bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF m‐AMSA ON RAT ISOLATED HEART
Authors: Merkin M. S. , Shinar E. , Shefer A. , Gotsman M.S. , Hasin Y. 
Published: June 2007

SUMMARY1. m‐AMSA (4′[9‐acridinylamino]methansulphon‐m‐anisidide) is a new cytoxic agent now under clinical trial.2. We used the rat isolated perfused heart model in order to investigate the cardiac effects of m‐AMSA.3. The results of the dose‐response study indicate that m‐AMSA has an acute moderate negative inotropic effect. The 90% effect (25% decrease in developed force compared to the control) was observed at drug concentration of 1.5 μg/ml. The refractory period (as measured by stimuli of twice diastolic threshold intensity) increased progressively as the drug concentration was increased (up to 2.5 μg/ml).4. Measurements of the strength‐duration and strength‐interval relationship showed that m‐AMSA induced a significant reduction (P < 0.005) in excitability and prolongation of refactoriness.5. We suggest that m‐AMSA has a membranal cardiotoxic effect in addition to its known intracellular cytotoxic effect.
SODIUM PREFERENCE AND EXCRETION IN SPONTANEOUSLY HYPERTENSIVE RATS ON VARIOUS DIETS
Authors: Wang H. , Ikeda K. , Kihara M. , Nara Y. , Horie R. , Yamori Y. 
Published: June 2007

SUMMARY1. Stroke‐prone spontaneously hypertensive rats (SHRSP) and stroke‐resistant SHR (SHRSR) exhibited an increased preference for a 2% NaCl solution, relative to water, in comparison with normotensive Wistar‐Kyoto (WKY), but the preference was lost quickly in SHRSP with unbroken exposure.2. Neither a high protein diet (50% fish protein) nor a low protein diet (5% protein) changed the salt water preference in SHRSR and the former abolished the preference more quickly in SHRSP.3. The fish protein diet, however, increased the ratio of urinary sodium excretion to dietary sodium intake in the first three days of exposure to a high salt intake in all groups.4. Results from this experiment suggest that an increased dietary protein intake can facilitate sodium excretion and may possibly ameliorate the adverse effect of a high sodium diet.
ANGIOTENSIN CONVERTING ENZYME INHIBITION DOES NOT PREVENT DEVELOPMENT OF ACTH‐INDUCED HYPERTENSION IN SHEEP
Authors: Spence Campbell D. , Coghlan John P. , Denton Derek A. , Fei David T. W. , Mills Eric H. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. The role of the renin‐angiotensin system in the onset of ACTH‐induced hypertension was examined in five conscious sheep.2. Captopril infusion alone (15 μg/kg per day) for 2 days produced a small fall in blood pressure.3. After 2 days of captopril ACTH was infused (20 μg/kg per day) for 3 days together with captopril. The blood pressure and electrolyte effects of ACTH administration were not modified by captopril pretreatment.4. These experiments establish that angiotensin II is not important in the onset of ACTH‐induced hypertension in sheep.
MIGRATION‐INDUCED CHANGES IN BLOOD PRESSURE: A CONTROLLED LONGITUDINAL STUDY
Authors: Poulter N. R. , Khaw K. T. , Mugambi M. , Peart W. S. , Sever† P. S. 
Published: June 2007

SUMMARY1. A longitudinal study of the effects of migration on blood pressure and related factors is being carried out in members of a black Kenyan population who migrate from a traditional rural community to an urban environment.2. Data on the first 139 migrants (78 male, 61 female) and 204 control non‐migrants (126 male, 78 female) who have been followed up for a period of 6 months are presented.3. Blood pressure changes rapidly on migration (within the first 2 months); thereafter trends between migrants and controls differ. Significant differences in systolic pressure between migrants and controls are found at all examinations during the 6 month follow‐up in both sexes. Diastolic pressure falls in controls but rises in migrants, the greatest difference being seen at the 6 month examination.4. Migration is associated with a marked increase in dietary sodium and a fall in potassium demonstrated by measurements of urinary electrolyte excretion in 3 × 12 h or 3 × 24 h urine collections.5. Analysis of covariance shows that the blood pressure differences between migrants and controls are partly explained by urinary sodium/potassium ratios and in some instances by body weight.
INCREASED SENSITIVITY OF RABBIT EAR ARTERY TO NORADRENALINE FOLLOWING PERIVASCULAR NERVE STIMULATION MAY BE A RESPONSE TO NEUROPEPTIDE Y RELEASED AS COTRANSMITTER
Authors: Glover W. E. 
Published: June 2007

