bluuebunny/crossref_metadata_2025_split huggingface dataset:
ENHANCED VASOCONSTRICTION BY SEROTONIN IN RABBIT CAROTID ARTERIES WITH ATHEROMA‐LIKE LESIONS IN VIVO
Authors: Sobey Christopher G. , Dusting Gregory J. , Woodman Owen L. 
Published: June 2007

SUMMARY1. In a new animal model which mimics the cellular events of early human atherosclerosis, atheroma‐like lesions were produced by positioning a hollow silastic collar around the common carotid arteries of rabbits. The functional significance of these arterial lesions on blood flow responses to vasoactive agents was then studied in anaesthetized rabbits in vivo.2. After 1 week of lesion development, resting blood flow was lower in atherosclerotic (cuffed) carotid arteries compared with the contralateral, sham‐operated control arteries.3. Intra‐carotid injection of serotonin (0.01–1 μg) produced dose‐dependent increases in blood flow in control arteries, but produced either smaller increases or decreases in flow in cuffed arteries. Serotonin caused complete vasospasm (zero blood flow) in one of six rabbits.4. Acetylcholine (0.0001–0.01 μg, intra‐carotid) produced smaller increases in blood flow in cuffed arteries compared with controls.5. These data support the proposal that morphological and functional alterations in large arteries in the early stages of atherogenesis play an important role in determining blood flow in vivo. The increased vascular reactivity to serotonin which accompanies development of the lesions might contribute to vasospasm.
CHLORIDE ION INGESTED WITH SODIUM AFFECTS THE DEVELOPMENT OF CEREBRAL LESIONS IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Ikeda K. , Nara Y. , Yamori Y. 
Published: June 2007

SUMMARY1. To determine the effect of chloride ion on the development of hypertension and the incidence of cerebral lesions in stroke‐prone spontaneously hypertensive rats (SHRSP), groups of 10 rats were administered chronically with either 171 mmol/L sodium chloride or equimolar sodium provided as sodium citrate in the drinking water from the age of 12 weeks.2. The life span was significantly extended in SHRSP given sodium citrate (336 ± 28 vs 246 ± 26 days, mean ± s.e.m., P<0.05) but their development of hypertension was not different from SHRSP given sodium chloride.3. In order to determine the role of calcium homeostasis, calcium in urine was collected. Urinary calcium in SHRSP given sodium citrate was significantly decreased (1.0 ± 0.12 vs 1.8 ± 0.18 mg/ 24 h urine, P<0.05).4. If the normal life span is 320 ± 35 days, this suggests that chloride ion ingested with sodium accelerates the development of cerebrovascular diseases, and that increased urinary calcium excretion may be related to this adverse chloride effect on the development of hypertension in SHRSP.
EFFECT OF RESERPINE ON CATECHOLAMINE CONTENTS AND MET‐ENKEPHALIN AND β‐ENDORPHIN LEVELS IN THE HYPOTHALAMUS AND THE PITUITARY
Authors: Tang Fai 
Published: June 2007

SUMMARY1. The effects of reserpine treatment on the contents of catecholamines and opioid peptides have been studied in the rat hypothalamus and pituitary.2. Hypothalamic and pituitary catecholamines were drastically depleted following acute reserpine treatment.3. Reserpine treatment also resulted in a significant decrease in immunoactive met‐enkephalin content in both the hypothalamus (25%) and the anterior lobe (50%), but not in the neurointermediate lobe of the pituitary.4. No changes were observed in immunoactive β‐endorphin levels.5. These findings suggest that the met‐enkephalin contents in the hypothalamus and the anterior pituitary may be under catecholaminergic control.6. The lack of effect of acute reserpine treatment on immunoactive β‐endorphin contents might be due to the opposing effects of adrenergic and dopaminergic mechanisms.
METABOLIC BASIS OF CATECHOLAMINE‐INDUCED WATER TRANSPORT IN EVERTED GUT SACS OF MOUSE
Authors: Mary P. L. , Rao J. Prakasa 
Published: June 2007

