bluuebunny/crossref_metadata_2025_split huggingface dataset:
PASSIVE SMOKING AND CORONARY HEART DISEASE: A BRIEF REVIEW
Authors: Lam Tai Hing , He Yao 
Published: June 2007

SUMMARY1. Whether passive smoking or environmental tobacco smoke (ETS) can cause coronary heart disease (CHD) is controversial. We have undertaken a comprehensive review of the epidemiological studies regarding the relationship between ETS and CHD.2. We searched for all original papers and reviews and calculated pooled odds ratio using the Mantel‐Haensze. method.3. Ten prospective studies, nine case‐control studies and one cross‐sectional study were found. Almost all studies showed positive associations between ETS and CHD and a few were statistically significant, with dose‐response relationships being evident. Six review papers calculated pooled estimates of the relative risks, which ranged from 1.23 to 1.51. Other studies also showed that ETS could have other cardiovascular effects.4. The association observed is likely to be real. The criteria for causation of time sequence, consistency, coherence and biological plausibility are satisfied. We conclude that ETS may cause CHD, particularly in women who have never smoked.
TRANSCRIPTIONAL ACTIVATION OF CYTOCHROME P450 GENES BY DIFFERENT CLASSES OF CHEMICAL INDUCERS
Authors: Dogra Satish C. , Whitelaw Murray L. , May Brian K. 
Published: June 2007

SUMMARY1. We review here the molecular mechanisms underlying the xenobiotic induction of genes encoding cytochrome P450 (CYP) enzymes in the liver and other tissues. We will focus on four major families of CYP genes.2. Members of the CYP1 gene family are induced by polycyclic aromatic hydrocarbons and this process is mediated by the basic helix‐loop‐helix proteins: the Ah receptor and its heterodimeric partner Arnt. Considerable progress has been made in elucidating the molecular details of this induction process.3. CYP4 genes are activated by peroxisomal proliferators, a group of structurally diverse chemicals that also induce peroxisome proliferation. The transcriptional response is dependent on the peroxisome proliferator‐activated receptor and its partner RXR, both members of the nuclear receptor super‐family; their role in the induction process has been well characterized at the molecular level.4. In contrast, the mechanism of gene induction of CYP2 genes by phenobarbital and other structurally diverse inducers is not well understood and a specific phenobarbital‐responsive receptor has not been identified.5. Induction of the CYP3 gene family by the glucocorticoid dexamethasone appears to involve the glucocorticoid receptor, but this receptor is not apparently required for induction by metapyrone and a complete molecular understanding of the induction processes is lacking at present.
ASSOCIATION OF PRE‐ISCHAEMIC DISTURBANCES IN ENERGY METABOLISM WITH POSTISCHAEMIC DYSFUNCTION OF THE RAT ISOLATED WORKING HEART
Authors: Pisarenko Oleg I. , Lakomkin Vladimir L. , Studneva Irina M. , Korchazhkina Olga V. , Kuzmin Alexander I. , Kapelko Valeri I. 
Published: June 2007

SUMMARY1. Metabolic and functional effects of two protocols of preconditioning were compared in rat isolated hearts subjected to 20 min global ischaemia (37°C) and reperfusion (30 min Langendorff + 15 min working). Prior to the ischaemic period, hearts were perfused according to Langendorff (control group) or were preconditioned by three 5 min cycles or two 10 min cycles of ischaemia and reperfusion (PC‐I and PC‐II groups, respectively).2. There was no difference in the contractile function between the two preconditioned groups at the onset of sustained ischaemia, although the PC‐II group showed enhanced release of adenosine (Ado), inosine, hypoxanthine and xanthine into the interstitium accompanied by losses of tissue adenine nucleotides (ΣAN = ATP + ADP + AMP), total creatine (ΣCr = phosphocreatine + creatine) and activation of glycolysis following the preconditioning period. During reperfusion, the PC‐I group showed enhanced functional recovery, higher contents of ΣAN and ΣCr, and the smallest lactate dehydrogenase release compared with these indices in the control and PC‐II groups. Postischaemic myocardial dysfunction was similar in the control and PC‐II groups.3. Functional recovery of hearts in both preconditioned groups was positively correlated with myocardial contents of ATP, ΣAN and ΣCr at the end of reperfusion, but not with pre‐ischaemic Ado release into the interstitium. The results suggest that pre‐ischaemic disturbances of energy metabolism, rather than activation of Ado receptors or stunning, may contribute to efficacy of multiple preconditioning in the rat isolated heart.
ASSOCIATION STUDY OF THE 5’ FLANKING REGIONS OF ENDOTHELIAL‐NITRIC OXIDE SYNTHASE AND ENDOTHELIN‐1 GENES IN FAMILIAL PRIMARY OPEN‐ANGLE GLAUCOMA
Authors: Tunny Terry J. , Richardson Kimberley A. , Clark Charles V. 
Published: June 2007