SUMMARY1. Neuropeptide Y (NPY 10‐10‐10‐7 mol/l) had little or no effect on the perfusion pressure of rabbit isolated ear arteries but potentiated the brief contractile responses to injections of noradrenaline, histamine or brief periods of electrical stimulation (2–20 Hz for 5 s). This effect was slowly reversible.2. Similar potentiation was seen following long periods of electrical stimulation (2–40 Hz for 1–5 min) which produced well sustained increases in perfusion pressure.3. Following even longer periods of electrical stimulation (10–30 min) during which the perfusion pressure was not maintained, responses to noradrenaline and histamine were potentiated but the responses to electrical stimulation for 5 s were greatly reduced.4. The increase in sensitivity following prolonged electrical stimulation may be due to NPY released as a cotransmitter.
HYPERTENSION CORRECTED AND ALDOSTERONE RESPONSIVENESS TO RENIN‐ANGIOTENSIN RESTORED BY LONG‐TERM DEXAMETHASONE IN GLUCOCORTICOID‐SUPPRESSIBLE HYPERALDOSTERONISM
Authors: Woodland E. , Tunny T. J. , Hamlet S. M. , Gordon R. D. 
Published: June 2007

SUMMARY1. Two males with glucocorticoid‐suppressible hyperaldosteronism had hyperaldosteronism, hypertension and hypokalaemia corrected by continuous administration of physiological doses of dexamethasone for more than a year.2. During long‐term dexamethasone treatment:(a) Plasma renin activity increased from subnormal to high normal levels, with normal posture‐mediated increases;(b) Plasma aldosterone became responsive to angiotensin infusion, a new observation;(c) A fall in plasma aldosterone between 0800 h (recumbent) and 1000 h (upright) was replaced by a rise;(d) Plasma aldosterone became suppressible with salt loading.3. These findings are consistent with a shift to more normal control of aldosterone by renin‐angiotensin, once abnormal responsiveness to ACTH has been nullified.
A RANDOMIZED CONTROL TRIAL OF A VEGETARIAN DIET IN THE TREATMENT OF MILD HYPERTENSION
Authors: Margetts B. M. , Beilin L. J. , Armstrong B. K. , Vandongen R. 
Published: June 2007

SUMMARY1. The effect of an ovo‐lacto‐vegetarian (OLV) diet on blood pressure was assessed in a randomized, controlled, crossover trial in 58 mild untreated hypertensive subjects recruited from the Perth Centre for the 1983 NHF Risk Factor Prevalence Survey.2. Subjects were randomly allocated to one of three groups; the first maintained their usual diet throughout 12 weeks; the other two were given an OLV diet for either the first or second 6 weeks of the 12‐week trial.3. Introduction of an OLV diet was associated with a significant fall in systolic blood pressure, on average of the order of 5 mmHg, which was unrelated to change in urinary sodium, potassium or body weight.4. It was concluded that a vegetarian diet may have an adjunctive role in control of mild hypertension, but that in view of likely problems with acceptability those dietary components responsible for the blood pressure differences need to be identified.
RETARDED DEVELOPMENT OF HYPERTENSION IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS FOLLOWING CHRONIC ALCOHOL CONSUMPTION
Authors: Howe P. R. C. , Rogers P. F. , Smith R. M. 
Published: June 2007

SUMMARY1. The influence of chronic alcohol consumption on blood pressure was examined in normotensive Wistar/Kyoto rats (WKY) and in stroke‐prone spontaneously hypertensive rats (SHR‐SP).2. Ethanol, administered in drinking water from 5 weeks of age to produce moderate blood alcohol levels, substantially retarded the development of hypertension in SHR‐SP and caused a mild reduction of blood pressure in WKY.3. Alcohol withdrawal caused an acute rise in blood pressure in both strains, followed by a reduction to the subnormal levels previously induced by alcohol treatment.4. This sustained antihypertensive effect of alcohol was not attributable to reductions of body weight or fluid intake.
EFFECT OF MAGNESIUM ON PASSIVE FLUXES OF LITHIUM IN THE HUMAN ERYTHROCYTE
Authors: Wiley J. S. , Bonacquisto L. , Doyle A. E. 
Published: June 2007

SUMMARY1. Extracellular Mg2+ is known to inhibit the passive Na+ and K+ fluxes in the human erythrocyte. In this study the effect of extracellular Mg2+ on Li+ efflux was measured in erythrocytes from 29 normotensive and essential hypertensive subjects.2. Magnesium produced a variable inhibition of between 0 and 47% in Li+ efflux in different subjects and this effect was unrelated to initial cell Li+, blood pressure or to an action on the co‐ or counter‐transport pathways for this cation.3. A positive correlation was observed between the magnitude of the passive Li+ efflux and its inhibition (0 to 47%) by Mg2+ ions. Thus Mg2+ has an inhibitory effect on passive Li+ permeability which is unrelated to essential hypertension.
TOTAL BODY SODIUM IN IMMATURE SPONTANEOUSLY HYPERTENSIVE AND WISTAR KYOTO RATS
Authors: Harrap Stephen B. , Doyle Austin E. 
Published: June 2007