SUMMARY1. Catecholamine‐induced water transport was measured using an everted gut sac technique. Adrenaline, noradrenaline and isoprenaline induce dose‐dependent increases in water transport by the proximal intestinal sacs. Use of selective adrenergic agents revealed the possible involvement of α1‐ and β2‐receptors in mediation of catecholamine stimulation of water transport in this segment.2. Inhibition of glycolysis reduced the effect mediated through α1‐receptors, while the inhibition of oxidative phosphorylation blocked the β2‐receptor mediated increase in water transport.3. Basal transport of water was also significantly reduced by inhibition of glycolysis but was significantly elevated by blockage of oxidative phosphorylation.4. Suppression or stimulation of glycolysis was paralleled by similar changes in lactic acid release from the gut wall.5. It is concluded that the energy for the catecholamine‐induced water transport is contributed by glycolysis and oxidative phosphorylation coupled to α1‐ and β2‐receptors, respectively. Under basal conditions water transport is mainly dependent on glycolysis in the segment of intestine examined.
KETOCONAZOLE AND PLASMA AND URINE STEROID LEVELS IN CUSHING'S DISEASE
Authors: Mortimer Robin H. , Cannell Graeme R. , Thew Caroline M. , Galligan John P. 
Published: June 2007

SUMMARY1. Plasma and urine steroid and plasma ACTH levels were measured for 2 weeks in eight subjects (six female, two male) with Cushing's disease with each given 200 mg ketoconazole orally four times daily.2. Treatment was associated with major falls in excretion of free cortisol and the cortisol metabolites tetrahydrocortisol, 5α‐tetrahydrocortisol and tetrahydrocortisone.3. Plasma cortisol and ACTH levels did not change significantly.4. Excretion of the androgen metabolites, androsterone, 11β‐hydroxyandrosterone and aetiocholanolone was also reduced but there was no significant fall in plasma testosterone. Plasma levels of progesterone, 17α‐hydroxyprogesterone and 11β‐deoxycortisol and excretion of pregnanediol, pregnanetriol and tetrahydrodeoxycortisol rose with treatment.5. Analysis of steroid precursor/product ratios indicated that ketoconazole significantly inhibited 11β‐hydroxylase and 17,20‐lyase but not 17α‐hydroxylase in these patients with Cushing's disease.
INTRACELLULAR pH AND SODIUM‐PROTON EXCHANGE ACTIVITY OF LYMPHOCYTES IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Di‐yuan Li , Kobayashi Ayame , Nara Yasuo , Ikeda Katsumi , Mori Chuzo , Yamori Yukio 
Published: June 2007

SUMMARY1. At the age of 20 weeks, intracellular pH (pHi) of circulating lymphocytes suspended in HCO3−‐free NaCl media was not significantly different between stroke‐prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar‐Kyoto rats (WKY).2. The initial recovery rate of pHi in lymphocytes tended to be greater in SHRSP than in WKY after the addition of 60 mmol/L or 120 mmol/L of NaCl, but there was no statistically significant difference.3. The H+ equivalent efflux rate, which was a true reflection of Na+‐H+ activity, was significantly greater in SHRSP than in WKY (P<0.05). The difference in H+ equivalent efflux rate was not due to the difference in cellular buffering power between the two groups (P>0.05). An increased Na+‐H+ exchange activity may play a partial role in the pathogenesis of hypertension.
COMPARISON OF VASOPRESSOR EFFECTS OF NITRO ARGININE IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS AND WISTAR‐KYOTO RATS
Authors: Kobayashi Yuta , Ikeda Katsumi , Kakizoe Eiichi , Shinozuka Kazumasa , Nara Yasuo , Yamori Yukio , Hattori Keisuke 
Published: June 2007

SUMMARY1. NG‐nitro‐L‐arginine (NO2Arg) is a guanidine nitro arginine derivative and an inhibitor of endothelium‐dependent vascular relaxation. Significant rise of the systolic blood pressure was observed after 1 week administration of NO2Arg in food (0.023% in weight, about 2.8 mg of NO2Arg/rat per day) in female rats of stroke‐prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar‐Kyoto rats (WKY). The rises were not different between SHRSP (21 mmHg) and WKY (23 mmHg).2. In ring preparations of the thoracic aorta of NO2Arg‐administered rats of both strains, relaxation by acetylcholine decreased markedly compared with those of the control rats (to 43–44%). On the contrary, glyceryltrinitrate‐induced relaxation was slightly but significantly increased in the aorta of WKY after NO2Arg administration and the same tendency was observed in SHRSP.3. The rise of blood pressure and the decrease of acetylcholine‐induced relaxation suggested that NO2Arg inhibited the endothelium‐dependent relaxation not only in WKY but also in SHRSP. The relaxation of the thoracic aorta preparation of SHRSP by acetylcholine was much less (ca 38%) than that of WKY; however, that of SHRSP by glyceryltrinitrate was slightly less (ca 74%), indicating that endothelium‐dependent relaxation declined in vascular preparation of SHRSP.4. The present results suggest that endothelium‐dependent relaxation has some contribution on blood pressure regulation in the hypertensive state, although a decline of endothelium‐dependent relaxation is evident in vascular preparation of SHRSP compared with WKY.
POTENTIATION BY ALDOSTERONE OF VASOPRESSIN‐INDUCED CALCIUM KINETICS IN VASCULAR SMOOTH MUSCLE CELLS
Authors: Okada Koji , Ishikawa San‐e , Saito Toshikazu 
Published: June 2007

