bluuebunny/crossref_metadata_2025_split huggingface dataset:
RELATIVE CONTRIBUTIONS OF EXTRACELLULAR Ca2+ AND Ca2+ STORES TO SMOOTH MUSCLE CONTRACTION IN ARTERIES AND ARTERIOLES OF RAT, GUINEA‐PIG DOG AND RABBIT
Authors: Low AM , Kotecha N. , Neild TO , Kwan CY , Daniel EE 
Published: June 2007

SUMMARY1. These studies describe the functional effects of modulation of the sarcoplasmic reticulum (SR) Ca2+ stores at three levels of the vasculature: (i) large arteries (rat and guinea‐pig aorta); (ii) small resistance arteries (rat tail artery, rabbit mesenteric artery, dog mesenteric artery); and (iii) arterioles (guinea‐pig submucosal arterioles of the small intestine).2. All tissues responded to phenylephrine (PE; 10 μmol/L) with a transient contraction in Ca2+‐free Krebs', reflecting Ca2+ release from PE‐sensitive Ca2+ stores. After pretreatment with cyclopiazonic acid (CPA; 30 μmol/L) or thapsigargin (TSG; 1 μmol/L), putative SR Ca2+ pump inhibitors, the PE‐induced contraction in a Ca2+‐free medium was significantly inhibited in arterial tissues at all levels of the vasculature. Similarly, ryanodine (RYA; 30 μmol/L), an agonist that enhances Ca2+ release from the SR, also reduced the PE contraction in a Ca2+‐free solution.3. CPA or TSG alone in the presence of extracellular Ca2+, caused marked and sustained contraction in the rat and guinea‐pig aorta and marked but transient or no contraction in the resistance arteries. In the rat and guinea‐pig aorta, RYA caused a slowly developing tension. Little increase in basal tension was produced by RYA in resistance arteries and arterioles.4. The findings show that an agonist‐releasable Ca2+ pool is present at all levels of the vasculature that is independent of the size of the vessels and suggest that under normal physiological conditions there is an intimate balance between the roles of the plasma membrane and of the SR in the maintenance of vascular contractility. It appears that the role of the SR diminishes as the arteries become smaller, while Ca2+ fluxes across the plasma membrane predominates.
SYMPOSIUM Experimental Biology 1995 Endothelin Receptors: Role in Renal Function and Dysfunction ENDOTHELIN RECEPTORS IN NORMAL AND DISEASED KIDNEYS
Authors: Nambi Ponnal 
Published: June 2007

SUMMARY1. Endothelin‐1 (ET‐1), the most potent vasoconstrictor yet identified, mediates a multitude of responses in various tissues including the kidney. The biological responses of ET‐1 are mediated by specific cell surface receptors classified as ETA and ETB. Species differences are observed in the distribution as well as function of these ET receptors.2. Involvement of ET has been demonstrated in a number of renal diseases, including ischaemia‐induced acute renal failure, chronic renal failure, radiocontrast and cyclosporin‐induced nephrotoxicity. ET antibodies as well as ET receptor antagonists have been shown to be beneficial in these disease models.
SYMPOSIUM Experimental Biology 1995 Endothelin Receptors: Role in Renal Function and Dysfunction ENDOTHELIN IS A KEY MODULATOR OF PROGRESSIVE RENAL INJURY: EXPERIMENTAL DATA AND NOVEL THERAPEUTIC STRATEGIES
Authors: Bruzzi Isabella , Benigni Ariela 
Published: June 2007

SUMMARY1. Glomerulosclerosis and tubulointerstitial damage are common histological abnormalities of many renal diseases that progress to end‐stage renal failure.2. In some models of renal damage, glomerulosclerosis seems to be associated with increased glomerular capillary pressure.3. Due to the positive correlation of glomerulosclerosis and proteinuria in both experimental models and in humans, abnormal permeability to macromolecules has also been considered a possible determinant of glomerulosclerosis.4. Abnormally filtered macromolecules have an intrinsic toxicity to the kidney due to protein over‐reabsorption, possibly leading to tubulointerstitial damage.5. Endothelin‐1 (ET‐1) is a vasoconstrictor peptide that induces mitogenesis and the accumulation of matrix proteins by mesangial cells.6. Evidence is available that ET‐1 plays a role in progressive renal disease in different experimental models, including renal mass reduction, lupus nephritis, streptozotocin‐induced diabetes and puromycin‐induced nephrosis.
NEW INSIGHTS INTO VASCULAR REACTIVITY: FROM ALTERED STRUCTURE TO NEURAL CONTROL*
Authors: Angus James A. 
Published: June 2007

