bluuebunny/crossref_metadata_2025_split huggingface dataset:
DIFFERENCES IN THE DENSITY OF BAROSENSITIVE NEURONS IN THE MEDULLA OF SPONTANEOUSLY HYPERTENSIVE AND WISTAR‐KYOTO RATS
Authors: Xiong Yu , Takayama Kiyoshige , Miura Mitsuhiko 
Published: June 2007

SUMMARY1. The density of barosensitive neurons in the medulla was examined in spontaneously hypertensive rats (SHR) and in normotensive Wistar‐Kyoto (WKY) rats. In control experiments, rats were sham‐operated, while in test experiments arterial baroreceptors were stimulated by pressor responses to i.v. administration of phenylephrine and the density of c‐Fos‐labelled neurons was immunocytologically examined.2. In both control and test experiments, c‐Fos‐labelled neurons were distributed in cardiovascular control sites: the nucleus trac‐tus solitarii (NTS) and the caudal and rostral ventrolateral medullas (CVLM/RVLM).3. In both WKY rats and in SHR, the total density of labelled neurons in test experiments was significantly higher than in control experiments.4. In control experiments, no significant difference was found in the distribution and density of labelled neurons in the NTS and in the CVLM/RVLM between WKY rats and SHR.5. In test experiments, no significant difference was found in the distribution and density of labelled neurons in the NTS between WKY rats and SHR.6. In test experiments in SHR, the density of labelled neurons in the CVLM just caudal to the obex level was significantly higher than that in WKY rats, whereas the density of labelled neurons in WKY rats in the RVLM just rostral to the obex level was significantly higher than that in SHR.7. These results indicate that stimulation of the arterial baro‐receptor induces strain‐specific differences in the density of barosensitive neurons in the CVLM/RVLM near the obex level.
CONTRACTILE PROPERTIES OF AFFERENT AND EFFERENT ARTERIOLES
Authors: Ito Sadayoshi , Abe Keishi 
Published: June 2007

SUMMARY1. The balance of vascular tone of the afferent and efferent arteriole is a crucial determinant of glomerular haemodynamics. Despite their intimate anatomical relationship in the juxtaglomerular apparatus, the mechanisms that regulate afferent and efferent arteriolar tone are different.2. In the afferent arteriole, two intrinsic mechanisms, the myogenic response and macula densa‐mediated tubuloglo‐merular feedback (TGF) play a dominant role, maintaining the glomerular filtration rate (GFR) at a constant level over a wide range of renal perfusion pressure. Studies have shown that these two mechanisms are modulated by nitric oxide (NO). In addition, an interaction between TGF and angiotensin II (AngII) seems to be essential to maintaining GFR despite large variations in daily intake of salt and water.3. In the efferent arteriole, neither myogenic response nor TGF seems to be important, while AngII is one major factor involved in the control of vascular resistance. In addition, recent studies have provided evidence that NO and prostaglandins produced by the glomerulus may control resistance of the downstream efferent arteriole.4. As the early segment of the efferent arteriole resides within the glomerulus, various autacoid hormones produced by the glomerulus may reach and directly act on this segment, thereby controlling the glomerular capillary pressure. Thus, it would be important to understand the differences in the mechanisms operating at the afferent and efferent arteriole, as well as their alterations in various physiological and pathological conditions.
LONG‐TERM SYMPATHO‐EXCITATORY EFFECT OF ANGIOTENSIN II: A MECHANISM OF SPONTANEOUS AND RENOVASCULAR HYPERTENSION
Authors: Fink Gregory D. 
Published: June 2007

SUMMARY1. The peptide hormone angiotensin II (AngII) is acknowledged to be an important factor in the pathophysiology of hypertension. This is particularly the case in hypertension caused by luminal narrowing of one renal artery, (i.e. renovascular hypertension). The primary mechanism by which AngII raises blood pressure, however, is disputed. Strong arguments can be made supporting either vascular contraction, effects on renal excretion of sodium and water, or trophic actions on cardiovascular structures as the key element. In this paper I review evidence that AngII influences blood pressure by modulating autonomic nervous system activity. Modulation can occur at both the peripheral and central aspects of the autonomic system, but I focus on brain pathways involved in determining sympathetic nervous system activity.2. Experimental and clinical investigations are cited to support the hypothesis that sympathetically mediated pressor effects are increased by both circulating and brain‐derived AngII in hypertension. Recent work points specifically to sympathetic pre‐motor neurons in the rostral ventrolateral medulla (RVLM) as a critical site of action of brain AngII in normoten‐sive and hypertensive animals.3. This same set of neurons appears to be an important relay in the sympatho‐excitatory response to circulating AngII initiated at circumventricular organs, particularly the area pos‐trema. AngII has important effects on the baroreflex. These do not mediate the sympatho‐excitation elicited by circulating AngII, but rather mask its expression.4. Substantial data support the hypothesis that increased blood concentrations of AngII in renovascular hypertension elevate blood pressure by causing neurogenic vasoconstriction mediated through the area postrema and RVLM.
TISSUE VARIATION OF ACUTE HAEMODYNAMIC CHANGES BY NG‐NITRO‐L‐ARGININE IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE AND WISTAR‐KYOTO RATS
Authors: Higashino H. , Simeonova K. , Lambev I. , Suzuki A. 
Published: June 2007

