bluuebunny/crossref_metadata_2025_split huggingface dataset:
INVOLVEMENT OF NITRIC OXIDE IN CORONARY VASCULAR RESPONSES TO 5‐HYDROXYTRYPTAMINE IN THE ANAESTHETIZED GREYHOUND
Authors: Woodman Owen L. , Dusting Gregory J. 
Published: June 2007

SUMMARY1. The effect of the intracoronary (i.c.) injection of 5‐hydroxytryptamine (5‐HT; 0.1–1.0 μFg/ kg) was examined before and after inhibition of nitric oxide (NO) synthesis with N‐nitro‐l‐arginine (NOLA; 5 mg/ kg i.c.) in nine anaesthetized greyhounds. Before administration of NOLA, 5‐HT increased coronary blood flow (CBF) but decreased large coronary artery diameter indicating simultaneous dilatation of resistance vessels and constriction of large arteries.2. The administration of NOLA significantly decreased large coronary artery diameter and increased systemic arterial pressure. There was no significant effect on coronary vascular resistance or heart rate. In the presence of NOLA, the 5‐HT‐induced constriction of the large coronary artery was enhanced and the dilatation of the resistance vessels was reduced. In addition there was a secondary reduction in CBF, a response that was not observed before NOLA treatment.3. The response to NOLA suggests that a basal release of NO is important in the regulation of coronary and systemic vascular tone. Nitric oxide is an important mediator of coronary vasodilator responses to 5‐HT, and in addition the release of NO modulates 5HT‐induced constriction of large coronary arteries.
NEUROPEPTIDE Y IN CORTISOL‐INDUCED HYPERTENSION IN MALE VOLUNTEERS
Authors: Whitworth Judith A. , Williamson Paula M. , Brown Mark A. , Morris Margaret J. 
Published: June 2007

SUMMARY1. Cortisol‐induced blood pressure rises in men are not accompanied by increases in plasma catecholamines. The present study examines the effects of cortisol on the sympathetic co‐transmitter, neuropeptide Y (NPY).2. Eight normal men were given cortisol 200 mg/day over 5 days and haemodynamic, metabolic and hormonal measures were taken. Plasma NPY‐like immunoreactivity (NPY‐LI) concentrations were measured by direct radio‐immunoassay.3. Cortisol significantly increased systolic, diastolic and mean arterial pressure, bodyweight, plasma glucose and total white cell concentration and decreased plasma potassium and total eosinophil count, as in previous studies. Plasma NPY concentrations were not altered significantly during cortisol treatment, but increased following cessation of cortisol treatment (P= 0.006).4. The essentially unchanged pattern for NPY concentration with cortisol treatment resembles that previously reported for adrenaline and noradrenaline, but the increase in NPY on cortisol withdrawal was not seen for adrenaline or noradrenaline. These data do not support a role for sympathetic activation in the genesis of cortisol‐induced hypertension.
SEX DIFFERENCES IN THE PARASYMPATHETIC NERVE CONTROL OF RAT HEART
Authors: Du X‐J. , Dart A. M. , Riemersma R. A. 
Published: June 2007

SUMMARY1. As it has been shown that oestrogen enhances the cholinergic muscarinic activity in the central nervous system, we studied sex differences in the responses to parasympathetic nervous stimulation in the rat heart using in vivo and in vitro preparations.2. In in situ perfused, innervated hearts, stimulation of bilateral vagus nerves (15 Hz with 1 μmol/L physostigmine) inhibited sympathetic nerve stimulation (5 Hz) induced noradrenaline release to a greater extent in female than in male rats (54 ± 5 vs 72 ± 5% of control). Similarly, vagus nerve stimulation at 1–20 Hz reduced heart rate (HR) more in females than males, and this sex difference became more marked in the presence of physostigmine. The chronotropic effect of vagal stimulation was attenuated after ovariectomy but potentiated after castration when compared with sham‐operated controls. In contrast, the muscarinic agonist methacholine reduced neural NA release and HR equally well in both sexes.3. In anaesthetized rats, reduction in HR and mean arterial pressure by vagus nerve stimulation (1–20 Hz) was more pronounced in females than in males after inhibition of acetylcholinesterase with physostigmine.4. The results indicate that activation of parasympathetic nerve leads to greater presynaptic and postsynaptic effects in female than in male rat hearts, presumably due to a higher level of acetyl‐choline release following nerve activation.
THE EFFECT OF HIGH PERFUSION RATES ON THE ENDOTHELIAL DIFFUSION BARRIER IN RAT MESENTERIC ARTERIES IN VITRO
Authors: Lew Michael J. , Madeley Lisa J. 
Published: June 2007