SUMMARY1. Total body sodium of male and female spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats was estimated weekly during the first 8 weeks of life by measuring exchangeable sodium (ENa). Blood pressure and sodium intake was measured from weeks 4 to 8.2. SHR had significantly higher blood pressure and sodium intake than WKY from 4 to 8 weeks of age.3. ENa was higher in SHR than WKY throughout the first 8 weeks of life.4. Relative sodium retention was observed in SHR during weeks 5 to 8 despite a significant rise in SHR blood pressure and fall in sodium intake.5. These findings suggest a change in the renal pressure/natriuresis relationship at this age in the SHR.
IN VITRO CALCIUM DEPENDENCE OF ARTERIAL SMOOTH MUSCLE IN HUMAN HYPERTENSION
Authors: Lipe S. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. Digital arteries, removed at autopsy from 12 hypertensives and 11 normotensives, have been compared in vitro for the calcium dependence of contractures produced by potassium chloride and noradrenaline, and the potency of verapamil to antagonize contractures to noradrenaline.2. No significant differences were found between the vessels from the hypertensives and normotensives for the pD2 values or the maximum response to either potassium chloride or noradrenaline in bathing solutions containing 2.5, 1.0, 0.5 or 0 mmol/l calcium chloride.3. There were also no significant differences between the vessels, from the hypertensive or normotensives, in the pD2 values for the addition of calcium chloride to arteries exposed to potassium chloride or noradrenaline in a calcium free bathing medium, in the ability of verapamil to shift the pD2 values for noradrenaline, nor in the ability of verapamil to reduce the maximum responses to noradrenaline (except at the two highest concentrations of verapamil tested).4. It is concluded that it is unlikely to be a primary abnormality of the mechanisms regulating calcium ion entry and release in vascular smooth muscle in human hypertension.
STUDIES ON THE VASODILATOR ACTIONS OF BUCINDOLOL IN THE RAT
Authors: Marwood John F. , Stokes Gordon S. 
Published: June 2007

SUMMARY1. Experiments were performed in anaesthetized rats to investigate the vasodilator actions of the β‐adrenoceptor antagonist bucindolol. Bucindolol (3 mg/kg) lowered blood pressure significantly in rats pretreated with (i) prazosin (0.4 mg/kg) (ii) prazosin (0.4 mg/kg) plus propranolol (0.5 mg/kg) or (iii) labetalol (0.5 mg/kg). Thus, a portion of the hypotensive effect of bucindolol was independent of effects on α‐ or β‐adrenoceptors. This was attributed to direct vasodilatation.2. In reserpinized anaesthetized rats bucindolol increased heart rate and thus had an intrinsic sympathomimetic action (ISA). The ISA was equipotent with that of isoprenaline at the 0.25 nmol/kg dose level, but declined with increasing bucindolol doses, probably due to the onset of β‐adrenoceptor blockade.3. In isolated perfused rat tail arteries constricted by perfusing with a high‐K+ Krebs solution, bucindolol (10−5 mol/l, 10−4 mol/l) caused a significant reduction in perfusion pressure indicative of vasodilatation. Since the perfusate contained 10−6 mol/l propranolol, the vasodilatation was not due to β‐adrenoceptor stimulation.4. These results are consistent with a direct vasodilator action of bucindolol. We suggest bucindolol lowers blood pressure by a complex mechanism involving β‐adrenoceptor blockade, α‐adrenoceptor blockade, vasodilatation and perhaps β2‐adrenoceptor stimulation.
DYNAMIC CHANGES IN PLASMA INACTIVE RENIN LEVELS IN BARTTER'S SYNDROME AFTER ADMINISTRATION OF CAPTOPRIL AND ANGIOTENSIN II
Authors: Nagai Hiroyuki , Matsunaga Masato , Ogawa Kazuya , Pak Chun Ho , Kanatsu Kazuro , Hara Akira , Kono Tsuyoshi , Kawai Chuichi 
Published: June 2007

SUMMARY1. Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome.2. A single oral dose of captopril (8‐25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC.3. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.
ACUTE TOLERANCE TO DIAZEPAM IN MICE: PHARMACOKINETIC CONSIDERATIONS
Authors: Yoong Y. L. , Lee H. S. , Gwee M. C. E. , Wong P. T.‐H. 
Published: June 2007