SUMMARY1. The acute effects of nitric oxide synthase inhibition on the haemodynamics in stroke‐prone spontaneously hypertensive (SHRSP) and normotensive Wistar‐Kyoto (WKY) rats were investigated using radiolabeled microspheres.2. Intravenous administration of 3 and 6 mg/kg NG‐nitro‐L ‐arginine (l.‐NNA) caused a significant increase in total peripheral resistance, a decrease in cardiac output and an increase in blood pressure in both SHRSP and WKY rats.3. Significant decreases in regional blood flow (RBF) in the lung, muscle and stomach of WKY rats were observed following L‐NNA administration.4. NG‐nitro‐L ‐arginine produced a 70% increase in brain regional blood flow at a dose of 6 mg/kg only in SHRSP.5. There was a variation in the involvement of nitric oxide (NO) in different tissues.6. It is concluded that hypertension in SHRSP augments NO‐mediated vasodilation.
EFFECTS OF VERATRIDINE ON THE ACTION POTENTIALS AND CONTRACTILITY OF RIGHT AND LEFT VENTRICLES FROM NORMO‐ AND HYPERTENSIVE RATS
Authors: Nand Vinita , Doggrell Sheila A. , Barnett Carolyn W. 
Published: June 2007

SUMMARY1. We have studied the effects of prolonging the opening of sodium channels with veratridine on the action potentials (AP) and contractility of isolated right and left ventricles of Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). It was examined whether the effects of veratridine were altered in the SHR right ventricle in the absence of hypertrophy. The main aim of the present study was to test the hypothesis that the effects of veratridine were altered in the SHR left ventricle in the presence of hypertrophy.2. The tail‐cuff pressures of 14‐ and 22‐week‐old, but not 5‐week‐old, SHR were greater than those of the WKY rat. At 14 weeks of age the SHR left, but not right, ventricle had developed hypertension‐associated hypertrophy.3. The AP and contractions and the ability of veratridine to prolong the AP and act as a positive inotrope were similar in the right ventricles from 22‐week‐old WKY rats and SHR. The effects of veratridine and the AP and contractions of left ventricles of 5‐, 14‐ and 22‐week‐old WKY rats and of 5‐ and 14‐week‐old SHR were also similar.4. The AP of the left ventricles of 22‐week‐old SHR were prolonged by 3 ms at the action potential duration (APD)50 and APD90 levels. The contractions to cardiac stimulation and the maximum combined force responses to cardiac stimulation and isoprenaline were reduced in the left ventricles of 22‐week‐old SHR compared with WKY rats and younger SHR.5. The effectiveness of veratridine in prolonging the AP and augmenting the contractions to cardiac stimulation was reduced in the hypertrophied left ventricle of 22‐week‐old, but not 14‐week‐old, SHR.6. In summary, the response to prolonging the opening of sodium channels with veratridine is not altered in the SHR right ventricle. However, in left ventricles of the hypertrophied 22‐week‐old, but not 14‐week‐old, SHR the effects of veratridine are reduced and this demonstrates that the response to prolonging the opening of sodium channels is changed in persistent hypertension‐associated hypertrophy.
PSYCHOMOTOR PERFORMANCE DURING INITIAL STAGE OF EXPOSURE TO HALOTHANE, ENFLURANE, ISOFLURANE AND SEVOFLURANE IN MICE
Authors: Komatsu Hisao , Nogaya Junko , Kuratani Norihumi , Ueki Masaaki , Yokono Satoshi , Ogli Kenji 
Published: June 2007

