bluuebunny/crossref_metadata_2025_split huggingface dataset:
BLOOD PRESSURE RESPONSE TO NOREPINEPHRINE AND ANGIOTENSIN II IN THE OFFSPRING OF PARATHYROIDECTOMIZED MOTHER RATS
Authors: Nakanishi Hitoshi , Fujii Tomoko 
Published: June 2007

SUMMARY1. The basal blood pressure and the drug‐stimulated pressor response were studied in male offspring in the sixth generation (5d‐PTx‐F6) of rats parathyroidectomized on day 5 of pregnancy.2. The systolic blood pressure in conscious 5d‐PTx‐F6 rats measured by a tail cuff was significantly higher (P < 0.001) than in control rats.3. Venous plasma renin activity was significantly lower (P < 0.001) in the 5d‐PTx‐F6 rats. Plasma levels of calcium, sodium, and potassium in the 5d‐PTx‐F6 rats and in the controls did not differ.4. Systolic arterial pressure response to intravenously (i.v.) administered angiotensin II (150 ng/kg) in the 5d‐PTx‐F6 rats was significantly greater than in the controls (P < 0.05), when blood pressure was measured directly through a pressure transducer under anaesthesia.5. Pressor responses to norepinephrine (5 μg/kg, i.v.) in the 5d‐PTx‐F6 rats were significantly lower (P < 0.05) than in the controls, when blood pressure was measured directly under anaesthesia.6. The findings suggest that the 5d‐PTx‐F6 rats undergo functional alterations of the renin‐angiotensin and sympathetic nervous systems for cardiovascular regulations.
CALCIUM CONTENT OF THE ERYTHROCYTES: A SENSITIVE AND EASY HANDLING METHOD FOR MEASURING FREE CALCIUM IONS, AND MODULATION OF THE Ca2+ ION CONCENTRATION BY THE CALCIUM ANTAGONISTS NIFEDIPINE AND PENTOXIFYLLINE
Authors: Friederichs E. , Rädisch T. , Winkler H. 
Published: June 2007

SUMMARY1. A method for determining free Ca2+‐ions in the erythrocyte is described, using a commercially available ORION‐Ca‐electrode and calomel reference electrode assembly, where changes in free Ca2+‐ion concentration upon addition of 0.01% digitonin could be measured.2. The average value found for fresh cells from 20 healthy donors at 37°C (pH = 7.4) was 0.20 ± 0.04 μmol/L referred to a haematocrit of 10%.3. Decrease of the simultaneously determined adenosinetriphosphate (ATP) concentration indicates that ATP is presumably needed to activate the Ca‐ATPase.4. In vitro addition of the calcium antagonists pentoxifylline and nifidepine, respectively, induced a normalization of the intraerythrocytic Ca2+‐ion concentration after previous increase with the ion carrier ionophore A23187.5. The advantages and possible clinical applications of this method are discussed.
CORTICAL CONTROL OF TONGUE CONTRACTILITY IN THE RAT UNDER KETAMINE ANAESTHESIA
Authors: Marco L. A. , Reed T. F. , Aides L. D. , Chronister R. B. , Brown C. B. , White L. E. 
Published: June 2007

SUMMARY1. Cortico‐lingual and linguo‐cortical interconnectivity was investigated in ketamine‐anaesthetized rats mounted onto a stereotaxic apparatus. The tip of the tongue was tied to a force displacement transducer to monitor tongue retrusions. The tongue cortical area was exposed in one or both hemispheres to record evoked potentials or spontaneous electroencephalographic (EEG) activity, or to stimulate electrically with single square pulses of up to 50 V and 0.25 ms pulse width.2. The results showed that (i) tongue retrusions elicited by electrical stimulation were identical to those induced by ketamine; (ii) ketamine‐induced tongue contractions correlated in time with cortical EEG potentials which were easily distinguished from the background noise; (iii) haloperidol (2.5 mg/kg, i.m.) suppressed the cortically evoked tongue contractions as well as the ketamine‐induced contractions.3. These results suggest that ketamine‐induced tongue retrusions may involve the cortex in their mediation if not their generation and that this may provide a basis for the suppression of dyskinetic activity during sleep or unconsciousness.
DETERMINANTS OF SMOOTH MUSCLE SENSITIVITY
Authors: Head Richard J. 
Published: June 2007

SUMMARY1. Deviation supersensitivity and post‐junctional supersensitivity are important determinants in the control of the response of smooth muscle.2. Post‐junctional supersensitivity is a process whereby effector cells have augmented responsiveness as a consequence of an impaired physiological stimulus. Deviation supersensitivity which occurs as a result of inhibition of sites of loss or inactivation of the transmitter substance noradrenaline and its analogues also produces an enhanced response of smooth muscle cell preparations.3. The enzymes monoamine oxidase and catechol‐O‐methyl transferase are irreversible sites of loss of noradrenaline. Functional impairment of these enzymes results in deviation supersensitivity.4. The complexities involved in unravelling the contribution of noradrenaline metabolizing enzymes to deviation supersensitivity are highlighted with emphasis upon the pioneering work of Professor de la Lande in this field.
MECHANISMS OF ADAPTIVE SUPERSENSITIVITY IN SMOOTH MUSCLES VS CARDIAC MUSCLE: A BRIEF REVIEW
Authors: Fleming William W. 
Published: June 2007