SUMMARY1. The present review covers two aspects of the author's research into the pharmacology of vascular reactivity of isolated vessels and in the intact circulation. First, how ‘normal’ reactivity is altered by injury or disease and, second, how novel drugs have allowed insight into the role of the cotransmitter neuropeptide Y and ‘N’ type calcium channels in neurotransmitter release.2. Acute endothelium removal in the femoral artery of the anaesthetized dog confirmed the obligatory role of these cells in the dilatation response to intra‐arterial acetylcholine (ACh). After 4 weeks, conduit arteries respond with a thickened neoin‐tima following acute endothelial injury but, provided macrophage‐derived foam cells are absent, the artery relaxes normally to ACh.3. In the dog coronary vasculature, stable collateral arteries have a marked neointima of non‐contractile smooth muscle cells that are lined with endothelium. Reactivity to vasodilator stimuli is normal while that to vasoconstrictor stimuli is impaired.4. In the conscious rabbit, superficial femoral artery (SFA) occlusion stimulates profound angiogenesis but, despite these changes to the hindlimb vasculature, reactivity to vasodilator and vasoconstrictor agents from day 1 to 6 months following SFA is unaltered.5. Endothelial dysfunction is discussed in relation to hypertension, hypercholesterolaemia and congestive heart failure.6. The novel ‘N’ type calcium channel antagonist co‐conotoxin GVIA, was used to explore the role of ‘N’ type channels in cardiac and vascular neurotransmitter release in conscious rabbits.7. The novel putative Yi‐selective neuropeptide Y antagonist 1229U91 was shown to inhibit nerve‐mediated contractions of isolated mesenteric, but not femoral, artery segments in the rat. This regional difference in a possible cotransmitter role of the peptide is discussed.
EFFECT OF GENOTYPE ON THE ANGIOTENSIN‐CONVERTING ENZYME mRNA LEVEL IN HUMAN ATRIA
Authors: Tamaki Shinji , Iwai Naoharu , Ohmichi Nobuyuki , Shimoike Hitoshi , Izumi Masafumi , Nakamura Yasuyuki , Kinoshita Masahiko , Katsuyama Kazuhiko , Sugita Takaaki , Watarida Shouji , Mori Atsumi 
Published: June 2007

SUMMARY1. To clarify the mechanism of the association between I/D polymorphism of the angiotensin‐converting enzyme (ACE) gene and various cardiovascular diseases, ACE mRNA levels in human atrial appendages were assessed in relation to the genotype of the ACE gene.2. Angiotensin‐converting enzyme mRNA levels were positively correlated with age and tended to show a positive correlation with mean pulmonary pressure (niPA). Multiple regression analysis indicated that age and mPA, but not the genotype of the ACE gene, were predictors of ACE mRNA levels in human atrial appendages.3. The present study indicates that I/D polymorphism of the ACE gene is not simply reflected in ACE mRNA levels and that further study is needed to determine the mechanism of the association between this polymorphism and various cardiovascular diseases.
IMPROVING EFFECT OF CARTEOLOL ON BODYWEIGHT AND CARBOHYDRATE AND LIPID METABOLIC RESPONSES IN THE OLETF RAT
Authors: Saitoh Yuichi , Tani Takeshi , Asahi Yoshihiko , Man Zhiwei , Kawano Kazuya , Ikunaga Hideyuki 
Published: June 2007

SUMMARY1. Carteolol, a non‐selective beta‐blocker with intrinsic sympathomimetic activity, admixed in a pellet diet was administered to Otsuka Long‐Evans Tokushima Fatty (OLETF) rats, an animal model of spontaneous non‐insulin‐dependent diabetes mellitus with mild obesity. A high dose of carteolol (0.02%) suppressed bodyweight gain without affecting food and water consumption until the appearance of glycosuria. Carteolol tended to reduce the cumulative incidence of glycosuria at 26 weeks after the beginning of administration (55,17 and 25% in control rats, and in rats fed a low (0.002 %) and high dose of carteolol, respectively).2. At the 26th week of administration, the high dose of carteolol decreased visceral fat weight, such as that of retroperitoneal and epididymal adipose tissue, whereas the liver and the kidney were not affected.3. Although plasma glucose and triglyceride levels in non‐fasted rats were elevated with age, carteolol tended to delay the increases in those parameters. Carteolol suppressed the increase in plasma glucose levels, which indicate the diabetic pattern, in a 25th week oral glucose tolerance test.4. These findings indicate that carteolol induces improvements in bodyweight and carbohydrate and lipid metabolism in an obese condition. Consequently, carteolol may be useful for the treatment of hypertension with obesity in order to prevent cardiovascular events.
NITRIC OXIDE DEFICIENCY INDUCES MYOCARDIAL INFARCTION IN HYPERCHOLESTEROLAEMIC STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Ikeda Katsumi , Nara Yasuo , Tagami Motoki , Yamori Yukio 
Published: June 2007

