bluuebunny/crossref_metadata_2025_split huggingface dataset:
SHORT TERM VITAMIN E SUPPLEMENTATION HAS NO EFFECT ON PLATELET FUNCTION, PLASMA PHOSPHOLIPASE A2 AND LYSO‐PAF IN MALE VOLUNTEERS
Authors: Silbert Peter L. , Leong Lillian L. L. , Sturm Marian J. , Strophair Julie , Taylor Roger R. 
Published: June 2007

SUMMARY1. Based largely upon in vitro studies, vitamin E has been reported to inhibit phospholipase A2 activity, to alter phospholipid metabolism and reduce platelet aggregation.2. The effect of dietary supplementation with D‐α‐tocopherol (1500 iu/day for 14 days) was studied in nine males, 41–63 years old, comparing active treatment with a preceding placebo period.3. Despite an increase from 2.6±0.8 (s.d.) × 10‐5 mol/L to 6.0±1.8 10‐5 mol/L in plasma vitamin E there were no significant changes in the aggregation of diluted whole blood or platelet rich plasma to adenosine diphosphate (ADP) or collagen, in plasma phospholipase A2 activity or plasma lyso‐platelet‐activating factor (lyso‐PAF) (bioassay after in vitro acetylation to PAF).4. High dose vitamin E dietary supplementation had no effect on these phospholipid and platelet parameters.
RENOVASCULAR HYPERTENSION: INFORMATION FROM EXPERIMENTS USING CONSCIOUS DOGS
Authors: Anderson W. P. , Woods R. L. , Gao Y. 
Published: June 2007

SUMMARY1. Evidence from experiments in conscious, instrumented dogs shows that hypertension from renal artery stenosis is due to: (i) the stimulus, the mechanical resistance of the stenosis; and (ii) the secondary responses to this, especially angiotensin II (initially) and cardiovascular hypertrophy.2. The hydraulic resistance of the stenosis is responsible for about 20–25% of the rise in blood pressure.3. Angiotensin II is initially the most important secondary response to the stenosis. Within days, however, other as yet undetermined factors become dominant in the maintenance of the hypertension. The most important of these factors is probably cardiovascular hypertrophy.4. These secondary factors are homeostatic, in that they mitigate the effects of stenosis on renal function.
NON‐ADRENERGIC, NON‐CHOLINERGIC NEURAL CONTROL OF THE AIRWAYS
Authors: Stretton David 
Published: June 2007

SUMMARY1. In addition to the classical cholinergic bronchoconstrictor and adrenergic bronchodilator neural mechanisms, there is a large volume of evidence to suggest the existence of neural pathways within the airways of a variety of species which are neither adrenergic nor cholinergic, the non‐adrenergic, non‐cholinergic (NANC) mechanisms. With respect to airway smooth muscle tone, NANC neural responses may induce either contraction (excitatory, e‐NANC) or relaxation (inhibitory, i‐NANC). Early investigations of NANC mechanisms in both human and other animal airways suggested a role for neuropeptides as the putative neurotransmitters.2. Excitatory NANC (e‐NANC) bronchoconstrictor responses are believed to be mediated by the release of sensory neuropeptides from a subpopulation of non‐myelinated C‐fibre primary afferent neurones in the airways. e‐NANC nerves, which release tachykinins such as substance P (SP), neurokinin A (NKA) and the peptide calcitonin gene‐related peptide (CGRP, produced as a result of alternative splicing of the calcitonin gene) are selectively degenerated by the nerve toxin capsaicin (an extract from hot peppers), with the subsequent abolition of the e‐NANC responses. Tachykinin receptors have been detected by radio‐ligand receptor binding studies and visualized by autoradiographic mapping, and exogenous addition of these peptides elicits a bronchoconstrictor response in both human and other animal airways. In addition to these effects on airway smooth muscle tone, tachykinins produce an increase in microvascular permeability (and associated oedema formation), mucus hypersecretion and cause an exaggerated cholinergic bronchoconstrictor response. Thus, tachykinins may play a role in the inflammatory process and contribute to the neurogenic inflammation as seen in asthma.3. Inhibitory NANC (i‐NANC) bronchodilator responses were believed to be due to the release of peptides such as vasoactive intestinal peptide (VIP) and peptide histidine isoleucine/methionine (PHI/M). VIP is believed to be co‐localized to cholinergic nerves in the airways and is co‐released upon cholinergic nerve stimulation. Recent evidence, however, would suggest that, together with VIP and related peptides, another substance may mediate i‐NANC responses in the airways. Nitric oxide (NO), which is formed from arginine in a reaction catalysed by the enzyme NO synthase, has been shown to mediate bronchodilator responses evoked in both human and other animal airway smooth muscles following nerve stimulation in vitro.4. NANC neural mechanisms play an important role in the maintenance and regulation of bronchomotor tone, either via the direct effects of the transmitters released or by neuromodulation of autonomic control mechanisms. The study of NANC nerves in the airways has led to a greater understanding of the interaction between different nerve types in the respiratory tract and provided new insights into, and understanding of, the pathogenesis of airway disease.
EFFECT OF STRESS ON SEROTONIN, NOREPINEPHRINE, EPINEPHRINE AND CORTICOSTERONE CONTENTS IN THE SOFT‐SHELLED TURTLE
Authors: Mahapatra Manjula S. , Mahata Sushil K. , Maiti Biswaranjan 
Published: June 2007