SUMMARY1. Arteries from Wistar‐Kyoto rat mesenteries were cannulated with glass cannulae and perfused with Krebs’ solution at controlled rates and distending pressure. Arterial diameter was measured and concentration—response curves generated with agonists applied via the perfusate (luminal) and via the solution bathing the outside of the preparation (extraluminal).2. The α1‐adrenoceptor selective agonist methoxamine was about three times more potent when applied extraluminally than intraluminally in arteries perfused at either 25 or 500 μL/ min, but the lipophilic α1‐adrenoceptor selective agonist SKF 89748‐A was equally potent with either mode of application.3. The extraluminal/intraluminal potency differentials for both methoxamine and noradrenaline were abolished by perfusion for 30 min at a rate calculated to give a high shear stress (100 dyn/cm2).4. The potency of luminally applied acetylcholine was reduced less than two‐fold by the high shear perfusion, and the ability of acetylcholine to maximally relax the arteries was unchanged.5. It is concluded that (i) the endothelium of small arteries reduces the potency of luminally applied lipophobic agonists by acting as a diffusion barrier; (ii) the ability of the endothelium to act as a diffusion barrier is easily damaged by shear stress in vitro; and (iii) the ability of acetylcholine to relax arteries in vitro is a poor index of the full functioning of the endothelium.
EFFECTS OF DILTIAZEM ON [3H]‐ACETYLCHOLINE RELEASE IN RAT CENTRAL NERVOUS SYSTEM
Authors: Tsuda Kazushi , Tsuda Seiko , Masuyama Yoshiaki , Goldstein Menek 
Published: June 2007

SUMMARY1. In the present study, we examined the effects of a Ca2+ channel blocker, diltiazem, on [3H]‐acetylcholine (ACh) release in the rat CNS.2. Diltiazem inhibited the electrically stimulated [3H]‐ACh release in a dose‐related fashion in striatal slices of Sprague‐Dawley (SD) rats. The basal release of [3H]‐ACh was not significantly affected by diltiazem except at a high concentration.3. The stimulation‐evoked [3H]‐ACh release was not different between spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats.4. The inhibitory effect of diltiazem on the stimulation‐evoked [3H]‐ACh release was significantly greater in SHR than in WKY rats.5. The results show that diltiazem inhibited the stimulation‐evoked ACh release in the rat CNS. The pronounced effect of diltiazem in SHR suggests that the inhibition of central cholinergic activity might contribute, at least partially, to the hypotensive mechanisms of the Ca2+ channel blocker.
PRORENIN AND ACTIVE RENIN CONCENTRATIONS IN OVARIAN FOLLICULAR FLUID INCREASE AFTER THE LH PEAK IN SUPEROVULATED HEIFERS
Authors: Hagemann A. , Nielsen A. H. , Assey R. J. , Hyttel P. , Boland M. P. , Roche J. F. , Poulsen K. 
Published: June 2007

SUMMARY1. The aim was to analyse the in vivo variations with time of prorenin and active renin and their relationship to steroid hormones in ovarian follicular fluid during follicular growth in heifers.2. Thirty one beef heifers were assigned to two groups after oestrous synchronization: an unstimulated and a follicle‐stimulating hormone (FSH)‐treated (superovulated) group. Within each group, animals were slaughtered at different times of the follicular phase of the oestrous cycle. Ovarian follicular fluids were aspirated and analysed for the concentrations of active renin, prorenin, oestradiol‐17β (E2) and progesterone (P4).3. Prorenin and active renin concentrations in follicular fluid remained constant until the luteinizing hormone (LH) peak, after which time they increased four‐ and two‐fold, respectively, in superovulated heifers.4. In follicular fluid, prorenin and active renin correlated negatively with oestradiol and E2/P4 ratio but positively with progesterone during follicular growth in superovulated heifers. Prorenin also correlated negatively with oestradiol and E2/P4 ratio in unstimulated heifers.5. The increase of renin concentrations in ovarian follicles after the LH peak and the correlations to steroid hormones suggest an important role of the ovarian renin‐angiotensin system in bovine follicular growth and maturation.
HYPERPROLIFERATION OF AORTIC SMOOTH MUSCLE CELLS AND FIBROBLASTS FROM YOUNG SHR RATS IS NOT SHARED BY ENDOTHELIAL CELLS
Authors: Battle Thierry , Arnal Jean‐François , Michel Jean‐Baptiste 
Published: June 2007

