATP during exercise. These include creatine phosphate (CP), muscle glycogen, blood‐borne glucose, lactate and free fatty acids (FFA), derived from either adipose tissue or intramuscular triglyceride stores.2. During high‐intensity short‐duration exercise, CP degradation and the breakdown of muscle glycogen to lactate are the major energy yielding pathways, although oxidative metabolism can make a significant contribution. The ‘anaerobic’ substrates are also important fuels during the transition from rest to steady state exercise.3. The oxidative metabolism of carbohydrate and lipid supplies most, if not all, of the ATP during prolonged submaximal exercise. Muscle glycogen, blood glucose and FFA are the key fuels. The relative importance of the various substrates for exercise metabolism is primarily determined by exercise intensity and duration, although training status, dietary manipulation and environmental factors can modify the metabolic response to exercise.
Carotid Artery Intima–Medial Thickness Is Increased In Chronic Renal Failure
Authors: Zoungas Sophia , Ristevski Sonya , Lightfoot Paul , Liang Yu‐Lu , Branley Pauline , Shiel Louise M , Kerr Peter , Atkins Robert , McNeil John J , McGrath Barry P 
Published: March 2003

SUMMARY1. Chronic renal failure (CRF) is associated with rapidly progressive atherosclerotic vascular disease. In the present study, carotid arterial intima–medial thickness (IMT) was assessed in a large cohort of patients with CRF and matched controls and related to risk factors.2. A total of 159 subjects with CRF (serum creatinine ≥ 0.40 mmol/L) aged > 50 years (mean (±SD) 63.8±7.7 years) and 159 healthy controls matched for age, sex and smoking status were studied.3. The IMT was determined using B‐mode ultrasound measurements of the far wall of both common carotid arteries and presented as the mean IMT. Fasting plasma homocysteine (tHcy) was measured in the CRF group.4. Intima–medial thickness was significantly greater in CRF patients than controls (0.89±0.17 vs 0.73±0.13 mm, respectively) after matching for age, sex and smoking status. Heart rate and pulse pressure were also significantly increased. The tHcy was increased two‐fold in the CRF group (27.7±11.3 μmol/L; normal < 13.0 μmol/L) and did not correlate with carotid IMT.5. Compared with controls after adjusting for traditional risk factors, patients with CRF exhibit significantly increased IMT.
Fluvastatin Normalizes The Decreased Turnovers Of Glutathione And Ascorbic Acid In Watanabe Heritable Hyperlipidaemic Rabbits
Authors: Suzumura Kuniharu , Kasahara Emiko , Ohnishi Yasuyo , Chien Kuang‐Chang , Inoue Masayasu 
Published: March 2003

SUMMARY1. Fluvastatin, a 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitor, has been reported to decrease the oxidizability of plasma lipids in hyperlipidaemic subjects. In order to elucidate one of the mechanisms of this in vivo, we investigated the effects of fluvastatin and pravastatin on the decreased turnovers of reduced glutathione (GSH) and ascorbic acid (AA) in Watanabe heritable hyperlipidaemic (WHHL) rabbits.2. These drugs (30 mg/kg per day) equally decreased plasma levels of lipids after a 4 week treatment period. However, only fluvastatin significantly decreased thiobarbituric acid‐reactive substances, which were increased in the plasma of WHHL.3. Although these drugs did not affect the steady state levels of total glutathione and low molecular weight thiols in the liver and kidney, fluvastatin markedly normalized the rate of GSH turnover in these tissues, as determined by using L‐buthionine‐(
S,
R)‐sulphoximine, a specific inhibitor of GSH synthesis.4. Fluvastatin also increased the clearance of AA from the circulation in WHHL.5. These results suggest that, in addition to its hypolipidaemic action, fluvastatin has the potential to improve the turnover of anti‐oxidants, which is closely related to the amelioration of the redox status in the body.
Anticardiolipin Antibodies In Spontaneously Hypertensive Rats (Shr), Stroke‐Prone Shr And Normal Wistar Rats
Authors: Todorova M , Baleva M , Nikolov K , Higashino H , Kamenov Z 
Published: March 2003

SUMMARY1. Anticardiolipin antibodies (ACA) can be detected in the serum of patients with autoimmune disturbances, ischaemic heart disease, myocardial infarction, neurological disorders and other medical conditions. Elevated values of these autoantibodies can be associated with recurrent fetal loss, arterial and venous thrombosis and thrombocytopenia.2. In the present study, we investigated the presence of ACA in three rat strains, namely normal Wistar rats (WR), spontaneously hypertensive rats Okamoto‐Aoki (SHR) and stroke‐prone SHR (SHRSP). All animals were examined at four ages: 1, 4, 10 and 12 months of age. Anticardiolipin antibodies were determined by ELISA.3. Anticardiolipin antibody levels in normal WR, which were used as controls, were lowest at 1 month and increased significantly from the 4th month on. At the prehypertensive age (1 month), ACA levels in SHR and SHRSP were significantly higher compared with control WR, decreased with age and were significantly lower at 4, 10 and 12 months compared with age‐matched WR.4. These differences may be a result of immunological disorders in SHR.
Dexmedetomidine And Haemodynamic Responses To Acute Central Hypovolaemia In Conscious Rabbits
Authors: Blake Dw , Ludbrook J , Leeuwen Af Van 
Published: March 2003