SUMMARY1. Endothelium‐derived substances are important regulators of the microcirculation. Endothelium‐derived nitric oxide (NO), which is catalysed by nitric oxide synthase (NOS), is a potent modulator of vascular tone in the human ophthalmic artery, which is normally in a state of constant vasodilation due to the actions of NO. Endothelin‐1 (ET‐1) produces vasoconstriction of the anterior optic nerve vasculature and may be associated with glaucomatous optic neuropathy. The aetiology of primary open‐angle glaucoma (POAG) remains largely unknown. Thus, alterations in the regulatory sequences of the genes coding for endothelium‐derived NOS (eNOS) and ET‐1 may have important effects in the development of POAG and were looked for in the present study.2. In 56 patients with familial POAG and in 100 control subjects with no family history of hypertension or POAG, we examined the 5’ flanking sequences of the eNOS and ET‐1 genes, which contain many positive and negative regulatory regions affecting gene transcription, using polymerase chain reaction‐based single strand conformation polymorphism analysis, to search for alterations. No variant in the promoter region of the ET‐1 gene was observed in familial POAG or controls. Using three primer sets spanning 706 b.p. of the eNOS gene, we observed alterations in 11 of 56 (20%) familial POAG members and in seven of 100 (7%) controls. Sequence analysis demonstrated a C/T substitution at the 5’ sequence position nucleotide (nt) ‐690 from the transcription start site, which lies between the CAMP regulatory element (nt ‐726 to ‐732) and an activator protein‐1 binding domain (nt ‐655 to ‐661).3. In summary, genotypic and allelic frequency analysis found no association between alterations in the promoter region of the ET‐1 gene and familial POAG. A variant in the promoter region of the eNOS gene was seen in a significant percentage of familial POAG patients. Future expression studies will determine whether this polymorphism results in altered eNOS gene expression.
UNIDIRECTIONAL TRANSFER OF D‐XYLOSE ACROSS THE RAT PLACENTA
Authors: Štaud F. , Fendrich Z. , Karlíček R. , Pávek P. 
Published: June 2007

SUMMARY1. The transplacental transfer Of D‐Xylose was investigated in the present study.2. Umbilical perfusion of the rat term placenta was used to study materno‐foetal (M‐F) and foetomaternal (F‐M) transfer of this compound.3. D‐Xylose was found to cross the rat term placenta very quickly in the M‐F direction, with subsequent accumulation in the foetal compartment (the F‐M ratio being 2.23 at the end of the experiments). In contrast, no transfer in the F‐M direction was observed.4. A possible facilitation of the transplacental transfer of D‐Xylose from the mother to foetus in rats is suggested.
IS INSULIN RESISTANCE LINKED TO HYPERTENSION?
Authors: Brands Michael W. , Hall John E. , Keen Henry L. 
Published: June 2007