SUMMARY1. To study the hypertensive genotypic influence on growth kinetics of the three aortic wall cell types.2. Using young spontaneously hypertensive (SHR) and Wistar‐Kyoto (WKY) rats weighing 160–180 g, we compared the proliferative properties of endothelial cells (EC), smooth muscle cells (SMC) and fibroblasts that were isolated from the thoracic aorta of each strain and cultured. Growth‐arrested cells were exposed to P <‐thymidine after stimulation with 150 μg/mL endothelial cell growth supplement. Proliferation assays were performed by cell seeding on decellularized aortic explants and cell counting 2, 4, 5, 6 and 7 days after seeding. The influence of SMC from SHR on the growth kinetics of EC was evaluated by co‐cultures in transwell systems.3. After stimulation, SMC from SHR exhibited a greater P <‐thymidine incorporation rate than those from WKY rats (ratios over controls: 3.90 ± 0.48 [7] vs 1.85 ± 0.25 [7] respectively, P < 0.05). This was also true for adventitial SHR fibroblasts: (13.1 ± 0.6 [6] vs 9.9 ± 1.0 [6] WKY P < 0.05). On the contrary, there was no difference in the P<‐thymidine incorporation rates between EC of each strain, regardless of the passage and the time considered. Cell proliferation on matrix explants confirmed the hyperproliferation of SMC and fibroblasts from SHR, while EC of each strain proliferated equally. Smooth muscle cells from SHR did not influence the growth kinetics of EC in co‐culture and vice versa.4. The changes in growth patterns of aortic cells isolated from young prehypertensive SHR seem to be restricted to SMC and fibroblasts.
HEMATOLOGICAL ALTERATIONS AFTER ACUTE EXPOSURE TO HYPERBARIC OXYGEN IN RATS
Authors: Amin Hesham M. , Hakim Tawfic S. , Camporesi Enrico M. 
Published: June 2007

SUMMARY1. Acute exposure to hyperbaric oxygen (HBO) is associated with a significant increase in haematocrit which returns to the control level after 24 h of recovery in room air. In this study we report changes in blood viscosity in Sprague‐Dawley rats after acute exposure to HBO.2. The rats were divided into three groups: a control group included rats not exposed to HBO (CON), a group studied immediately after acute exposure to HBO at 283.7 kPa for 6 h (HBO), and a group allowed to recover for 24h in room air after HBO exposure (REC).3. The viscosity of the whole blood, plasma and red blood cells (RBC) suspension was measured in the three groups. A significant increase in whole blood viscosity was detected in HBO and REC groups compared with CON (P<0.05), but no changes in the viscosity of the plasma or RBC suspension were noted.4. A significant decrease in oxygen delivery index was found in the REC group compared with the CON and HBO groups (P<0.05).5. In a subgroup of rats, several blood parameters known to influence blood viscosity were evaluated. A significant increase in plasma colloid oncotic pressure was noted in HBO rats compared with CON (P<0.01). A marked increase in platelet count and fibrinogen concentration was detected in HBO and REC rats compared with CON (P<0.05). Furthermore, a significant increase in total leukocytic count was noticed in REC group compared with CON and HBO (P<0.001).6. We conclude that acute exposure to HBO induces a significant increase in whole blood viscosity which cannot be explained solely by the increase in haematocrit. Alterations in several blood components could lead to this phenomenon.
ω‐CONOTOXIN GVIA AND PRAZOSIN, BUT NOT FELODIPINE, CAUSE POSTURAL HYPOTENSION IN RABBITS
Authors: Hawkes Anna L. , Angus James A. , Wright Christine E. 
Published: June 2007

