bluuebunny/crossref_metadata_2025_split huggingface dataset:
ROLE OF THE BRAIN RENIN‐ANGIOTENSIN SYSTEM IN THE MAINTENANCE OF BLOOD PRESSURE IN CONSCIOUS SPONTANEOUSLY HYPERTENSIVE AND SINOAORTIC BARORECEPTOR‐DENERVATED RATS
Authors: Paul Jeremy RA , Bunting Michael W. , Widdop Robert E. 
Published: June 2007

SUMMARY1. Evidence suggesting an involvement of the brain renin‐angiotensin system (RAS) in the development/maintenance of hypertension in spontaneously hypertensive rats (SHR) relies, in part, on early experimental data reporting centrally mediated antihypertensive effects of saralasin. However, recent data using non‐peptide ATi receptor antagonists does not always support this theory because these compounds usually do not lower blood pressure when given centrally.2. In the present study we have re‐assessed the central effects of saralasin in conscious SHR as well as in sinoaortic baroreceptor‐denervated (SAD) rats. Both of these models exhibit heightened sensitivity to the central pressor effects of angiotensin II (AngII) and, thus, any potential antihypertensive activity would provide functional evidence of activated brain RAS mechanisms in these models.3. In SHR, saralasin failed to lower mean arterial pressure (MAP) when given intracerebroventricularly (i.e.v.) as bolus or infusion doses that blocked the centrally mediated pressor effect of AngII.4. In SAD rats, there was a marked impairment of the baroreceptor‐heart rate reflex function and enhanced centrally mediated pressor responses to AngII. However, i.e.v. saralasin infusions again did not alter MAP.5. Collectively, these results suggest that the central RAS is not involved in the maintenance of MAP in SHR and SAD rats, both of which are models exhibiting a functional hyper‐responsiveness to AngII.
ASTROCYTE‐CONDITIONED MEDIUM INDUCES BLOOD‐BRAIN BARRIER PROPERTIES IN ENDOTHELIAL CELLS
Authors: Yamagata Kazuo , Tagami Motoki , Nara Yasuo , Mitani Mitsuaki , Kubota Akiyoshi , Fujino Hideaki , Numano Fujio , Kato§ Taiji , Yamori# Yukio 
Published: June 2007

SUMMARY1. We evaluated the induction of endothelial barrier functions by the type 1 astrocyte‐derived supernatant in culture using horseradish peroxidase (HRP) as a parameter.2. A gel filtration fraction (molecular weight 16‐20 kDa) of type 1 astrocyte‐derived supernatant reduced plasmalemmal vesicles and induced tight junctions in endothelial cells.3. In addition, this fraction promoted the uptake of [3H]‐glucosamine by endothelial cells. This cell activity disappeared after heating at 95°C for 10 min and was sensitive to trypsin.4. These results suggest that a type 1 astrocyte‐derived protein factor(s) promotes proteoglycan synthesis with a resultant increase in charge selectivity in endothelial cells and plays an important role in the induction of blood‐brain barrier functions.
SUPRAMEDULLARY MODULATION OF SYMPATHETIC VASOMOTOR FUNCTION
Authors: Verberne Anthony JM , Lam William , Owens Neil C. , Sartor Daniela 
Published: June 2007

SUMMARY1. Supramedullary structures including the ventral medial prefrontal cortex (MPFC) and the midbrain cuneiform nucleus (CnF) project directly and indirectly to premotor sympatho‐excitatory neurons of the rostral ventrolateral medulla (RVLM) that are critically involved in the generation of sympathetic vasomotor tone.2. Electrophysiological studies have demonstrated that activation of depressor sites within the MPFC is associated with splanchnic sympathetic vasomotor inhibition and inhibition of the activity of RVLM sympathoexcitatory neurons.3. Antidromic mapping and anatomical studies support the notion that a relay in the nucleus tractus solitarius is involved in the cardiovascular response to MPFC stimulation.4. The midbrain CnF, which lies adjacent to the midbrain periaqueductal grey, is a sympathoexcitatory region of the midbrain reticular formation. Sympathoexcitatory responses evoked from the CnF are associated with short‐latency excitation of RVLM neurons.5. Cuneiform nucleus stimulation induces the expression of mRNA for the immediate early genes c‐fos and NGFI‐A in midbrain, pontine and hypothalamic structures.6. The MPFC and CnF are supramedullary structures with opposing modulatory influences on sympathetic vasomotor drive, whose roles in cardiovascular control mechanisms warrant further investigation.
DETECTION OF WEAKLY EXPRESSED GENES IN THE ROSTRAL VENTROLATERAL MEDULLA OF THE RAT USING MICROPUNCH AND REVERSE TRANSCRIPTION‐POLYMERASE CHAIN REACTION TECHNIQUES
Authors: Comer AM , Yip S. , Lipski J. 
Published: June 2007