SUMMARY1. To observe the effect of nitric oxide (NO) on the myocardium, the NO synthesis inhibitor NG‐nitro‐L‐arginine (L‐NNA) was administered to hypercholesterolaemic stroke‐prone spontaneously hypertensive (SHRSP) rats.2. Hypercholesterolaemic SHRSP were produced by feeding SHRSP a high fat and high cholesterol diet (HFC) for 2 weeks. The rats were then divided into three groups: (i) the N group, which were fed the HFC diet containing 0.023% L‐NNA and 1% NaCl in their drinking water (n = 10); (ii) the NH group, which were fed the HFC diet containing 0.023% L‐NNA and 1% NaCl in their drinking water which also contained 80 mg/L hydralazine (n = 10); and (iii) the C group, which were fed the HFC diet and 1% NaCl in their drinking water (n = 10).3. All rats in the N and NH groups died within 35 days of the initiation of L‐NNA administration. Rats in the N and NH groups had significantly increased serum creatine phosphokinase, lactate dehydrogenase, glutamic oxaloacetic transaminase and serum total cholesterol levels compared with rats in the C group.4. Fibrosis in response to necrosis was histopathologically observed in the hearts of all rats in the N and NH groups without exception. Occlusion or intimal thickening in the arteries adjacent to the necrotic regions was also observed.5. These results suggest that nitric oxide deficiency induces myocardial infarction in hypercholesterolaemic SHRSP. These NO‐deficient hypercholesterolaemic SHRSP offer a new model of myocardial infarction in rats.
RENAL REGULATION OF PHOSPHATE EXCRETION IN ENDOTOXAEMIC RATS
Authors: Mimura Yoshikazu , Uno Keizo , Nakamura Takuro 
Published: June 2007

SUMMARY1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)‐treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia.2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n= 8) or saline vehicle (n = 9). Thirty‐minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx‐ (n= 7) and saline‐treated (n = 8) rats.3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3′,5′‐cyclic mono‐phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late‐phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH‐mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline, and constant dopamine excretion were observed in endo‐toxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle.4. To test whether renal tubular sensitivity to parathyroid hormone related‐protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx‐ (n = 7) and saline‐treated rats (n= 7) was examined. Parathyroid hormone related‐protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx‐ than in saline‐treated rats.5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH‐mediated phosphaturia after PTH infusion.
FEASIBILITY OF CONDUCTING CARDIOVASCULAR OUTCOME RESEARCH IN AUSTRALIAN GENERAL PRACTICE: RESULTS FROM THE ANBP2 PILOT STUDY
Authors: Reid CM , Nelson M. , Beckinsale P. , Ryan P. , Wing LMH , Beilin LJ , Brown MA , Jennings GLR , Johnston CI , Marley J. , McNeil JJ , Morgan TO , Shaw J. , Steven ID , West MJ 
Published: June 2007

SUMMARY1. The present study aimed to determine the feasibility of conducting a 5 year cardiovascular outcome trial of the treatment of 6000 elderly hypertensive patients in Australian general practices.2. General practitioners (GPs) were invited to participate by mail and personal follow‐up. Patient records were reviewed to identify subjects for a blood pressure (BP) screening programme. Blood pressure was measured on three occasions and eligible subjects were included if the average BP was 160 mmHg systolic or 90 mmHg diastolic if systolic BP was 140 mmHg.3. Seven hundred and forty‐one GPs were approached and 89 were enrolled in the study (12% of mail invites and 75% of those receiving a personal contact). In 16 practices where screening was completed, 82 000 records were reviewed to identify 4% patients eligible for screening. Twenty‐two per cent of eligible subjects attended screening. Of 1938 subjects screened, 180 (9%) had BP 5=160/90 mmHg. Forty‐seven percent of subjects (n = 916) were receiving antihypertensive therapy and 184 (20%) were withdrawn from therapy. One hundred and sixteen (63%) of these subjects had BP return to study entry levels within 6 weeks. Fifty‐seven newly diagnosed and 81 previously treated subjects were randomized (7% of the screened population).4. Based on the high participation rate of GPs, the response rate of patients to attend a BP screening programme and the 7% randomization to screening ratio for entry into the study, the ANBP2 pilot study has demonstrated that it is feasible to recruit subjects from Australian general practices to a cardiovascular outcome trial.
ENDOTOXIN ALTERS THE SYSTEMIC DISPOSITION OF NITRIC OXIDE SYNTHASE INHIBITORS IN THE AWAKE SHEEP
Authors: Rutten AJ , Bersten AD , Whiting MJ 
Published: June 2007