SUMMARY1. Adult soft‐shelled turtles were exposed to hyperosmotic and dehydration stresses.2. Acute treatment for 0.5, 1 or 2 h with sodium chloride (3.6%, single intramuscular injection, 2 mL volume) caused depletion of pineal serotonin contents followed by elevation of norepinephrine and epinephrine levels. In addition, it depleted corticosterone and norepinephrine from the adrenal gland.3. The serotonin level also decreased with a concomitant increase of 5‐hydroxyindoleacetic acid but without any discernible change in catecholamine content after chronic treatment with sodium chloride (3.6%, 0.5 mL daily for 7 days).4. Dehydration for 7 days brought about depletion of serotonin and epinephrine levels and elevation of norepinephrine level.5. The findings suggest that hyperosmotic stress has a definite influence on pineal‐paraphyseal serotonin, 5‐hydroxyindoleacetic acid, norepinephrine and epinephrine concentrations, and adrenal corticosterone and norepinephrine contents in Lissemys turtles. Dehydration stress also modulates pineal‐paraphyseal serotonin, norepinephrine and epinephrine concentrations.
COMPARISON OF INOTROPIC AND CHRONOTROPIC RESPONSES IN RAT ISOLATED ATRIA AND VENTRICLES
Authors: Brown Lindsay , Sernia Conrad , Newling Ross , Fletcher Peter 
Published: June 2007

SUMMARY1. The positive inotropic and chronotropic responses to adrenoceptor agonists (noradrenaline, phenylephrine), to compounds which increase cAMP by post‐adrenoceptor mechanisms (forskolin, theophylline and dibutyryl cAMP) and to calcium chloride were measured in isolated rat atria and papillary muscles from both ventricles.2. Noradrenaline produced similar maximal inotropic responses to calcium chloride in all tissues. Forskolin gave similar responses to calcium chloride in atrial but not ventricular tissues; the reverse was observed with dibutyryl cAMP. Phenylephrine and theophylline produced significantly smaller inotropic responses than calcium chloride in all tissues, especially in ventricular tissues.3. Maximal chronotropic responses to noradrenaline, theophylline and dibutyryl cAMP were similar. Forskolin produced significantly greater responses while calcium chloride and phenylephrine produced significantly smaller responses than noradrenaline.4. These results show that the maximal positive inotropic response of some agonists is markedly dependent on the tissue chosen. Further, chronotropic responses in right atria do not mimic inotropic responses in left atria.
NEUROPEPTIDE Y RADIO‐IMMUNOASSAY: CHARACTERIZATION AND APPLICATION
Authors: Allen Roberta , Boublik Jaroslav , Hauger Richard L. , Scott Neal , Rivier Jean , Brown Marvin R. 
Published: June 2007

SUMMARY1. A sensitive and specific neuropeptide Y (NPY) radio‐immunoassay has been developed. This radio‐immunoassay does not detect the NPY‐related peptides pancreatic polypeptide or peptide YY. NPY extracted from rat plasma using sequential C18 sorbent and affinity chromatography co‐eluted with synthetic rat NPY when applied to high pressure liquid chromatography.2. The procedure of stabilization of platelets followed by high speed centrifugation reduced basal values of NPY by 60%, and this may be consistent with removal of platelets that release NPY. Administration of the cholinesterase inhibitor physostigmine (0.3 mg/kg), intravenously, produced a small but significant increase (39%) from basal concentrations of NPY.3. NPY concentrations in young (2‐3‐month‐old) Sprague‐Dawley and Fisher 944 rats were similar; however, NPY concentrations were significantly increased (55%) in 2‐year‐old Fisher 944 rats. Similar to plasma concentrations of noradrenaline, NPY levels increase with age.
CARDIOVASCULAR DISEASE RISK FACTORS IN AUSTRALIAN ABORIGINES
Authors: O'Dea Kerin 
Published: June 2007