SUMMARY1. The aim was to compare the effect of N‐type calcium channel blockade by ω‐conotoxin GVIA (ω‐CTX) with α1‐adrenoceptor or L‐type calcium channel blockade on postural adaptation in conscious rabbits.2. Orthostatic responses were assessed by rapidly tilting the rabbits through 90° for 1 min. Tilts were performed before, 30 and 60 min after i.v. bolus administration of vehicle (propylene glycol 0.17mL/kg; n = 8), prazosin (0.5mg/kg; n= 8), felodipine (30μg/kg; n= 8) or ω‐CTX (3 & 7 μg/kg; n = 9).3. Prazosin, felodipine or ω‐CTX caused significant falls in mean arterial pressure (MAP) with corresponding increases in heart rate (HR). Vehicle administration had no effect on MAP but caused a small fall in HR.4. Before drug or vehicle administration, a small rise in MAP and HR occurred in response to tilt in all rabbits. In the vehicle treatment group, similar responses were observed to tilt at 30 and 60 min. Postural hypotension was observed in the prazosin treatment group, but not following administration of felodipine. Tilts 30 and 60 min after ω‐CTX (3μg/kg) caused an increase in HR but no change in MAP, different to the small pressor response observed following vehicle administration. However, following administration of ω‐CTX 7 μg/kg (total dose, 10μg/kg), significant falls in MAP with tachycardia were observed in response to tilt.5. In conclusion, orthostatic hypotension was observed following acute αl‐adrenoceptor or N‐type calcium channel blockade in the conscious rabbit. These findings are compatible with the expectation that agents which are directly sympatholytic interfere with postural adaptation. In contrast, L‐type calcium channel antagonism with felodipine did not elicit postural hypotension.
HUMAN BUCCAL EPITHELIAL CELLS AS A POTENTIAL BIOCHEMICAL PREDICTOR OF ESSENTIAL HYPERTENSION: IDENTIFICATION OF KEY CELLULAR PROCESSES
Authors: McMurchie Edward J. , Head Richard J. 
Published: June 2007

SUMMARY1. Human cheek cell Na+/H+ antiporter activity (measured as the rate of proton‐dependent 22Na+ uptake) was determined in seven normotensive (NT) and four hypertensive (HT) subjects following preincubation of cheek cells with a low molecular weight fraction isolated from NT saliva together with the ionophore, nigericin.2. Cheek cells preincubated in this manner exhibited greater Na+/H+ antiporter activity with the mean values being 4.2 nmol Na+.mg protein. 5min for the NT group and 1.7 for the HT group.3. It is possible that stimulation of Na+ transport is due to cellular accumulation of K+ ions during preincubation which, in the presence of the K+/H+ selective ionophore, nigericin, can cause cellular reacidification promoting further 22Na+ uptake via the Na+/H+ antiporter.
INHIBITION OF RAT GLOMERULAR MESANGIAL CELL SODIUM/HYDROGEN EXCHANGE BY HYDROGEN PEROXIDE
Authors: Shaw Sidney , Naegeli Patricia , Etter Jean‐Daniel , Weidmann Peter 
Published: June 2007

SUMMARY1. pHi regulation In glomerular mesangial cells (GMC) includes both Na+/H+ and Cl‐/HCO3‐ exchange. As a fall in pHi may protect against H2O2‐mediated GMC damage during ischaemia‐reperfusion, the involvement of these mechanisms in the GMC pHi response to H2O2 was assessed using confluent GMC grown in RPMI medium with 20% fetal calf serum (10–15 passages).2. Cells were loaded with BCECF‐AM and pHi evaluated using standard fluorometric‐ratio techniques. In HEPES buffer, GMC exposure to H2O2 dose‐dependently (25μmol/L‐1 mmol/L) decreased pHi over 10 rnin from 7.3 ± 0.1 to 6.7 ± 0.1 (at 100 μmol/L) partly due to rapid non‐competitive inhibition of amiloride‐sensltive Na+/H+ exchange.3. BCECF fluorescence in free solution was unchanged by H2O2 whereas the pHi decrease was abolished by nigericin/K+ clamp. Buffer capacity by direct titration was not changed by H2O2 and averaged 100 ± 9 nmol/2.6±106 cells/pH unit. Similarly, zero‐Na+/high‐K+ buffer, used to minimize Passive H+ entry, did not prevent the fall in pHi while GMC H+‐formation/extrusion, assessed by the rate of extracellular acidification in low‐capacity buffer (0.05 mmol/L), was rapidly inhibited.4. In contrast, following only a brief 3 min exposure to 1 mmol/L H2O2, HCO3‐/CO2 buffer potentiated the inhibition of Na+/ H+ exchange from 50 to 80% of control and reduced the acidification from pHi 6.6 ± 0.1 to 7.15 ± 00.05. This effect was reversed (to pHi 6.8 ± 0.07) by pretreatment with 200 μmol/L DIDS, an inhibitor of Cl‐/HCO3‐ exchange.5. Thus, the decrease in GMC pHi in Fespohsë to H2O2 In HEPES, partly mediated by inhibition of Na+/H+ exchange and a possible redistribution of intraceliular H+, is antagonized in HCO3‐/CO2 through a DIDS‐sensitive Cl‐/HCO3‐ exchange mechanism. This may act to negate potentially protective effects of low pHi and potentiate oxidative damage to membrane lipids, enzymes and intracellular organelles on reperfusion.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: NSAID: AN UPDATE ON THEIR ANALGESIC EFFECTS
Authors: Walker J. S. 
Published: June 2007