SUMMARY1. Effects of the α2‐adrenoceptor agonist dexmedetomidine on vasoconstrictor and heart rate (HR) responses to acute central hypovolaemia were studied in eight chronically instrumented rabbits. We compared intravenous (i.v.) and fourth ventricular (V4) dexmedetomidine (0.1–10 μg/kg) and the reversal of effects by the α2‐adrenoceptor antagonist idazoxan and the opioid agonist alfentanil.2. Gradual inflation of an inferior vena cava (IVC) cuff reduced cardiac index (CI) by 8%/min, with progressive vasoconstriction and increased HR. In control rabbits, at approximately 40% baseline CI, there was sudden decompensation with failure of vasoconstriction and a fall in mean arterial pressure (MAP).3. Dexmedetomidine (i.v. and V4) reduced resting MAP and HR and caused an earlier decompensation during central hypovolaemia. Intravenous dexmedetomidine (3 and 10 μg/kg) also reduced the slope of the initial vasoconstrictor response and the maximum HR.4. The effects of dexmedetomidine were reversed by the antagonist idazoxan, which prevented the decompensation phase. Intravenous alfentanil was also effective in restoring the vasoconstrictor response and delaying decompensation with hypovolaemia after dexmedetomidine. Combining dexmedetomidine with an opioid, such as alfentanil, may provide the benefit of reduced sympathetic tone without increased risk of cardiovascular collapse.
Localization Of Tachykinin Receptors And Fos‐Like Immunoreactivity Induced By Substance P In Guinea‐Pig Brain
Authors: Yip Jane , Chahl Loris A 
Published: March 2003

SUMMARY1. In the present study, a comparison was made between the distribution of tachykinin NK1 and NK3 receptor immunoreactivity and the distribution of Fos‐like immunoreactivity induced by the tachykinin agonist substance P (SP) in the guinea‐pig brain.2. In agreement with results from previous studies in rat brain, NK1 receptor‐immunoreactive neurons were found to be widely distributed throughout the brain in the striatum and in diencephalic and mesencephalic structures, while NK3 receptor‐immunoreactive neurons were mainly in telencephalic structures. Considerable overlap was observed between NK1 and NK3 receptor distributions.3. Substance P induced Fos‐like immunoreactivity (Fos‐LI) in extensive areas of the guinea‐pig brain. The induction of Fos‐LI was markedly inhibited in many areas by pretreatment with the NK1 receptor antagonist SR 140333. The NK3 receptor antagonist SR 142801 reduced Fos‐LI staining in fewer areas, although a reduction was observed in the cortex, striatum and hypothalamus.4. In general, tachykinin receptors were located at sites corresponding to areas of functional activation by SP, as shown by Fos‐LI. These results extend previous studies by adding a functional dimension to tachykinin receptor localization studies.
Glutathione Metabolism In Cyclosporine A‐Treated Rats: Dose‐ And Time‐Related Changes In Liver And Kidney
Authors: Jiménez R , Galán AI , González de Buitrago JM , Palomero J , Muñoz ME 
Published: March 2003

SUMMARY1. We investigated the simultaneous effects of cyclosporine A (CsA) treatment in rats on glutathione metabolism, oxidative status and their interorgan relationship in the liver and kidney.2. Reduced and oxidized glutathione (GSH and GSSG, respectively), lipid peroxidation and the activity of several enzymes of the glutathione cycle were evaluated in adult Wistar rats treated daily (i.p.) with saline, CsA vehicle (olive oil) or CsA (10 and 20 mg/kg per day) for either 1 or 4 weeks (short‐ and long‐term treatments, respectively).3. Cyclosporine A treatment elicited a significant depletion in liver GSH content and a decrease in the GSH/GSSG ratio that was unrelated to either the time of treatment or the dose used; these effects were already evident after 1 week of treatment. Renal GSH levels remained unaffected or increased, while those of GSSG increased markedly in all CsA‐treated rats, leading to decreases in the GSH/GSSG ratio, except in rats treated in the short term with the lower dose of CsA. These changes in the GSH/GSSG ratio were time and dose dependent. Short‐term CsA treatment using the higher dose and long‐term treatment with both doses of CsA progressively enhanced lipid peroxidation, which was reflected by increased levels of thiobarbituric acid‐reactive substances in both hepatic and renal homogenates. Hepatic γ‐glutamylcysteine synthetase activity was increased after long‐term treatment with both doses of CsA, whereas the activity of GSH hepatic peroxidase and GSH transferase was not significantly modified in any of the experimental groups. In contrast, renal γ‐glutamyl transpeptidase activity decreased in a progressive fashion, with the magnitude of this decrease being dose and time dependent. The plasma levels of total glutathione increased only in rats treated in the long term, regardless of the dose of CsA used, and remained unaltered in animals treated in the short term.4. In summary, the data collected indicate that CsA treatment alters the interorgan homeostasis of glutathione and the oxidative status of the rat liver and kidney, which is associated with increases in lipid peroxidation in both organs, and also induces modifications in the activity of some enzyme related to the glutathione cycle.