SUMMARY1. We evaluated the haemodynamic effects and systemic disposition of the nitric oxide synthase (NOS) inhibitor NL‐nitro‐L‐arginine (NOLA) after intravenous (i.v.) administration of two different doses (5 and 20 mg/kg) in awake healthy sheep and awake sheep given a continuous i.v. infusion of endotoxin (lipopolysaccharide, 12 ng/kg per h, i.v., for 18 h). In addition, we determined the systemic disposition of another NOS inhibitor, NL‐nitro‐L‐arginine methylester (L‐NAME; 20 mg/kg, i.v.) in awake healthy sheep only.2. ArL‐Nitro‐L‐arginine produced a dose‐dependent decrease in heart rate (HR) and cardiac output (CO) together with a dose‐dependent increase in mean arterial pressure (MAP) and peripheral vascular resistance (PVR) when compared to baseline. In endotoxic sheep NOLA produced a greater increase in MAP and mean pulmonary arterial pressure (MPAP).3. In healthy sheep there was a dose‐related increase in total body clearance (CI) of NOLA. The CI increased from 0.028 L/min after the lower dose to 0.032 L/min after the higher dose. The infusion of endotoxin caused an increase in CI of NOLA to 0.040 and 0.047 L/min, respectively, and a decrease in plasma slow half‐life (t1/2 from 825 to 546 min and from 780 to 453 min, respectively.4. NL‐Nitro‐L‐arginine methylester was rapidly cleared from the plasma with a slow half‐life of approximately 7.5 min and there was a simultaneous appearance of NOLA in the plasma.5. These results support the view that nitric oxide has a significant role in regulating vascular tone in healthy and endotoxic sheep and indicate that the increases in CI of NOLA with an increase in its dose and the presence of endotoxin will be important in influencing appropriate dosage regimens in clinical studies.
SKELETAL MUSCLE RESTING METABOLISM IN COLD‐ACCLIMATED RATS: EFFECT OF AGE, NORADRENALINE AND HYPEROSMOLARITY
Authors: Cox Jason P. , Gibbs Colin L. 
Published: June 2007

SUMMARY1. A myothermic technique has been used to measure the resting metabolism of small bundles of a fast twitch muscle, extensor digitorum longus (EDL), and a slow twitch muscle, soleus (SOL), in 7‐week‐old rats. At 27°C, mean (± SEM) resting heat rates were 2.33 ± 0.41 and 2.09 ± 0.37 mW/g in EDL and SOL, respectively (n= 16).2. Seven‐week‐old rats were cold acclimatized at 4°C for 1–4 weeks and the metabolic rates of the fast and slow twitch muscles were monitored and compared with 7‐ and 11‐week‐old controls. There was a 160% increase in metabolic rate from week 7 to week 11, but the increase also occurred in the control group.3. In accordance with several literature reports, noradrenaline at concentrations of 10”7 and 10”6 mol/L had no effect on either the control or cold‐acclimatized resting heat rate.4. The osmolarity of the physiological solution bathing the muscle bundles was increased by lOOmosmol using sodium sulphate. Basal metabolism increased by similar amounts (approximately 250%) in both the fast and slow muscle bundles. Periods of cold exposure had no significant effect on the magnitude of the increment.5. Bumetanide, a potent inhibitor of Na+‐Cl− co‐transport, produced only a slight reduction in the heat increments caused by hyperosmolar challenge.
ALTERATIONS OF mRNA LEVELS OF ai‐ADRENOCEPTOR SUBTYPES WITH MATURATION AND AGEING IN DIFFERENT RAT BLOOD VESSELS
Authors: Xu Kai‐ming , Tang Fai , Han Chide 
Published: June 2007