SUMMARY1. The volume of work reporting insulin resistance in multiple forms of chronic hypertension has generated tremendous interest in whether this abnormality is an important factor in causing hypertension. Insulin resistance, however, is an imprecise term used interchangeably to describe widely disparate types of impairment in insulin action throughout the body and the type of insulin resistance has major ramifications regarding its potential for inducing long‐term increases in blood pressure (BP).2. Hepatic insulin resistance (impaired insulin‐mediated suppression of hepatic glucose output) is the primary cause of fasting hyperinsulinaemia and is a cardinal feature of obesity hypertension. Evidence from chronic insulin infusion studies in rats suggests hyperinsulinaemia can increase BP under some conditions; however, conflicting evidence in humans and dogs leaves in question whether hyperinsulinaemia is a factor in hypertension induced by obesity.3. Peripheral insulin resistance (impaired insulin‐mediated glucose uptake, primarily of an acute glucose load in skeletal muscle) also present in obesity hypertension, but now reported in lean essential hypertension as well, is linked most notably to impaired insulin‐mediated skeletal muscle vasodilation. This derangement has also been proposed as a mechanism through which insulin resistance can cause hypertension.4. The present review will discuss the lack of experimental or theoretical support for that hypothesis and will suggest that a direct link between insulin resistance and BP control may not be the best way to envision a role for insulin resistance in cardiovascular morbidity and mortality.
SEX STEROID CONTROL OF MOOD, MENTAL STATE AND MEMORY
Authors: Fink George , Sumner Barbara EH , McQueen Judith K. , Wilson Helen , Rosie Roberta 
Published: June 2007

SUMMARY1. Sex steroid hormones exert profound effects on mood and mental state. Thus, in women, oestrogen is thought to protect against depression and delay the onset of schizophrenia and Alzheimer's disease.2. Our studies in the female rat show that oestradiol, in its positive feedback mode for gonadotrophin release, increases the expression of genes for the 5‐hydroxytryptamine 5‐HT2A receptor and the serotonin transporter (SERT) in the dorsal raphe nucleus and the density of 5‐HT2A receptor and SERT sites in regions of the forebrain that, in the human, are concerned with cognition, mental state, emotion and memory.3. In the male rat, castration decreases while oestrogen and testosterone, but not 5α‐dihydrotestosterone (5α‐DHT), increase the density of 5‐HT2A receptors in forebrain. The fact that 5α‐DHT has no effect suggests that the action of testosterone depends on its conversion to oestradiol by aromatase.4. In intact rats, the density of 5‐HT2A receptors in cerebral cortex is significantly higher in prooestrous female than in male and dioestrous female rats, showing that the spontaneous, preovulatory surge of oestradiol that reaches a peak at 12.00 h of pro‐oestrus also increases the density of 5‐HTZA receptors in cortex.5. Oestrogen and testosterone (by way of its conversion to oestrogen) also stimulate the expression of the arginine vasopressin gene in the bed nucleus of the stria terminalis of the rodent, a mechanism that plays a key role in olfactory memory.6. These actions of sex steroid hormones are discussed in the context of genomic versus non‐genomic mechanisms, the recent discovery that there are two oestradiol receptors with different distributions in brain, the significance of our findings for our understanding of the control of mood, mental state and memory and the mechanism by which oestrogen stimulation of the 5‐HT2A receptor could delay the onset of Alzheimer's disease.
MECHANISMS UNDERLYING THE DECREASE IN CIRCULATING ANGIOTENSIN II CONCENTRATION AFTER SODIUM LOADING
Authors: Duggan KA , Ye VZC 
Published: June 2007