SUMMARY1. The present study describes the use of reverse transcription‐polymerase chain reaction (RT‐PCR) to detect weakly expressed neurotransmitter receptor mRNA in tissue micropunched from the rostral ventrolateral medulla (RVLM) and other discrete areas of the medulla oblongata of the rat.2. Micropunches were made from 240 fJim transverse medullary sections. Punched regions included the RVLM, hypoglossal nucleus (XIIn), ventrolateral subnucleus of the nucleus tractus solitarius (NTS) and spinal trigeminal nucleus (STN). RNA was extracted and reverse transcribed into cDNA, which was probed for the presence of seven genes: glyceralde‐hyde phosphate dehydrogenase (GAPDH), neuron‐specific enolase (NSE), tyrosine hydroxylase (TH), phenylethanolamine N‐methyltransferase (PNMT), glucocorticoid receptor (GCR), mineralocorticoid receptor (MCR) and the adenosine 5‐triphosphate (ATP) receptor subunit P2X2‐1. Each transcript was detected using a semi‐nested PCR protocol, which used three primers.3. Tyrosine hydroxylase was detected in the RVLM and NTS and PNMT was also detected in the RVLM, which agrees with the distribution of catecholamine neurons in the medulla. Expression of GCR mRNA was detected in the RVLM and the XIIn but not in the NTS (it was not probed for in the STN punches). The P2X2‐1 receptor message was detected in all areas. Expression of MCR mRNA was detected in the RVLM only.4. This method offers a simple way to detect the presence of low‐abundance receptor mRNA in discrete brain regions.
PRESSOR RESPONSES TO BRAIN DOPAMINERGIC STIMULATION
Authors: van den Buuse Maarten 
Published: June 2007

SUMMARY1. Systemic administration of a dopamine D2 receptor agonist, such as quinpirole, causes a centrally mediated rise in blood pressure (BP) with a maximum at 1‐2 min after injection. At 30 min after injection, when BP has returned to baseline, further treatment with these drugs has little effect on BP. Moreover, the antihypertensive effects of sympathoinhibitory drugs, such as clonidine and rilmenidine, is markedly inhibited. Increased circulating levels of vasopressin contribute to the initial rise in BP, but return to baseline thereafter. Differential changes in sympathetic vasomotor tone may be involved in the apparent de‐sensitization induced by quinpirole.2. Stimulation of the region of origin of the mesolimbic dopamine (DA) system in the brain, the ventral tegmental area, causes a long‐lasting increase in BP. In this model, circulating levels of vasopressin are moderately increased through a non‐dopaminergic mechanism. Dopaminergic stimulation causes a functional potentiation of the effect of vasopressin, resulting in an increase in BP.3. Spontaneously hypertensive rats (SHR) display several changes in central dopaminergic responses. Dopamine levels in the brain are normal, while resting DA activity appears reduced. Partial depletion of forebrain DA levels, particularly in the nigrostriatal system, causes an inhibition of the development of hypertension and normalizes deficient functional responses to dopaminergic drugs in the SHR.4. These results show that brain DA is involved in several aspects of cardiovascular regulation and may be involved in the development of hypertension. The widespread involvement of brain DA systems in behavioural, hormonal and cardiovascular mechanisms suggests that these systems play an important role in the integration of stress and environmental stimuli with homeostatic mechanisms in the body.
INHIBITION OF K+ TRANSPORT IN HUMAN SICKLE CELL ERYTHROCYTES BY OKADAIC ACID AND SODIUM FLUORIDE
Authors: Gharaibeh Nayef Saleh Al‐Rohil , Al‐Sheyyab† Mahmoud 
Published: June 2007