SUMMARY1. Aborigines from all over Australia develop unusually high prevalence rates for obesity, non‐insulin dependent diabetes mellitus (NIDDM) and cardiovascular disease when they make the transition from their traditional hunter‐gatherer lifestyle to a Westernized lifestyle.2. There is no evidence that they experienced these diseases as hunter‐gatherers. Data from the few extant traditionally orientated groups in very remote areas of northern Australia indicate that they were very lean (BMI < 20 kg/m2), with low blood pressure, and that neither blood pressure nor BMI rose with age.3. In addition, fasting glucose and cholesterol levels were low (usually below 4 mmol/L). However, in view of their extreme leanness and regular physical activity, fasting insulin and triglyceride levels were inappropriately elevated, suggestive of insulin resistance.4. When Westernized diabetic Aborigines reverted temporarily to a traditional hunter‐gatherer diet and lifestyle, all of the metabolic abnormalities of diabetes were greatly ameliorated (fasting glucose and triglyceride levels fell markedly and glucose tolerance and insulin secretion improved). In addition, they lost weight and there was a reduction in the major risk factors for cardiovascular disease (reduction in hypertriglyceridaemia and blood pressure, increase in bleeding time).5. The hunter‐gatherer lifestyle was associated with increased physical activity and a low‐fat, high‐fibre diet of low‐energy density and high‐nutrient density derived from very lean wild meat, and uncultivated vegetable foods. It has important therapeutic implications for the treatment and prevention of many of the chronic degenerative diseases of affluent Western societies.
CARDIOVASCULAR RESPONSES TO NIFEDIPINE IN ANAESTHETIZED RATS WITH ABNORMAL BLOOD GAS/PH LEVELS
Authors: Achike Francis I. , Dai Soter 
Published: June 2007

SUMMARY1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose‐anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis, or hypercarbia with acidosis.2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2 with 5% CO2 at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2 at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air.3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions.4. The control animals showed a dose‐dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection.5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls.6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role than PO2 or PCO2 abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated rats.
THROMBOXANE A2 RECEPTOR STIMULATION SIMILARLY POTENTIATES PRESSOR RESPONSES TO 5‐HYDROXYTRYPTAMINE IN PERFUSED HINDQUARTERS OF NON‐DIABETIC AND ALLOXAN DIABETIC RATS
Authors: Sikorski Bogdan W. , Hodgson Wayne C. , King Roger G. 
Published: June 2007

SUMMARY1. Dose‐response curves were obtained to bolus injections of 5‐hydroxytryptamine (5‐HT) in Krebs'‐perfused hindquarters of male Wistar rats. Vasoconstrictor responses to 5‐HT (5.7–363 nmol/kg) were significantly attenuated in hindquarters of alloxan‐treated 14 day diabetic rats compared with non‐diabetics.2. Infusion of the thromboxane A2 (TxA2)‐mimetic U46619 (317 and 31.7, but not 3.17 nmol/L) significantly potentiated vasoconstrictor responses to 5‐HT in Krebs'‐perfused hindquarters of non‐diabetic and diabetic rats. The degree of potentiation was similar for both groups.3. In Krebs'‐perfused hindquarters of non‐diabetic rats, infusion of the α1‐adrenoceptor agonist methoxamine (8.96 μmol/L, which caused a rise in perfusion pressure intermediate in magnitude to that produced by infusion of 31.7 and 317 nmol/L U46619) did not significantly affect responses to bolus injections of 5‐HT.4. The same concentration of methoxamine did not cause a significant potentiation of vasoconstrictor responses to 5‐HT (except for the two highest 5‐HT doses, 182 and 363 nmol/kg) in hindquarters of diabetic rats. This potentiation was significantly less than that due to 317 nmol/L U46619, although there was no significant difference between the rise in basal perfusion pressures produced by these concentrations of methoxamine and U46619.5. Infusion of the TxA2 receptor antagonist AH23848 (111 nmol/L) inhibited the potentiating effect of U46619 (317 nmol/L) on responses to 5‐HT in both non‐diabetic and diabetic rats.6. These results indicate that the potentiation of constrictor responses to 5‐HT by U46619 is mediated by activation of TxA2/prostaglandin H2 (PGH2) receptors, and suggest that a synergistic interaction of TxA2 and 5‐HT could be of importance in both normal and diabetic vasculature.
CLINICAL AND PATHOLOGICAL DIVERSITY OF PRIMARY ALDOSTERONISM, INCLUDING A NEW FAMILIAL VARIETY
Authors: Gordon Richard D. , Stowasser Michael , Tunny Terry J. , Klemm Shelley A. , Finn Wendy L. , Krek Anton L. 
Published: June 2007