SUMMARY1. The dose‐response relationship during the pre‐anaesthetic and pre‐equilibrium state of four inhalation anaesthetics (halothane, enflurane, isoflurane and sevoflurane) on fixed‐ratio schedule‐controlled behaviour was studied in mice.2. Animals exposed to halothane, enflurane and isoflurane showed a biphasic pattern (i.e. a significant incremental increase in psychomotor responses at low inspired concentrations (0.1‐0.4%) and decrements at greater concentrations) in a dose‐dependent manner. Mean peak responses (per cent of control) were 132.3 (P<0.01 vs control), 124.0 (P<0.05) and 116.7% (P<0.05) at 0.1% halothane, 0.3% enflurane and 0.2% isoflurane, respectively.3. Sevoflurane did not increase schedule‐controlled behavioural responses at any concentration.4. The effect of subanaesthetic concentrations of inhalation anaesthetics on psychomotor performance can be evaluated as changes in the response rate in schedule‐controlled behaviour.
FUNCTION IN NEUROTOXICITY: INDEX OF EFFECT AND ALSO DETERMINANT OF VULNERABILITY
Authors: Ray DE 
Published: June 2007

SUMMARY1. In neurotoxicity, functional indices may be the only available measures of effect, as many potent neurotoxic agents produce no morphological change. Examples of these are strychnine, dieldrin and pyrethroids, which produce excitation but no pathology, and barbiturates, xylene and lithium, which produce depression but no pathology.2. In other cases where both functional and morphological effects are seen, functional measures often produce the most convenient, if not always the most specific, indices of toxicity. Appropriate functional measures can be highly sensitive, both in humans and in experimental animals, and can also give vital mechanistic information. However, it is essential that functional measures are reproducible and interpretable (some behavioural measures are not) and also provide a reasonably exacting test of function (passive observation of resting behaviour can miss many effects).3. In addition to their use as an index of toxicity, changes in function, even within the normal range, can themselves influence susceptibility to toxins. Tissue perfusion can determine delivered dose and is influenced by function, while metabolic transformation is modified by nutritional state. Nutritional state can also influence absorption, with anaemia enhancing manganese toxicity and calcium deficiency enhancing lead toxicity. Functional activity can influence target susceptibility directly: thus, noise exposure enhances the ototoxicity of carbon monoxide, toluene or aminoglycoside antibiotics; noise, motor activity or anaesthesia all influence the central neurotoxicity of dinitrobenzene or metronidazole; motor activity enhances the peripheral nerve toxicity of lead or thallium; and nerve regeneration enhances the toxicity of hexane. These functional factors can be very important in determining individual susceptibility.
SYMPATHETIC MODULATION OF SENSORY NERVE ACTIVITY WITH AGE: HUMAN AND RODENT SKIN MODELS
Authors: Khalil Z , LeVasseur S , Merhi M , Helme RD 
Published: June 2007

SUMMARY1. Sensory nerves serve an afferent role and mediate neurogenic components of inflammation and tissue repair via an axon reflex release of sensory peptides at sites of injury. Dysfunction of these nerves with age could contribute to delayed tissue healing.2. Complementary animal and human skin models were used in the present studies to investigate changes in the modulation of sensory nerve function by sympathetic efferents during ageing. Laser Doppler flowmetry was used to monitor neurogenic skin vascular responses.3. The animal model used skin of the hind footpad of anaesthetized rats combined with electrical stimulation of the sciatic nerve, while the human model comprised capsaicin electrophoresis to the volar surface of the forearm. Sympathetic modulation was effected by systemic phentolamine pretreatment in animals and local application in the human model.4. The results obtained from the human model confirmed the reported decline in sensory nerve function and showed no change in sympathetic modulation with age. The results from the animal model confirm and expand results obtained from the human model.5. The use of low (5 Hz) and high (15 Hz) frequency electrical stimulation (20 V, 2 ms for 1 min) revealed a preferential response of aged sensory nerves to low‐frequency electrical stimulation parameters with differential sympathetic modulation that is dependent on the frequency o. stimulation.
Experimental Biology 1997 Symposium on Neurobiology of Thennoregulation: Role of Stress: POISONS AND FEVER
Authors: Gordon Christopher J. , Rowsey Pamela J. 
Published: June 2007