SUMMARY1. The present study was undertaken to examine the effect of aldosterone on arginine vaso‐pressin (AVP)‐induced Ca2+ kinetics in cultured rat vascular smooth muscle cells (VSMC). The pre‐incubation of cells with 1 X 10−6 mol/L aldosterone for 24 h did not affect the basal cytosolic free Ca2+ ([Ca2+]i) but enhanced the AVP‐induced mobilization of [Ca2+]i (1 X 10−8 mol/L AVP; 287 vs 401, 1 X 10−6 mol/L AVP; 430 vs 714 nmol/L).2. The pre‐incubation of cells with 1 X 10−7 mol/L aldosterone for 24 h did not show this enhancing effect on the AVP‐induced mobilization of [Ca2+]i. Without the preincubation, aldosterone did not change the basal [Ca2+]i or the AVP‐induced mobilization of [Ca2+]i. This enhancement was still observed in the Ca2+‐free solution containing 0.1 mmol/L EGTA (1 X 10−8 mol/L AVP; 169 vs 341 nmol/L).3. The enhancement by aldosterone of the AVP‐mobilized [Ca2+]i was completely blocked by the simultaneous administration of 1 X 10−4 mol/L spironolactone (1 X 10−8 mol/L AVP; 258 vs 265 nmol/L). The treatment with aldosterone also stimulated the AVP‐produced [45Ca2+] efflux during a 3 min period (1 X 10−8 mol/L AVP; 32 vs 49, 1 X 10−6 mol/L AVP; 50 vs 58% released from the resting intracellular [45Ca2+]‐contents).4. The present results indicate that aldosterone enhances the vascular action of AVP mediated through the stimulation of Ca2+ kinetics which may be dependent on the changes in the cellular signal transduction systems.
CARDIOVASCULAR SENSITIVITY CHANGES TO EICOSANOIDS IN RATS WITH EXPERIMENTALLY INDUCED DIABETES MELLITUS
Authors: Hodgson Wayne C. , Sikorski Bogdan W. , King Roger G. 
Published: June 2007

SUMMARYThis paper attempts to provide a short review of the evidence for:1. Increased platelet production of thromboxane A2 and reduced vascular production of prostacyclin in the human and also animal models of diabetes.2. Reduced depressor responsiveness to arachidonic acid of anaesthetized alloxan‐ and streptozotocin‐induced diabetic rats.3. Enhanced constrictor responsiveness to arachidonic acid in blood‐perfused hindquarters of alloxan‐induced diabetic rats.4. Potentiation by the thromboxane A2‐mimetic, U46619, of constrictor responses to 5‐hydroxy‐tryptamine in Krebs'‐perfused hindquarters and kidneys of both control and alloxan‐induced diabetic rats.5. Alterations during diabetes in production of, and responsiveness to, eicosanoids may contribute to the cardiovascular changes which occur in this disease.
THE EVOLUTION OF HYPERTENSIVE THERAPY
Authors: Robson R. D. 
Published: June 2007

SUMMARY1. During the past 30 years many antihypertensive agents, acting at differing levels on the mechanisms controlling arterial blood pressure, have been introduced.2. Whereas the usefulness of early drugs was limited by side effects, the discovery of successive classes of agents has resulted in the gradual introduction of drugs causing fewer adverse effects with consequent improvements in patient compliance.3. The recent appearance of angiotensin II antagonists and potassium channel openers, together with increased knowledge of the roles played by atrial natriuretic factor and endothelial cell‐derived autacoids in control of vascular tone, hold prospects for still further improvements in therapy.
GABAa AGONISTS AS TARGETS FOR DRUG DEVELOPMENT
Authors: Johnston Graham A. R. 
Published: June 2007