SUMMARY1. The non‐steroidal anti‐inflammatory drugs (NSAID) are a group of drugs that possess both analgesic and anti‐inflammatory properties. They are used to treat a variety of painful and inflammatory disorders such as postoperative pain, dental surgery, headache, acute and chronic musculoskeletal pain.2. There is now substantial evidence that NSAID produce analgesia by inhibiting prostaglandin (PG) synthesis both in the peripheral and central nervous system. However, other mechanisms of action should also be considered. There is a multiplicity of mediators capable of producing pain, and NSAID may act both on the peripheral and central nervous system to modulate such mediators. There is a growing body of evidence suggesting that NSAID can exert an effect on specific G‐protein dependent functions.3. There is significant intra‐ and interpatient variability in the response to NSAID. Development of tolerance after multiple doses may provide an explanation for the unsatisfactory response to NSAID in some patients.4. It has been suggested that the rate of decline of drug effect is characteristic of analgesia itself and indicates that an endogenous substance mediates the analgesic effect; possible candidates include serotonin.5. NSAID remain an important therapeutic option in the management of pain.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: NEUROTRANSMITTER MECHANISMS OF RAT VAGAL AFFERENT NEURONS
Authors: Lawrence Andrew J. 
Published: June 2007

SUMMARY1. The present study has employed anatomical and neurochemical techniques to assess whether the amino acid, l‐glutamate, may be considered as a potential neurotransmitter at rat vagal afferent neurons, with particular reference to baroreceptor afferents.2. Slide‐mounted sections of rat nodose ganglia were incubated with a high‐titre antibody to glutamate, and visualization of the resulting immunoreactivity indicated glutamate‐positive staining in a population of vagal afferent perikarya. In contrast, interstitial cells were devoid of immunostaining.3. Release of endogenous glutamate was measured by in vivo microdialysis in the nucleus tractus solitarius, the site of central vagal afferent terminals, and could be evoked with a depolarizing stimulus of KCl in a calcium‐dependent fashion. In addition, baroreceptor loading with an intravenous infusion of phenylephrine (30 μg/kg per min) increased the spontaneous efflux of glutamate to 148 ± 28% of basal levels, which was paralleled by an increase in mean arterial pressure (∼40 mmHg). Release of glutamate was also elevated two‐fold by intra‐cerebral administration of S‐nitroso‐N‐acetylpenicillamine (30 μmol/L), an effect that could be prevented by coadmini‐stration of methylene blue (10 μmol/L).4. These data suggest that neuronal glutamate may be formed in a population of vagal afferent cell bodies, presumably to act on soma membrane receptors. Furthermore, the excitatory amino acid is released in a neurotransmitter‐like fashion at the terminal region of vagal afferent neurons, where glutamate release is increased as a consequence of baroreceptor loading and also following activation of soluble guanylate cyclase. Thus, glutamate may be considered a candidate neurotransmitter of vagal baroreceptor afferent neurons, which may be modulated by nitric oxide or an endogenous nitrosothiol.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: SIGNALLING PATHWAYS IN CARDIAC FAILURE
Authors: Summers Roger J. , McMartin Lynne R. , Kompa Andrew , Gu Xinhua , Molenaar Peter 
Published: June 2007

SUMMARY1. Cardiac failure in humans and in animal models is associated with a marked desensitization of the catecholamine signalling pathway.2. β1‐ and β2‐ and possibly β3‐adrenoceptors (β‐AR) are found in the hearts of humans and common laboratory animals such as rats and guinea‐pigs. In rats and guinea‐pigs chronic stimulation of cardiac β‐AR leads to a rapid loss of β2‐AR whereas heart failure in humans is associated with a loss of β1‐AR or β1‐AR and β2AR.3. Desensitization is also associated with phosphorylation of β‐AR by β‐AR kinase β‐ARK) and uncoupling of receptors from the signalling pathway. β‐ARK but not β‐arrestin activity and mRNA are markedly increased in heart failure.4. Chronic β‐AR stimulation and heart failure are associated with increases in Giα but little if any change in Gsα.5. The roles of β&#x006d;̀ subunits of G‐proteins, adenylate cyclase subtypes and cAMP dependent protein kinase A in heart failure are unclear at present.