SUMMARY1. Acute sodium loading causes a rapid decrease in the circulating concentration of angiotensin II (AngII), which is apparent from 5 min after sodium administration. This could result from an increase in AngII catabolism and/or a decrease in AngII synthesis/secretion. However, the major determinant of AngII synthesis is thought to be a change in plasma renin activity, which occurs over a longer time frame (15 min).2. To investigate the mechanisms underlying the rapid decrease in plasma AngII engendered by sodium administration, we performed metabolic clearance studies in male New Zealand white rabbits before and after a hypertonic sodium load of 1.5 mmol/kg as 0.513 mol/L saline i.v. bolus.3. The metabolic clearance rate of AngII increased significantly from 42.2 ± 9.0 mL/min per kg before sodium to 110.8±33.7 mL/min per kg after sodium administration (P<0.05). The calculated or theoretical secretion rate decreased from 1470.7±404.2 to 573.5 ± 139.5 fmol/min per kg (P<0.025) in response to sodium.4. We conclude that an increase in AngII metabolism and a decrease in synthesis/secretion contribute to the reduction in circulating AngII, which occurs in the first 60–90 min after sodium loading.
ORIGIN AND FUNCTION OF EPOXYEICOSATRIENOIC ACIDS IN VASCULAR ENDOTHELIAL CELLS: MORE THAN JUST ENDOTHELIUM‐DERIVED HYPERPOLARIZING FACTOR?
Authors: Hoebel Bernhard G. , Steyrer Ernst , Graier Wolfgang F. 
Published: June 2007

SUMMARY1. In addition to their contribution to endothelium‐derived hyperpolarization, our understanding of the physiological function of epoxyeicosatrienoic acids (EET) within the vascular wall and the actual enzymes involved in the formation of the EET in endothelial cells is very limited. In the present study, the expression of potential cytochrome P450 (CYP) mono/epoxygenases was assessed in endothelial cells isolated from porcine and bovine aortas as well as in the human umbilical vein‐derived cell lines EA.hy926andECV304.2. Expression of CYP2B1, CYP2E1 and CYP3A could be found. The latter were inducible by dexamethasone/cloflbrate for 72 h, a procedure that also enhanced CYP epoxygenase activity in endothelial cells.3. Enzyme induction yielded increases in capacitative Ca2+ entry and membrane hyperpolarization in response to autacoids, such as bradykinin and thapsigargin. Thiopentone sodium, an inhibitor of endothelial CYP mono/epoxygenase(s), diminished autacoid‐induced capacitative Ca2+ entry and membrane hyperpolarization, while the effect of EET remained unchanged.4. Epoxyeicosatrienoic acids activated endothelial tyrosine kinase activity in a concentration‐dependent manner. Arachidonic acid, at 20‐fold higher concentrations, also increased tyrosine kinase activity. Because only the effect of arachidonic acid was inhibited by thiopentone sodium, an inhibitor of CYP mono/epoxygenases, these data suggest that arachidonic acid needs to be converted to the EET in order to stimulate tyrosine kinase.5. All these data provide clear evidence that the CYP epoxygenase‐derived arachidonic acid metabolites (EET) not only serve as potential endothelium‐derived hyperpolarizing factors but also constitute highly active intracellular messengers with a physiological role including the control of Ca2+ signalling, membrane potential and tyrosine kinase activity.
PACEMAKING IN THE HEART: THE INTERPLAY OF IONIC CURRENTS
Authors: Saint David A. 
Published: June 2007

SUMMARY1. There is still a degree of controversy about which currents drive pacemaking in the sinoatrial node or sinus venosus. Early attempts to identify a single ‘pacemaker current’ in these tissues, based on voltage‐clamp data, were largely unsuccessful, prompting the search for other mechanisms that may contribute to rhythmic activity.2. Whole‐cell patch‐clamp recording from single cells isolated from the sinus venosus of the toad has shown that a voltage‐dependent sodium current may play a role in pacemaking. This current has a transient component that contributes to the action potential upstroke and an inactivation‐resistant component that contributes to the diastolic depolarization. The relative importance of this current in pacemaking is still controversial.3. The development of computer models of pacemaking has contributed greatly to our understanding of how ionic currents can interact to produce rhythmic activity. Results are presented from one such model, ‘Oxsoft Heart', to illustrate the different contributions of If and INA and to highlight the concept that pace‐making is driven by the integrated activity of many processes, rather than by any one current in particular.4. Present models of pacemaking fail to accurately reproduce biological observations for certain situations. It is becoming clear that many processes contribute to pacemaking and have yet to be fully incorporated into models. Recent results regarding the role of intracellular calcium buffering and release and their implications, are discussed in this context.5. The control of pacemaking by neurotransmitters is discussed. The limitations of single cell models in reproducing many of the complex responses to nerve stimulation of multicellular tissue, such as postinhibitory rebound, are discussed and possible improvements to models are suggested.
KATP CHANNEL BLOCKING ACTIONS OF QUATERNARY IONS PLAY NO ROLE IN THEIR ANTIPROLIFERATIVE ACTION ON MOUSE LEUKAEMIA AND RAT VASCULAR SMOOTH MUSCLE CELLS IN VITRO
Authors: Piekarska Anna E. , Webster Lorraine , Saltis John , McPherson Grant A. 
Published: June 2007