SUMMARY1. Agents with selective actions on bicuculline‐sensitive GABAa receptors have been developed by systematically restricting the conformational mobility of the GABA molecule.2. THIP, a bicyclic isoxazole that represents GABA held in a relatively rigid and partially extended conformation, is an analgesic of potency comparable to that of morphine. THIP represents a lead compound for a novel series of analgesics acting independently of Naloxone‐sensitive opiate systems.3. ZAPA, a conformationally‐restricted analogue of GABA containing an isothiouronium moiety, is a selective agonist for low affinity GABAa receptors and is a lead compound for the development of a novel series of anthelmintics.4. (+)‐TACP, a cyclopentane analogue of GABA, may activate a different subclass of GABAa receptors from THIP.5. Pharmacological, molecular modelling and molecular biological studies provide evidence for a heterogeneity of GABAa receptors which might be exploited for drug development.
ARACHIDONIC ACID METABOLISM IN NICOTINE‐TREATED RATS AND NICOTINE‐INCUBATED RABBIT AORTIC SMOOTH MUSCLE CELLS
Authors: Hui S‐C. G. , Wang Z. , Zhang H. , Ogle C. W. 
Published: June 2007

SUMMARY1. The changes in plasma levels of thromboxane‐B2 (TXB2) and 6‐keto‐prostaglandin‐F1α(6‐keto‐PGF1α) were examined in rats given 5, 25, 50 or 100 μg/mL nicotine in drinking water for 10 days.2. The effect of nicotine on prostacyclin (PGI2) synthesis from endogenous arachidonic acid by cultured rabbit aortic smooth muscle cells was also studied.3. Plasma levels of TXB2 were increased dose‐dependently by treatment for 10 days with nicotine.4. 6‐Keto‐PGF1α values were lowered dose‐dependently, both in the plasma of nicotine‐treated rats and in rabbit aortic smooth muscle cells incubated with the alkaloid.5. The results suggest that endogenous synthesis of thromboxane‐A2 and PGI2, as reflected by TXB2 and 6‐keto‐PGF1α levels, respectively, is influenced by nicotine treatment. These findings may be related to cardiovascular diseases associated with cigarette smoking, but further studies are needed.
BRADYCARDIA DURING REVERSIBLE HYPOVOLAEMIC SHOCK: ASSOCIATED NEURAL REFLEX MECHANISMS AND CLINICAL IMPLICATIONS
Authors: Secher Niels H. , Jacobsen John , Friedman Daniel B. , Matzen Steen 
Published: June 2007

1. Heart rate response to reversible central hypovolaemia can be divided into three stages. In the first stage (corresponding to a reduction of the blood volume by approximately 15%) a modest increase in heart rate (<100 beats/min) and total peripheral resistance compensate for the blood loss, and a near normal arterial blood pressure prevails (preshock). During the second stage, a reduction of the central blood volume by approximately 30% results in a decrease in heart rate, total peripheral resistance and blood pressure due to activation of unmyelinated vagal afferents (C‐fibres) from the left ventricle. In the third stage, blood pressure falls further as haemorrhage continues and tachycardia (> 120 beats/ min) is manifest. This stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals.2. Recognition of the vasodepressor–cardioinhibitory reaction to a reduced circulating blood volume is important and suggests the need for immediate treatment with volume expansion in critically ill patients.
ARTERIAL BAROREFLEX CONTROL OF HEART PERIOD IS NOT RELATED TO BLOOD PRESSURE VARIABILITY IN CONSCIOUS HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Su Ding‐Feng , Cerutti Catherine , Barrès Christian , Julien Claude , Vincent Madeleine , Paultre Christian , Sassard Jèan 
Published: June 2007

SUMMARY1. The short‐term (within 30 min periods) and the long‐term (among 30 min periods) variabilities, expressed as variation coefficients, of blood pressure (BP) and heart period (HP) were studied using a computer analysis of BP recordings in freely moving genetically hypertensive (LH), normotensive (LN) and low BP (LL) rats of Lyon strains at ages 5, 9, 21 and 40 weeks. The baroreflex control of HP was estimated with the slope of the linear relationship between systolic BP (SBP) and HP (SBP‐HP slope) computed after phenylephrine and nitroglycerin injections.2. Short‐term variability of BP increased between 5 and 9 weeks of age and then remained stable. Hypertension was accompanied by an increase in both short‐and long‐term variabilities of diastolic BP in adult rats.3. A sharp increase in SBP‐HP slope was observed between 5 and 9 weeks of age in LN rats. SBP‐HP slope of LH rats increased slightly up to 21 weeks but remained lower than that of normotensive controls.4. The weak inverse correlation existing between SBP‐HP slope and BP variability appeared to be mediated by the BP level. In addition, atropine which is known to abolish almost completely the SBP‐HP slope, did not increase BP variability. It is concluded that SBP‐HP slope is not linearly associated with BP variability in conscious rats.
RELATIONSHIP BETWEEN ATP RESYNTHESIS AND CALCIUM ACCUMULATION IN THE REPERFUSED RAT HEART
Authors: Hasin Y. , Kneen M. M. , Craik D. J. , Nayler W. G. 
Published: June 2007