SUMMARY1. The effect of okadaic acid and sodium fluoride on swelling‐and N‐ethylmaleimide (NEM)‐stimulated KC1 cotransport was examined in blood cells from homozygote sickle cell anaemia patients.2. Blood was drawn into heparin or EDTA by vein puncture from sickle cell patients previously diagnosed in the haematology clinics of Princess Badee'a Teaching Hospital. A standard method for measuring flux by using radioactive rubidium was used.3. Okadaic acid strongly inhibited swelling‐stimulated KC1 cotransport if added before swelling. Okadaic acid and sodium fluoride added before NEM inhibited the activation of transport by NEM. Okadaic acid added after NEM did not inhibit transport.4. The inhibition of the effects of NEM by okadaic acid and sodium fluoride indicates that activation of the flux by NEM requires the action o. phosphatase.
RELATIONSHIP BETWEEN GASTRIC MUCUS SYNTHESIS, SECRETION AND SURFACE GEL EROSION MEASURED IN AMPHIBIAN STOMACH IN VITRO
Authors: Keogh JP , Allen A , Garner A 
Published: June 2007

SUMMARY1. The layer of adherent mucus that protects the surface of the stomach reflects a dynamic balance between biosynthesis of glycoprotein, secretion of preformed mucus and erosion of the adherent gel layer. The present study is the first in which all these processes have been measured concomitantly and was undertaken to define interrelationships between the three parameters.2. A chambered sac preparation of amphibian gastric mucosa is described. Biosynthesis was determined by specific incorporation of radiolabeled sugars into purified glycoprotein. Mucus secretion was determined by measuring the thickness of the adherent gel and erosion of the surface layer was assessed from the appearance of soluble mucin in the luminal solution.3. 16,16‐Dimethyl‐prostaglandin (PG. E2 stimulated glucosamine incorporation by 10‐fold, but did not alter the rate of incorporation of galactose. There was a rapid two‐fold increase in the thickness of the adherent mucus layer but no change in the rate of erosion. Dibutyryl‐cAMP also stimulated mucus release but, unlike PG, increased glycoprotein labelling by galactose.4. Both distention or the application of a cholinergic agonist increased adherent mucus thickness. Stimulation of mucus release in response to carbachol was accompanied by a decrease in glycoprotein labelling by galactose. In contrast, the adrenergic agent noradrenaline decreased secretion but did not influence labelling.5. These results indicate that biosynthesis and secretion of gastric mucus are subject to differential regulation. Moreover, the profile of incorporation of sugars in response to secreta‐gogues also differs, indicating the need for caution when interpreting effects on glycoprotein biosynthesis.
EFFECTS OF DRUGS ON UTEROPLACENTAL BLOOD FLOW AND THE HEALTH OF THE FOETUS
Authors: Lumbers Eugenie R. 
Published: June 2007

SUMMARY1. The placental vascular bed is normally fully dilated. Therefore, changes in vascular resistance elsewhere in the body can affect uteroplacental blood flow (UBF). For example, antihypertensive drugs, such as diazoxide, hydralazine and the angiotensin‐converting enzyme inhibitor captopril, cause falls in arterial pressure and, hence, in UBF.2. Angiotensin II (AngII), prostacyclin and nitric oxide (NO) all influence uteroplacental vascular tone. Angiotensin II in a pharmacological dose (62.5 μg/h) had a biphasic effect on UBF in the sheep. Initially, there was a rise in UBF as pressure rose; however, by 16–24 h, UBF had fallen. The AngII‐induced fall in UBF caused severe foetal hypoxia and hypercapnia.3. Prostacyclin may protect the uteroplacental circulation from vasoconstrictors such as AngII, as the vasoconstrictor effect of AngII in the uteroplacental circulation is enhanced followin. indomethacin.4. Oestrogen‐induced uterine artery vasodilation is nitrergic dependent. As well, nitrergic nerves alter the responsiveness of pregnant uterine arteries to noradrenaline.5. Thus, both systemic and local factors are important in the control of UBF and in promoting foetal health an. growth.
CURRENT ISSUES IN EXERCISE METABOLISM: THE CROSSOVER CONCEPT
Authors: Tipton Charles M. 
Published: June 2007