SUMMARY1. The tolerance to the hypnotic effect of diazepam developed after a single exposure to diazepam in the presence or absence of cycloheximide, which blocks liver enzyme induction, was studied.2. At the high dose (30‐35 mg/kg) used in this study, diazepam was found to be metabolized very rapidly in mice, consistent with previous findings using a much smaller dose (5 mg/kg).3. There was no significant difference in the pharmacokinetics of diazepam in control and tolerant mice as observed by monitoring the plasma and brain concentrations of diazepam and N‐desmethyldiazepam.4. It is concluded that acute tolerance to diazepam in mice may not be attributed to changes in pharmacokinetic factors.
INHIBITION OF ACETYLCHOLINESTERASE BY VARIOUS OPIOIDS
Authors: Sim M. K. , Chua M. E. 
Published: June 2007

SUMMARY1. The anti‐acetylcholinesterase (AChEase) activity of 15 opioids, namely morphine, nalorphine, oxymorphone, naloxone, naltrexone, N‐methylnaloxone, levorphanol, levallophan, dextrorphan, dextrallophan, levo‐methadone, dextro‐methadone, pethidine, leu‐enkephalin and U‐50,488H was investigated.2. Among the opioids, the morphinans (in terms of their dissociation constants) are the strongest inhibitors of the enzyme. These are followed by the phenanthrenes and the morphones, though two members of the latter group are non‐inhibitors. Levo‐methadone, dextro‐methadone, pethidine and leu‐enkephalin are also non‐inhibitors of the enzyme.3. The present results, together with our previous findings, support the suggestion that opioids which are poor or non‐inhibitors of AChEase are strong inhibitors of the ACh‐induced contraction of the toad rectus, whereas the reverse is true for inhibitors of AChEase.
VERAPAMIL‐INDUCED SECRETION OF ACTIVE AND INACTIVE RENIN IN CONSCIOUS SHEEP
Authors: Mzail A. H. K. , Noble A. R. 
Published: June 2007

SUMMARY1. Regulation of plasma active and inactive renin was investigated using conscious sheep with indwelling artery, vein and bladder catheters. Control and experimental studies were carried out in the same animals on different days.2. The calcium antagonist drug verapamil was given as an initial bolus injection (0.5 mg/kg) followed by a continuous infusion (0.1 mg/kg per h) over a 2.5 h period.3. Plasma active and inactive renin changed in parallel. Both were significantly increased within 15 min of the initial drug dose and both attained a peak increase after 45 min. Thereafter, the two forms of renin returned to basal levels despite continued infusion of the drug.4. Effective renal plasma flow (CPAH) was also transiently increased by verapamil and followed a similar time course to changes in plasma active and inactive renin concentration. Arterial blood pressure, however, remained suppressed by verapamil for the duration of the study.5. Verapamil did not alter urine flow or sodium and potassium excretion rates.6. These results are discussed in relation to the possible link between intrarenal haemodynamics and renin secretion in conscious and in anaesthetized animals and also in relation to the concept that variation in the relative amounts of active and inactive renin secreted in differing physiological situations represents a mechanism for regulating the renin‐angiotensin system.
ADRENALINE AND STRESS‐INDUCED INCREASES IN BLOOD PRESSURE IN RATS
Authors: Majewski H. , Alade P. I. , Rand M. J. 
Published: June 2007

SUMMARY1. Stress was induced by immobilizing the hind limbs of rats for 12 days and housing the rats in individual cages. Control rats were housed in groups without immobilization. Blood pressure and heart rate were measured through an indwelling carotid cannula.2. After 10 and 12 days of immobilization and isolation, the stressed rats had significantly higher blood pressures (ca. 10 mmHg) and higher cardiac adrenaline levels (ca. 90%). After adrenal medullectomy cardiac adrenaline levels were markedly reduced in both stressed and control rats. Furthermore, the stressing procedure did not cause a rise in blood pressure in adrenal‐medullectomized rats.3. Desipramine HCl (2 mg/kg per day), administered orally to block the neuronal uptake of adrenaline, prevented the elevation in blood pressures and cardiac adrenaline levels. Propranolol HCl (2.8 mg/kg per day), orally, also prevented the rise in blood pressure.4. The results are consistent with the hypothesis that activation of facilitatory prejunctional β‐adrenoceptors on sympathetic nerves by neuronally‐released adrenaline may be responsible for the raised blood pressure.
ENDOTHELIUM‐DEPENDENT RELAXATION IS UNALTERED BY HYPERTENSION, CHOLESTEROL OR INTIMAL THICKENING
Authors: Angus J. A. , Wright C. E. , Cocks T. M. , Satoh K. , Campbell G. 
Published: June 2007