SUMMARY1. The postulate that the composition of solutions used to reperfuse ischaemic hearts may modulate their ability to synthesize high‐energy compounds was tested in isolated rat hearts subjected to 30 min normothermic ischaemia and then reperfused with either Krebs'‐Henseleit buffer (K‐H) for 20 min (control reperfusion, CR), or a ‘myocardial protective solution’ (MPS) for 5 min, followed by 15 min K‐H (modified reperfusion, MR). The ‘myocardial protective solution’ was designed to protect against damage caused by sodium and calcium accumulation and by free radicals. Metabolic precursors were also included to promote and support adenosine triphosphate (ATP) resynthesis during reperfusion under both aerobic and hypoxic conditions.2. 31P nuclear magnetic resonance (NMR) was used to measure tissue ATP and creatine phosphate (CP), and atomic absorption spectrometry was used to measure Ca++. Early during CR, ATP recovered to 28% of the pre‐ischaemic value, but fell to 5.5% with continued perfusion. Similarly, CP recovered to 45.5% of the pre‐ischaemic level during early CR but fell to 25.5% with continued perfusion.3. Better maintenance of ATP was seen during MR with oxygenated MPS (O2‐MR), the final ATP remaining at 16.9% of the pre‐ischaemic level. During O2‐MR, CP recovered to 43.55 of the pre‐ischaemic level but was not maintained and fell to a final level of 29.5%.4. During MR with O2‐free MPS (non‐O2‐MR), there was no reperfusion‐associated fall in ATP or CP, with the levels maintained at 26.6% and 34.55, respectively.5. During 5 min CR, tissue Ca++ was elevated but this did not happen during 5 min reperfusion with O2‐MR or non‐O2‐MR. After 20 min reperfusion there was no significant difference in Ca2+between the groups (CR 16.56±1.33; O2‐MR 13.48±1.2; non‐O2‐MR 15.97±2.4 μmol/g dry weight). When reperfused with O2‐free histidine‐containing MPS, tissue Ca1+ increased substantially without any change in ATP (26.2 ± 1.65% at 20 min).6. Thus reperfusion injury, assessed by a secondary reduction in ATP, can be limited by the initial use of appropriately designed reperfusion ‘cocktails', and Ca++ overload is not the primary factor limiting ATP regeneration.
ANTAGONISM BY ENDOTHELIN OF CENTRALLY MEDIATED CARDIOVASCULAR EFFECTS OF POTASSIUM IN ANAESTHETIZED RATS
Authors: Shah Jui , Jandhyala Bhagavan S. 
Published: June 2007

SUMMARY1. We have previously demonstrated that cerebroventricular administration of potassium chloride (KCI) solutions produces dose‐dependent reductions in blood pressure and heart rate in anaesthetized rats and that these effects are significantly attenuated by ouabain, a selective inhibitor of the Na+‐pump. These observations suggest an important relationship between Na+, K+‐ATPase activity in the central nervous system (CNS) and neural mechanisms involved in the regulation of cardiovascular function.2. Since endothelin‐1 (ET‐1) has been shown to affect various ion transport mechanisms, including the Na+‐pump, the present studies were conducted to evaluate whether this peptide would antagonize central effects of KCI.3. The present studies demonstrate that cumulative doses of ET‐1 (0.8–3.2 pmol, intracerebrolateral ventricular administration, i.c.v.) produced significant attenuation of hypotension and bradycardia produced by i.c.v. injections of KCI (0.75 μmol/5 μL, i.c.v.); in a separate series, a single high dose of ET‐1 (4.0 pmol, i.c.v.) significantly reduced cardiovascular responses to various doses of KCI (0.375, 0.75, 1.25 μmol/5μL, i.c.v.).4. These studies suggest that endothelin may be involved in the regulation of arterial pressure since it is present in CNS and possesses a ouabain‐like effect. However, it is not conclusive that ET‐1 inhibits neuronal Na+‐pump, since alternative mechanisms can also account for the efficacy of the peptide to antagonize central effects of potassium chloride.