SUMMARY1. Since ancient times, athletes have consumed proteins because of the belief they were the necessary substrate for optimal performance. Even though this concept was proven to be incorrect before the beginning of the 19th century, the practice continued until several decades ago.2. By 1939, careful metabolic investigations on the changes in the respiratory exchange ratio had demonstrated that the metabolic transformations of lipids and carbohydrates were the primary sources of energy for muscula. exercise.3. Metabolic investigations on the profile of energy transformations during exercise have indicated that aspects related to exercise intensity, state of training, the availability of circulating free fatty acids, the activity of the sympathetic nervous system, resting levels of muscle and liver glycogen and muscle triglyceride concentrations have to be considered to explain a specifi. response.4. In 1994, Brooks and Mercier introduced the concept of ‘crossover’ in their review manuscript to explain the shift in substrate utilization from lipids to carbohydrates by trained subjects when the power output was increased. In addition, the concept was advanced to reconcile divergent results by different investigators.5. In 1995, Coggan and associates investigated the glucose kinetics of non‐trained and trained subjects performing power outputs equal to 80. Vo2max and concluded that the crossover concept was unable to explain their metabolic results from trained subjects.6. Because of the importance of the topic to exercise physiologists and the uncertainties the controversy has created for teachers and researchers, the American Physiological Society Section on Environmental and Exercise Physiology scheduled a Point‐Counterpoint forum at the 1997 Experimental Biology Meeting. The subsequent manuscripts of Brooks and Coggan are a result of that forum.
IMPORTANCE OF THE ‘CROSSOVER’ CONCEPT IN EXERCISE METABOLISM
Authors: Brooks George A. 
Published: June 2007

SUMMARY1. The ‘crossover’ concept is a model of substrate supply during exercise which makes the following predictions.2. Lipid is the major fuel (approximatel. 60%) for non‐contracting skeletal muscle and the body at rest.3. Energy flux, as determined by exercise intensity, is the major factor in determining the balance of substrate utilization during exercise. Thus, moderate and greater exercise intensities increase contraction‐induced muscle glycogenosis and glycolysis, increase recruitment of fast‐twitch muscle fibres, increase sympathetic nervous system activity and down‐regulate mitochondrial fatty acid uptake.4. Glycogen and glucose utilization scales exponentially to relative exercise power output with a greater gain in glycogen than in glucose use at high power. The relationship between free fatty acid flux and power output is an inverted hyperbola. Consequently, at high power outputs, the role of lipid oxidation is diminished.5. Factors such as endurance training, energy supply, as influenced by dietary manipulation, and prior exercise play secondary roles in determining the balance of substrate utilization durin. exercise.6. Comparisons of the metabolic responses in subjects engaged in activities requiring vastly different metabolic rates or comparisons of subjects of different gender, age or training status require normalization of dat. to total energy flux.
THE GLUCOSE CROSSOVER CONCEPT IS NOT AN IMPORTANT NEW CONCEPT IN EXERCISE METABOLISM
Authors: Coggan Andrew R. 
Published: June 2007

SUMMARY1. The basic premise of the ‘crossover’ concept (i.e. that the balance of carbohydrate (CHO) and fat utilization during exercise depends on the interaction between exercise intensity and the individual's endurance training status) has been accepted since at least the 1930s.2. The crossover concept differs from earlier perspectives mostly in its greater emphasis on the absolute exercise intensity as an important determinant of substrate selection during exercise. Because of this emphasis, it is argued that while trained subjects may utilize less CHO than their untrained counterparts during low‐ or moderate‐intensity exercise, this is not true during high‐intensity exercise, because during such exercise even trained persons must ‘crossover’ to CHO dependency. In fact, the crossover concept predicts that utilization of at least one CHO source (i.e. plasma‐borne glucose) should be greater in trained subjects during intense exercise. This increase in glucose utilization is hypothesized to be supported by an enhanced rate of gluconeogenesis.3. In direct contradiction of the crossover concept, the literature consistently shows that, compared with untrained individuals, trained subjects rely less on CHO for fuel, even during high‐intensity exercise. In particular, it has been shown that the rate of glucose utilization is lower in trained subjects under these conditions. Recent data from Dr Brooks’ own laboratory support this conclusion and also show that this reduction in glucose use is associated with a decrease in the rate of gluconeogenesis. These recent observations confirm prior studies of moderate‐intensity exercise.4. Based on the above, it is clear that the crossover concept cannot be considered an important new concept in exercise metabolism. Instead, the crossover concept actually serves to hinder understanding in this area.
MITOCHONDRIAL FUNCTION IN RAT RENAL CORTEX IN RESPONSE TO PROTEINURIA AND IRON
Authors: Harris David CH , Tay Yuet‐Ching 
Published: June 2007