SUMMARY1. Dysfunction of the thermoregulatory system is one of many pathologies documented in experimental animals and humans exposed to toxic chemicals. The mechanism of action responsible for many types of poison‐induced fevers is not understood. Some elevations in body temperature are attributed to the peripheral actions of some poisons that stimulate metabolic rate and cause a forced hyperthermia. Exposure to organophosphate (OP) pesticides and certain metal fumes appears to cause a prolonged, regulated elevation in body temperature (Tb).2. Activation of cyclo‐oxygenase (COX) and the production of prostaglandin (PG)E2 in central nervous system (CNS) thermoregulatory centres is required to elicit a fever. Activating the COX‐PGE2 pathway by a poison may occur by one of three mechanisms: (i) induction of cell‐mediated immune responses and the subsequent release of cytokines; (ii) induction of lipid peroxidation in the CNS; and (iii) direct neurochemical activation.3. Radiotelemetric monitoring of core temperature in unstressed rodents has led to an experimental animal model of poison‐induced fever. Rats administered the OP agents chlorpyrifos and diisopropyl fluorophosphate display an initial hypothermic response lasting approximately 24 h, followed by an elevation in diurnal core temperature for 24–72 h after exposure. The hyperthermia is apparently a result of the activation of the COX‐PGE2 pathway because it is blocked by the anti‐pyretic sodium salicylate. Overall, the delayed hyperthermia resulting from OP exposure involves activation of thermoregulatory pathways that may be similar to infectionmediated fever.
ELECTROPHYSICAL PROPERTIES, SYNAPTIC TRANSMISSION AND NEUROMODULATION IN SEROTONERGIC CAUDAL RAPHE NEURONS
Authors: Li Yu‐Wen , Bayliss Douglas A. 
Published: June 2007

SUMMARY1. We studied electrophysiological properties, synaptic transmission and modulation by 5‐hydroxytryptamine (5‐HT) of caudal raphe neurons using whole‐cell recording in a neonatal rat brain slice preparation; recorded neurons were identified as serotonergic by post‐hoc immunohistochemical detection of tryptophan hydroxylase, the 5‐HT‐synthesizing enzyme.2. Serotonergic neurons fired spontaneously (approximately 1 Hz), with maximal steady state firing rates of < 4 Hz. 5‐Hydroxytryptamine caused hyperpolarization and cessation of spike activity in these neurons by activating inwardly rectifying K+ conductance via somatodendritic 5‐HT1A receptors.3. Unitary glutamatergic excitatory post‐synaptic potentials (EPSP) and currents (EPSC) were evoked in serotonergic neurons by local electrical stimulation. Evoked EPSC were potently inhibited by 5‐HT, an effect mediated by presynaptic 5‐HTIB receptors.4. In conclusion, serotonergic caudal raphe neurons are spontaneously active in vitro; they receive prominent glutamatergic synaptic inputs. 5‐Hydroxytryptamine regulates serotonergic neuronal activity of the caudal raphe by decreasing spontaneous activity via somatodendritic 5‐HTIA receptors and by inhibiting excitatory synaptic transmission onto these neurons via presynaptic 5‐HTIB receptors. These local modulatory mechanisms provide multiple levels of feedback autoregulation of serotonergic raphe neurons by 5‐HT.
CENTRAL REGULATION OF AUTONOMIC FUNCTION: NO BRAKES?
Authors: Krukoff Teresa L. 
Published: June 2007

SUMMARY1. Nitric oxide (NO) is formed by neuronal NO synthase (nNOS) and acts as a non‐conventional neurotransmitter in the brain. A growing body of evidence supports the hypothesis that NO acts to decrease sympathetic output to the periphery; these effects may occur at several autonomic sites. The present review describes studies from our laboratory that address this hypothesis.2. Restraint stress activates putative NO‐producing neurons in many autonomic centres: preoptic area, medial septum, amygdala, hypothalamus, including the paraventricular nucleus (PVN), raphe nuclei, nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM). These results suggest that NO is directly or indirectly involved in regulating sympathetic output to the periphery.3. Systemic angiotensin II (Angll) activates putative NO‐producing neurons in the PVN. These neurons may be activated either by the increases in arterial pressure that accompany Angll injections or due to activation of AngII‐containing neural pathways.4. Hypotension is associated with the activation of putative NO‐producing PVN neurons, small numbers of which also project to the NTS or VLM. As the majority of activated neurons is in the magnocellular division, NO production may be related to the production of vasopressin.5. Adult spontaneously hypertensive rats (SHR) show increased gene expression of nNOS in the hypothalamus, dorsal medulla and caudal VLM. These differences are not present in young prehypertensive SHR, suggesting that the changes in gene expression in adult rats are associated with the increased sympathetic nerve activity found in these rats.6. Gene expression of nNOS is altered in the hypothalamus and caudal VLM of renal hypertensive rats at 3 and 6 weeks after surgical induction of hypertension. Contrasting results at the two time points may be due to differing underlying physiological processes that characterize the two stages of renal hypertension.7. Nitric oxide may affect sympathetic output through several possible mechanisms. These include affecting production of the second messenger cGMP and interactions with more classical neurotransmitters or with neurohormonal systems in the brain.
RELATIONSHIPS BETWEEN ISOMETRIC AND ISOTONIC MECHANICAL PARAMETERS AND CROSS‐BRIDGE KINETICS
Authors: Rossmanith Gunther H. , Tjokorda Oka B. 
Published: June 2007