SUMMARY1. The aim of the present study was to investigate the possibility that, in the two cell lines examined, alterations in cell growth caused by lipophilic quaternary ions may involve KATP channels. We examined the effect of tetraphenylphosphonium (TPP), tetraphenylboron (TPB), rhodamine 123, dequalinium chloride (DECA) and the non‐quaternary ion cisplatin on the proliferation of L1210 mouse leukaemia cells and rat smooth muscle cells in vitro. The KATP channel opener levcromakalim (LKM) and the Katp channel antagonist glibenclamide were also tested.2. From growth‐inhibition studies, the rank order of potency (based on pIC50 values) using L1210 leukaemia cells was: DECA (6.61) > cisplatin (6.09) = rhodamine 123 (6.01) > TPP (5.61) > TPB (4.25). Levcromakalim and glibenclamide were found to be inactive at the maximum concentrations used (100 μmol/L). A different rank order of potency was obtained in rat aortic smooth muscle cells: cisplatin (6.33) > DECA (5.67) > TPP (4.96) > rhodamine 123 (4.1). Tetraphenylboron (30μmol/L), LKM (100 μmol/L) and glibenclamide (100 μmol/L) were found to be inactive.3. When the negatively charged TPB (30 μmol/L) was combined with some of the active agents, the potency of the active agents was increased. Thus, in L1210 cells, rhodamine 123, DECA and TPP were all more potent at inhibiting cell growth in the presence of TPB. Tetraphenylboron had no effect on cisplatin in this cell line. In rat smooth muscle cells, TPB (30 μ mol/L) potentiated the effect of rhodamine 123 but had no effect on the actions of cisplatin, DECA or TPP.4. In functional studies, rhodamine 123 was a weak antagonist of the vasorelaxant responses to the KATP channel opener LKM in the porcine right circumflex artery in vitro. The pKB value obtained for rhodamine 123 at 100 μmol/L was 4.95. Dequalinium chloride was inactive.5. We found no correlation between the actions of the compounds tested to antagonize KATP channels and their ability to inhibit cell proliferation. In addition, compounds known to regulate KATP channel activity failed to influence proliferative rates. These results suggest that KATP channels are not involved in the antiproliferative action of TPP and other quaternary ions in the two cell lines studied.
EFFECTS OF ZAPRINAST ON RENAL NERVE STIMULATION‐INDUCED ANTI‐NATRIURESIS IN ANAESTHETIZED DOGS
Authors: Sekizawa Toshihiro , Shima Yuichiro , Yoshida Kozo , Tanahashi Masayuki , Yoshida Makoto , Suzuki‐Kusaba Mizue , Hisa Hiroaki , Satoh Susumu 
Published: June 2007

SUMMARY1. We examined whether zaprinast, a putative cGMP‐specific phosphodiesterase inhibitor, affects neural control of renal function in pentobarbital‐anaesthetized dogs.2. Renal nerve stimulation (1Hz, 1ms duration) reduced urine flow rate, urinary Na+ excretion (UNaV) and fractional excretion of Na+ (FENa) with little change in either renal blood flow (RBF) or glomerular filtration rate (GFR).3. Intrarenal arterial infusion of zaprinast (10 and 100 μg/kg per min) increased basal urine flow rate, UNaV and FENa but not RBF or GFR. Zaprinast infusion (100 μg/kg per min) also increased renal venous plasma cGMP concentration and urinary cGMP excretion.4. Renal nerve stimulation‐induced reductions in UNaV and FENa were attenuated during zaprinast infusion, whereas the reduction in urine flow rate was resistant to zaprinast.5. Renal nerve stimulation increased the renal venous plasma noradrenaline concentration and renal noradrenaline efflux, which remained unaffected during infusion of zaprinast (100 μg/kg per min).6. The results of the present study suggest that zaprinast induces natriuresis and counteracts adrenergically induced anti‐natriuresis by acting on renal tubular sites in the dog kidney in vivo.
MODULATORY EFFECTS OF TYPE‐C NATRIURETIC PEPTIDE ON SYMPATHETIC COTRANSMISSION IN THE RAT ISOLATED TAIL ARTERY
Authors: Mutafova‐Yambolieva Violeta N. , Westfall David P. 
Published: June 2007