SUMMARY1. Proximal tubular cell dysfunction in chronic glomerular disease (CGD) has been ascribed, in part, to reabsorption of transferrin‐iron from tubular fluid and subsequent cytosolic peroxidative injury. To investigate a possible role for altered mitochondrial function in tubular cell injury in CGD, renal cortical mitochondrial respiratory function was examined in rats with adriamycin nephrosis.2. State 4 (resting) respiration was increased in adriamycin nephrosis in comparison with control (51±2 vs 43±2ng atoms oxygen (0)/min per mg protein, respectively; P < 0.02).3. Mitochondrial iron concentration was increased in nephrotic rats compared with contro. (9.52±0.70 vs 5.97±0.26 nmol Fe/mg protein, respectively; P < 0.001) and rates of state 3, state 4 and uncoupled respiration and the severity of proteinuria correlated with mitochondrial iron concentration.4. To further define the relationship between mitochondrial iron accumulation and altered respiratory function, rats were loaded wit. iron.5. In comparison with control, acute iron loading of normal rats impaired creatinine clearanc. (1.48±0.02 vs 0.40±0.29 mL/min), increased kidney weight (1.33±0.07 vs 1.74±0.14g) and impaired mitochondrial enzyme activity (e.g. cytochrome oxidase 185.0±46.6 vs 362.0±32.8Alog [cytochrome C]/min per mg protein; P < 0.05), but had no significant effect on rates of mitochondrial respiration or on mitochondrial fragility.6. Mitochondrial iron concentration was not increased by iron loading, despite a similar increment in cytoplasmic iron to that seen in rats with adriamyci. nephrosis.7. In summary, resting mitochondrial respiration is increased in nephrotic rats in proportion to mitochondrial iron accumulation. Changes in mitochondrial oxygen consumption do not appear to be a primary event in the tubular cell injury of iron loading.
POTENTIATION OF DIPSOGENIC ACTIONS BY CENTRALLY ADMINISTERED TYPE‐C NATRIURETIC PEPTIDE IN SPONTANEOUSLY HYPERTENSIVE BUT NOT WISTAR‐KYOTO RATS
Authors: Goto Eiichi , Shibata Kazuhiko , Furukawa Tatsuo 
Published: June 2007

SUMMARY1. The effects of type‐C natriuretic polypeptides (CNP) on the central dipsogenic and pressor responses to angiotensin II (AngII) were studied by the administration of agents into the lateral cerebral ventricle under conscious and unrestrained conditions in normotensive Wistar‐Kyoto (WKY) and spontaneously hypertensive rats (SHR).2. The fluid intake induced by AngII (25 ng) and water deprivation were potentiated after pretreatment with CNP in SHR but not in WKY rats. However, carbachol‐induced water intake was not altered by pretreatment with CNP (2.5 μg) in either WKY rats or SHR.3. In contrast, CNP did not influence the pressor responses to AngII in either WKY rats o. SHR.
VOLUME‐ACTIVATED TAURINE TRANSPORT IS DIFFERENTIALLY ACTIVATED IN HUMAN CERVICAL CANCER HT‐3 CELLS BUT NOT IN HUMAN PAPILLOMAVIRUS‐IMMORTALIZED Z183A AND NORMAL CERVICAL EPITHELIAL CELLS
Authors: Chou Cheng‐Yang , Shen Meng‐Ru , Chen Tzer‐Ming , Huang Ko‐En 
Published: June 2007

SUMMARY1. Previous studies demonstrate that volume‐sensitive chloride currents are distinctly activated in cervical cancer cells, but not in human papillomavirus (HPV)‐immortalized and normal cervical cells. In the present study, the Na+‐independent volume‐activated transport of taurine in three cervical cell types was investigated.2. Osmotic swelling of cervical cancer HT‐3 cells suspended i. Na+‐free hypotonic medium led to increased membrane uptake of taurine. This taurine uptake was effectively blocked by various C1‐ channel blockers with a similar potency in blocking volume‐sensitive C1‐ channels: l,9‐dideoxyforskolin > 5‐nitro‐2‐(3‐phenyl‐propylamino)‐benzoic acid (NPPB) > 4‐acetamido‐4′‐isothiocyanastilbene‐2,2′‐disulphonic acid (SITS) > 4,4′‐diisothio‐cyanatostilbene‐2,2‐disulphonic acid (DIDS)>furosemide. The taurine influx was also abolished by pertussis toxin. In contrast, Na+‐independent volume‐activated taurine transport was not significantly activated in HPV‐immortalized Z183A cells and in normal cervical cells.3. Exposure of HT‐3 cells to hypotonic medium also resulted in a marked increase in taurine efflux. The volume‐activated taurine efflux was osmolality dependent and the pattern of pharmacological inhibition by C1‐ channel blockers was indistinguishable from that for taurine uptake.4. These results suggest that volume‐sensitiv. C1‐ channels in HT‐3 cells can mediate the transport of amino acids. In addition, the pertussis toxin‐sensitive G‐protein is linked with the activation of this transport mechanism.