SUMMARY1. The effect of cellophane wrap hypertension (WRAP) and hypercholesterolemia (1% cholesterol diet, CHOL) for 4 weeks was assessed on the endothelium‐dependent vasodilator response to acetylcholine in conscious rabbits after pharmacological autonomic blockade.2. Dose‐response curves for the hindlimb vascular resistance (ear artery pressure/lower aortic blood flow; Doppler flowmeter) and acetylcholine infusion (i.v.) doses were unaltered in sensitivity (ED50) for any of the treatment groups. The range and slope of the curves were significantly altered by WRAP, CHOL or WRAP plus CHOL for acetylcholine and adenosine infusions consistent with medial hypertrophy in resistance vessels and raised serum viscosity.3. The effect of intimai thickening on the response to endothelium derived relaxing factor (EDRF) was tested in dog carotid artery ring segments in vitro 4 weeks after endothelium removal.4. The relaxation responses to acetylcholine (EDRF‐dependent) and adenosine or nitroglycerin were not significantly altered by the neo‐intima.5. Therefore the response to EDRF released by acetylcholine in resistance vessels was unaltered by hypertension, hypercholesterolemia or both together. Neo‐intimal thickening in response to initial endothelium loss does not appear to alter EDRF responses in the carotid artery.
EFFECT OF SALT LOADING ON BLOOD PRESSURE AND EICOSANOID METABOLISM OF SPONTANEOUSLY HYPERTENSIVE RATS FED A FISH OIL ENRICHED DIET
Authors: Codde J. P. , Croft K. D. , Beilin L. J. 
Published: June 2007

SUMMARY1. This study investigated the effects of dietary modification of prostaglandin (PG) synthesis on blood pressure regulation in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats under conditions of normal and elevated salt intake.2. After an initial period of 4 weeks on either a 2‐series PG ‘inhibitory’ diet offish oil (maxEPA) or a control diet of saturated fat, half of each group received 1.5% saline for 1 week.3. Blood pressures were unaffected by diet during the period of normal salt intake, but following salt loading, the maxEPA‐fed SHR showed a blood pressure increase (mean = 21 mmHg) relative to the EPA‐fed rats on water.4. Rats on maxEPA showed impaired ability to generate serum thromboxane and diminished excretion of urinary 6‐keto‐PGF1α and PGE2. SHR on water showed greater serum TXB2 generating capacity than WKY, but diminished urinary PGE2 excretion.5. Thus, the increased blood pressure observed in the salt‐loaded SHR on the maxEPA diet may be explained by reduced renal PG synthesis resulting in either mild sodium retention and/or increased vascular reactivity.
NATRIURETIC EFFECT OF CHRONICALLY ADMINISTERED α‐HUMAN ATRIAL NATRIURETIC POLYPEPTIDE IN SODIUM DEPLETED OR REPLETED CONSCIOUS SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kondo K. , Kida O. , Sasaki A. , Kato J. , Tanaka K. 
Published: June 2007

SUMMARY1. Hypotensive and natriuretic effects of chronically administered α‐human atrial natriuretic polypeptide (α‐hANP) were investigated in conscious spontaneously hypertensive rats (SHR) and Wistar‐Kyoto rats (WKY) in both sodium depletion and repletion.2. Systolic blood pressure was significantly reduced in SHR and WKY in both sodium deplete and replete states.3. Urinary sodium excretion was significantly increased in SHR and tended to be increased in WKY on sodium repletion, but remained unchanged on sodium depletion.4. It is suggested that extracellular fluid volume may be an important determinant factor of the natriuretic action of ANP but may not affect the hypotensive effect.
A COMPARISON OF THE EFFECTS OF END‐TO‐SIDE PORTACAVAL SHUNTING AND SIDE‐TO‐SIDE MESOCAVAL SHUNTING ON HEPATIC HAEMODYNAMICS IN THE DOG
Authors: Jenkins S. A. , Taylor A. , Johnson J. , Shimlrty S. K. , Baxter J. N. , Shields R. 
Published: June 2007

SUMMARY1. Functional liver blood flow and hepatic artery flow were measured before and after either end‐to‐side portacaval or side‐to‐side mesocaval shunting in dogs.2. Functional liver blood fell by approximately 50% following both portacaval and mesocaval shunting.3. The hepatic artery response was variable after both portacaval and mesocaval shunts.4. It is concluded that side‐to‐side mesocaval shunts do not preserve hepatic blood flow or produce a greater compensatory increase in hepatic artery flow than conventional portacaval shunts.