SUMMARY1. Of 93 patients with primary aldosteronism seen during a 20 year period, 52 had an aldosterone‐producing adenoma (APA) removed (five more await surgery), 14 had bilateral adrenal hyperplasia (BAH), three had glucocorticoid‐suppressible hyperaldosteronism (GSH), one had adrenal carcinoma and 18 are yet to be categorized.2. Seventy‐three presented with hypertension and hypokalaemia. Others had markedly suppressed renal venous plasma renin activity (PRA) or elevated plasma aldosterone (PA)/PRA ratio, in new or resistant hypertensives.3. The PA/PRA ratio was the most reliable screening test.4. Diagnosis depended on the failure of suppression of aldosterone by salt loading and fludrocortisone.5. Differentiation of BAH from APA depended on adrenal venous sampling comparing adrenal and peripheral venous PA/cortisol ratios.6. A new familial variety of primary aldosteronism is described, with two affected members in each of three families.7. Primary aldosteronism should be looked for in resistant and low‐renin hypertension as well as in hypertension with hypokalaemia, and other family members should have PA/PRA measured if they are hypertensive.
EFFECTS OF ENDOTHELIN‐1 ON ARTERIAL PRESSURE AND MYOCARDIAL CONTRACTILITY IN THE CONSCIOUS NORMOTENSIVE RABBIT
Authors: Roberts‐Thomson P. , McRitchie R. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. We studied the effects of an intravenous bolus of endothelin‐1 on arterial pressure and myocardial contractility in the conscious rabbit.2. Endothelin produced an initial fall in arterial pressure accompanied by an increase in heart rate. This was followed by a dose‐dependent increase in arterial pressure, peaking about 7 min after injection, accompanied by a reciprocal fall in heart rate.3. Left ventricular rate of change of pressure (LV dP/dt) increased with endothelin except at higher doses (0.8 and 1.6 nmol/kg), where in some animals it decreased.
SECRETION OF MEDULLIPIN I BY ISOLATED KIDNEYS PERFUSED UNDER ELEVATED PRESSURE
Authors: Muirhead E. E. , Brooks B. , Byers L. W. , Brown P. , Pitcock J. A. 
Published: June 2007

SUMMARY1. Medullipin I (Med I) is a hormone extracted from renal papillae and its renomedullary interstitial cells (RIC). Med I is stimulated by elevation of the renal artery perfusion pressure.2. When isolated normal rat kidneys were perfused either with oxygenated blood or with 5% albumin bubbled with O2 at elevated perfusion pressures, Med I appeared to be secreted into the renal venous effluent (RVE). Addition of Tween 20, treatment of the assay rat with SKF 525A, inhibitor of cytochrome P‐450 and removal of the liver from the systemic circulation prevented vasodepression of both the RVE and extracted Med I. The lipid in the RVE gave the same dose–response as extracted Med I.3. Lowering the renal artery perfusion pressure below normal inhibited the secretion of Med I. As the perfusion pressure was elevated Med I secretion appeared to increase.4. Previous observations and the present study support the view that the renin–angiotensin system and the Medullipin system are double feedback systems involved in blood pressure control.
INCREASE IN REACTIVITY OF HUMAN PLATELET GUANYLATE CYCLASE DURING AGGREGATION POTENTIATES THE DISAGGREGATING CAPACITY OF SODIUM NITROPRUSSIDE
Authors: Chirkov Y. Y. , Belushkina N. N. , Tyshchuk I. A. , Severina I. S. , Horowitz J. D. 
Published: June 2007