SUMMARY1. Alterations of mRNA levels of ai‐adrenoceptor subtypes during maturation and ageing were determined by reverse trans‐cription‐polymerase chain reaction (RT‐PCR) in aortae and renal, pulmonary and mesenteric arteries isolated from 3,12 and 24‐month‐old rats.2. The steady state levels for α1A‐, α1B‐ and α1D‐adrenoceptors in aorta declined with maturation and ageing. In renal artery there was a decrease in mRNA for the α1B‐adrenoceptor in aged rats. However, in mesenteric and pulmonary arteries there were no changes in mRNA levels for the three subtypes of α1‐adrenoceptors as a result of maturation and ageing.3. The results suggest that expression of α1‐adrenoceptors is changed heterogeneously in different blood vessels during maturation and ageing in rats.
A NITRIC OXIDE DONOR (SPERMINE‐NONOATE) PREVENTS THE FORMATION OF NEOINTIMA IN RABBIT CAROTID ARTERY
Authors: Yin ZL , Dusting GJ 
Published: June 2007

SUMMARY1. In the present study we investigated the effect of spermine diazeniumdiolate (spermine‐NONOate), a nitric oxide donor, on the early development of atheroma‐like lesions induced by a peri‐arterial collar in rabbits.2. Spermine‐NONOate was given locally by incorporating the compound (1 mg/mL) into a silastic collar, which was applied on one common carotid artery of rabbit while the other carotid artery had a placebo collar (without compound) applied.3. Fourteen days postimplantation, both carotid arteries were dissected free for histological study (n = 6).4. After 14 days with collars, treatment with spermine‐NONOate had significantly reduced (by 74%) the thickness of the neointima in comparison with the contralateral collared artery without compound. Blood pressure did not change during treatment. Nitric oxide, detected as nitrite, was still released from spermine‐NONOate silastic collars after 14 days implantation.5. These results suggest that locally administered spermine‐NONOate is effective in slowing the development of neointima in this model.
CHRONIC INTRARENAL INFUSION OF LOW‐DOSE ANGIOTENSIN II IN DOGS INCREASES ARTERIAL PRESSURE WITHOUT IMPAIRMENT OF RENAL FUNCTION
Authors: Stevenson Kathleen M. , Fitzgerald Sharyn M. , Evans Roger G. , Anderson Warwick P. 
Published: June 2007

SUMMARY1. To determine whether chronic angiotensin II (AngII) infusion into the renal artery, at a dose which increases systemic arterial pressure, reduces glomerular filtration rate (GFR) and renal blood flow, AngII was infused at 0.5 ng/kg per min into the renal artery or intravenously in chronically instrumented dogs for 1 month.2. Mean arterial pressure (MAP) rose significantly (P < 0.05) during the infusion of AngII into the renal artery (+7 ± 2 nunHg on days 26‐30). There were no significant changes in GFR or renal blood flow. When the same dose of AngII was infused intravenously, MAP did not change significantly (−2 ± 2mmHg) and there were no significant changes in GFR or in renal blood flow.3. We conclude that AngII infused into the renal artery for 1 month, at a dose which was initially subpressor, causes a rise in arterial pressure that is not associated with impairment of renal function.
ASSOCIATION OF THE BRAIN NATRIURETIC PEPTIDE GENE WITH BLOOD PRESSURE AND HEART WEIGHT IN THE RAT
Authors: Zhang Li , Xu Dong , West Malcolm J. , Summers Kim M. 
Published: June 2007

SUMMARY1. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important in the control of body fluid homeostasis, blood pressure (BP) regulation and vascular remodelling. The genes for these peptides may, therefore, be involved in the pathogenesis of genetic hypertension. We have previously described a quantitative trait locus (QTL) for BP in the ANP gene region on rat chromosome 5. We have now assessed the possibility that this QTL lies at the closely linked BNP locus.2. Intra‐arterial BP and heart weight were measured in 12‐week‐old (n = 207) and 24‐week‐old (n= 88) F2 rats derived from crosses between Wistar‐Kyoto normotensive rats and spontaneously hypertensive rats. We designed polymerase chain reaction primers to amplify a microsatellite in the BNP gene from genomic DNA. Analysis of variance was used for cosegregation analysis. Linkage mapping and localization of QTL was performed using the Mapmaker computer package.3. A significant correlation was found between genotype for the BNP gene and systolic BP (P < 0.001) in 12‐week‐old rats. The ANP gene, but not the BNP gene, was associated with systolic BP in 24 week rats. There was no segregation of heart weight with BNP genotype at 12 or 24 weeks of age. The BNP gene mapped approximately 20 cM from the ANP gene in our rat hybrids, away from the previously described QTL. There was evidence for a second BP locus near to but distinct from the BNP gene.4. These results suggest that BP QTL are present in the natriuretic peptide gene region but that the ANP and BNP genes themselves have no major effect on BP in this cross.