SUMMARY1. Isometric and isotonic measures have been widely used both to characterize muscular contraction in striated muscle and to compare the mechanical properties of striated muscle types for a wide variety of species. The interrelationship of these measures and their interpretation, in terms of underlying cross‐bridge mechanisms, requires clarification.2. We demonstrate that a strain‐dependent three‐state model can simulate these isometric and isotonic mechanics and offer a unified explanation for these mechanics in terms of cross‐bridge kinetics.3. Our exploration reveals the partial view each individual measure of mechanics provides and emphasizes the complementary insights the various isometric and isotonic measures give of the underlying cross‐bridge kinetics.
CYTOCHROME P‐450‐DEPENDENT ARACHIDONATE METABOLITES AND RENAL FUNCTIONS IN THE LYON HYPERTENSIVE RAT
Authors: Messer‐Létienne I. , Bernard N. , Benzoni D. , Sassard J. 
Published: June 2007

SUMMARY1. The present work aimed to assess the role of cytochrome P‐450 (CP‐450) metabolites of arachidonic acid such as epoxy‐eicosatrienoic (EET) and hydroxyeicosatetraenoic acids (HETE) in the renal vasoconstriction and decreased natriuresis exhibited by genetically hypertensive (LH) rats of the Lyon strain.2. The experiment was performed on single‐pass isolated perfused kidney preparations from 8‐week‐old male LH rats and their low blood pressure (LL) controls. The effects of miconazole (an inhibitor of the formation of EET) and of 17‐octadecynoic acid (17‐ODYA, an inhibitor of both EET and HETE synthesis) were studied before and after stimulation of the kidneys with two noradrenaline (NA) infusions (65 and 110 nmol/L).3. Unstimulated LH kidneys (n= 12) differed from LL {n= 12) by increased vascular resistance (RVR) and decreased glomerular filtration rate and urinary sodium excretion (UNaV).4. Miconazole (1 μmol/L) did not change the functions of LH and LL unstimulated kidneys, but blunted the vasoconstrictor response to NA (110 nmol/L), the difference being significant in LH kidneys only (1.7±0.2 vs 3.6±1.2 mmHg/mL per min per g; P<0.05).5. Addition of 17‐ODYA (3 μmol/L) to miconazole did not modify RVR in LH and LL kidneys or the response to NA infusion. On the contrary, it increased UNaV, the differences being significant in LH kidneys only (22.9±1.4 vs 17.5±1.4 μmol/min per g; P<0.05 after NA 110 nmol/L).6. It is suggested that EET may contribute to the elevated RVR and HETE to the reduced ability to excrete sodium, of LH kidneys.
RESTORATION OF NITRIC OXIDE FUNCTION IN HUMAN HYPERLIPIDAEMIA, CONGESTIVE HEART FAILURE AND LIVER CIRRHOSIS
Authors: Chin‐Dusting Jaye PF , Kaye David M. 
Published: June 2007

SUMMARY1. There is accumulating evidence for a range of abnormalities in the nitric oxide (NO) signalling cascade in human cardiovascular disorders.2. In the present review we assess the literature detailing such evidence in early (hyperlipidaemia) and end‐stage (heart failure) disease, with emphasis on the mechanisms by which the disturbances are thought to occur.3. Strategies for the correction of disturbed NO signalling in these states are reviewed and include both prescribed pharmacological interventions, such as lipid‐lowering therapy and novel uses of angiotensin‐converting enzyme inhibitors, as well as non‐pharmacological interventions, such as exercise and dietary supplementation with l‐arginine and n‐3 polyunsaturated fatty acids.4. In addition to a decreased production/function of NO, the possible detrimental effects of a chronic elevation in NO production in patients with liver cirrhosis, together with a novel use of antibiotics to correct this perturbation, is outlined.