SUMMARY1. Rat type‐C natriuretic peptide (CNP) has been studied for its effects on the neurogenically induced overflow of adenosine 5′‐triphosphate (ATP), adenosine 5′‐diphosphate (ADP), adenosine 5‐monophosphate (AMP), adenosine (ADO) and noradrenaline (NA) in endothelium‐free segments of rat isolated tail artery. The overflow of each was evoked by electrical field stimulation (EFS) of 0.5 ms pulses at 8 Hz for 3 min and the amount of ATP, ADP, AMP and ADO was quantified by high‐performance liquid chromatography (HPLC)‐fluorescent detection, while the amount of NA was quantified by HPLC‐electrochemical detection.2. Type‐C natriuretic peptide (100 nmol/L) was found to cause a significant reduction of the overflow of all adenine purines and NA. However, at lower concentrations (1 and 10 nmol/L), CNP caused a significant reduction of the overflow of NA but did not change ATP overflow.3. The overflow of ADP, AMP and ADO was significantly reduced by either concentration of CNP, so that the ratio ATP:ADP was diminished from 1:2 in controls to 1:1 after 1 nmol/L CNP and to 1:1.2 after 10 nmol/L CNP.4. The production of inorganic phosphate (Pi) in response to the exogenous application of ATP was significantly reduced by 1,10 or 100 nmol/L CNP.5. Type‐C natriuretic peptide exerts neuromodulatory effects on the neurogenically induced release of the cotransmitters ATP and NA in rat tail artery, consisting of an inhibition of the release of both ATP and NA. This effect is accompanied by inhibition of the breakdown of ATP by ecto‐ATPases. Either effect results in apparent CNP‐induced differential modulation of the overflow of the cotransmitters ATP and NA.
ANGIOTENSIN‐CONVERTING ENZYME INHIBITION IN PIGLETS INDUCES PERSISTENT RENAL ABNORMALITIES
Authors: Guron Gregor , Sundelin Birgitta , Wickman Anna , Friberg Peter 
Published: June 2007

SUMMARY1. We have previously shown that neonatal angiotensin‐converting enzyme (ACE) inhibition or angiotensin II type I (AT1) receptor antagonism during the first three postnatal weeks in the rat produces persistent abnormalities in renal function and histology, indicating an essential role for the reninangiotensin system (RAS) in normal renal development.2. The aim of the present study was to investigate whether the pig kidney, which shows a high resemblance to the human kidney, is dependent on an intact RAS neonatally for normal renal development, analogous with findings in rats.3. Piglets received daily i.p. injections of either enalapril (10 mg/kg) or vehicle from 2 to 24 days after birth. Urine concentrating capacity, renal functional parameters and renal histology were assessed in 8‐week‐old pigs.4. Urine osmolality after 20 h water deprivation was 673 ± 55 and 928 ± 50 mOsm/kg (P < 0.05) in enalapril‐ and vehicle‐treated pigs, respectively. There were no significant differences between groups in plasma creatinine or urea concentrations.5. Semiquantitative analysis of renal histology showed significant interstitial fibrosis and inflammation, tubular atrophy and thickened walls of interlobular arteries in enalapril‐treated pigs.6. The present study demonstrates that an intact RAS is required for normal renal development in the pig, similar to previous observations made in rodents.