SUMMARY1. Basal and stimulated guanylate cyclase activity during ADP‐induced human platelet aggregation in comparison with the actions of sodium nitroprusside (SNP) on platelets was investigated.2. Sodium nitroprusside exhibited both ex vivo and in vitro antiplatelet effects, as assessed by inhibition of subsequent ADP‐induced aggregation in platelet‐rich plasma. A strong correlation between decrease in aggregation and increase in platelet guanylate cyclase activity in the presence of SNP was obtained.3. When SNP was administered after the induction of aggregation, it caused acceleration of disaggregation (in reversible aggregation) and produced disaggregation (under conditions of otherwise irreversible aggregation) which was time‐dependent.4. Platelet aggregation was accompanied by a transient increase in platelet cyclic GMP content and guanylate cyclase activation by the nitric oxide (NO) donor SNP. Changes in guanylate cyclase activity were haem‐associated and probably reflected saturation of enzyme by haem.5. Maximal SNP disaggregating effect coincided with peak guanylate cyclase responsiveness to SNP.6. The present investigation provides evidence that increased responsiveness of platelet guanylate cyclase to NO during aggregation facilitates disaggregation in the presence of SNP. Thus, availability of NO (endogenous or exogenous) at sites of incipient platelet aggregation in vivo may play a pivotal role regarding limitation of this process.
DEVELOPMENT OF TOLERANCE TO KAVA IN MICE
Authors: Duffield P. H. , Jamieson D. 
Published: June 2007

SUMMARY1. The development of tolerance to the aqueous extract of kava, and to the lipid soluble extract (kava resin) was tested in mice.2. Tolerance to the unknown pharmacologically active ingredient(s) developed very rapidly, given parenterally, in the aqueous extract. A minimally effective daily dose (50 mg/kg) of the aqueous extract for 3 days was sufficient to produce tolerance to a test dose of 150 mg/kg, which is close to the ED50. As tolerance was evident at the first test period it can be assumed to be physiological tolerance.3. Kava resin decreased spontaneous motility and caused a loss of muscle control. A minimally effective daily dose of kava resin (100 mg/kg) did not produce tolerance to the above effects of a weekly test dose of kava resin (166 mg/kg) within 7 weeks. In a further experiment the dose was raised to 150 mg/kg twice daily and this schedule caused partial tolerance to occur within 3 weeks, but very little further tolerance developed over the ensuing 2‐week period.4. To try to induce learned (behaviourally acquired) tolerance a dose of 166 mg/kg kava resin was injected daily and animals were tested each day while under the influence of the drug. However, even under these conditions, there was no tolerance evident within 3 weeks, when the experiment was terminated.5. It appears difficult to induce the development of physiological or learned tolerance to kava resin in mice.
EXERCISE‐LOADED BLOOD PRESSURE AND Li‐Na COUNTERTRANSPORT SYSTEM IN THE ERYTHROCYTE MEMBRANE AS PREDICTORS OF MILD ESSENTIAL HYPERTENSION PROGNOSIS
Authors: Saito Toshihiro , Onuma Noriyoshi , Yamamoto Mitsuyuki , Kai Noriyuki , Yamamoto Kazutoshi , Iwata Jiro , Yamada Kenjiro , Deguchi Fujio , Inagaki Yoshiaki 
Published: June 2007

SUMMARY1. The blood pressure response to exercise loading, Na concentration in the erythrocyte and Li–Na countertransport (Li–Na CT) system in the erythrocyte membrane in 40 male volunteers and 98 patients with mild essential hypertension were investigated. Subjects were divided into a juvenile group (<36 years) and a middle‐aged (>36 years and <65 years) group. Exercise‐loaded blood pressure in patients with mild essential hypertension was followed up for more than 5 years.2. Systolic blood pressure (SBP) at 6 min during exercise loading was significantly higher in the mild hypertension group compared with the control group.3. Patients with high SBP at exercise loading in the mild hypertension group transferred more often to the moderate hypertension group within 5 years.4. No difference in the haemodynamic parameter at rest was noted in the transferred group for moderate hypertension and the non‐transferred group.5. A higher blood pressure response to noradrenaline was noted in the transferred group compared with the non‐transferred group of the juvenile group.6. High Na concentration in the erythrocyte and acceleration of the Li–Na CT system in the erythrocyte membrane were noted in the mild hypertension group compared with the volunteer group.7. A correlation between SBP at exercise loading and Li‐Na CT system in the erythrocyte membrane was noted. This correlation was strongly noted in subjects less than 50 years old.8. From these results it was concluded that SBP at exercise loading and Li–Na CT system in the erythrocyte membrane are useful as indicators for the prognosis of mild essential hypertension.