SUMMARY1. Depending upon the type of cell being studied, adaptive supersensitivity has been traced to molecular changes in receptors, the Na+/K+ pump or the G‐protein/adenylate cyclase system.2. Evidence is reviewed that indicates that adaptive supersensitivity in guinea‐pig atria is the result of changes in the G‐protein/adenylate cyclase system.
CYTOCHROMES P‐450 IN STEROIDOGENESIS: ARE THESE ENZYMES MORE SPECIFIC THAN THOSE OF DRUG METABOLISM?
Authors: Hall Peter F. 
Published: June 2007

SUMMARY1. In contrast to drug‐metabolizing cytochromes P‐450, the corresponding ster‐oidogenic enzymes appear to be highly specific with respect to substrates, reactions catalysed, and the sites in the substrate molecule that are attacked.2. Recent studies have shown that important exceptions to this generalization are encountered.3. The conversion of 11‐deoxycorticosterone to aldosterone requires three enzymatic reactions, the last of which (aldehyde synthetase), like the first two, requires a P‐450 mono‐oxygenation. The involvement of P‐450 in this third step (from alcohol to aldehyde) was demonstrated by photochemical action spectra and determination of stoichiometry. The three reactions were shown to be catalysed by a single enzyme as demonstrated by immunoprecipitation and the use of a homogenous enzyme.4. The conversion of pregnenolone and progesterone to the corresponding Δ16‐C19 steroids, which are pheromones, is catalysed by a cytochrome P‐450 that also catalyses the conversion of progesterone to androstenedione (that is, C21 side‐chain cleavage; hydroxylase/lyase). The synthesis of the Δ16 compounds requires cytochrome b5.5. The conversion of testosterone and epitestosterone to androstenedione is catalysed by P‐450b. Studies of kinetic isotope effects using deuterium and 18O2 show that P‐450b catalyses this reaction with epitestosterone via the formation of a gem diol, whereas, with testosterone as substrate, one‐third of the product is formed via the same mechanism while the remainder results from the mechanism described as dual hydrogen abstraction.
THE ROLE OF CYTOCHROMES P‐450 AND N‐ACETYL TRANSFERASE IN THE CARCINOGENICITY OF AROMATIC AMINES AND AMIDES
Authors: McManus Michael E. 
Published: June 2007

SUMMARY1. Epidemiological studies have clearly identified the aromatic amines 2‐naph‐thylamine, benzidine and 4‐aminobiphenyl as human carcinogens. Many other compounds of this class are suspected to be human carcinogens.2. At least 12 heterocyclic aromatic amines have been isolated from cooked food, nine of which have been shown to be carcinogenic in vivo. The significance of these compounds in the aetiology of human cancer is yet to be established.3. Specific forms of cytochrome P‐450 have been shown to be involved in the initial step in the activation (N‐hydroxylation) of aromatic amines and amides. A possible polymorphism exists for the N‐hydroxylation of 2‐acetylaminofluorene in human liver microsomes.4. N‐Acetyltransferase is involved in the further activation of arylhydroxamic acids and N‐hydroxyarylamines to reactive intermediates. Polymorphisms in the expression of this enzyme activity have been associated with certain types of human cancer.5. Polymorphisms in both cytochrome P‐450 and N‐acetyltransferase expression may be critical determinants in the susceptibility of individuals to the toxicity and carcinogenicity of aromatic amines and amides.
ISOMETRIC CONTRACTILE PROPERTIES AND CAFFEINE SENSITIVITY OF THE DIAPHRAGM, EDL AND SOLEUS IN THE MOUSE
Authors: Singh Yadhu N. , Dryden William F. 
Published: June 2007

SUMMARY1. Isometric contractile responses and caffeine sensitivity were studied in isolated mouse hemidiaphragm (HD), extensor digitorum longus (EDL) and soleus muscles.2. The maximum twitch and tetanic tensions developed by the EDL showed a greater temperature dependence than the soleus. The rates of force development and relaxation were more temperature sensitive in the soleus.3. For the HD, Q10 values for all contractile parameters were intermediate between those of the EDL and the soleus but closer to those of the EDL.4. The soleus was significantly more sensitive to caffeine than the EDL while the HD showed a response closer to that of the EDL than the soleus.5. Costal segments of the HD developed force more rapidly but were less caffeine sensitive than the vertebral or sternal segments.6. The results indicate that the mouse HD exhibits isometric contractile characteristics and caffeine sensitivity more closely resembling the EDL than the soleus but there is a variation in these properties between the different parts of the HD.
TAURINE: EFFECT ON MYOCARDIAL RELAXATION
Authors: Rahimi A. R. , Campbell K. B. , Knowlen G. G. , Kirkpatrick R. D. 
Published: June 2007

SUMMARY1. The effects of taurine on cardiac inotropic state and relaxation were studied in the isolated rabbit heart using solutions containing three concentrations of calcium: 0.7, 1.8 and 3.0 mmol/l.2. Increases in Ca2+ caused increases in inotropic indices, but had no effect on rate constant of relaxation.3. Taurine had a positive inotropic effect at Ca2+= 0.7 mmol/l, an equivocal effect at Ca2+= 1.8 mmol/l and a negative inotropic effect at Ca2+= 3.0 mmol/l.4. Taurine had no effect on the rate constant of relaxation at any Ca2+ concentration.5. Taurine modulates the positive inotropic effect of Ca2+ but neither taurine nor Ca2+ affect the rate constant of relaxation.
ACUTE HORMONAL AND RENAL EFFECTS OF ORAL DILEVALOL IN NORMAL MEN
Authors: Whitworth Judith A. , Gordon Deanna , Harpley Robin , Yeung Stella , Phillips Paddy 
Published: June 2007

SUMMARY1. Acute hormonal and renal effects of dilevalol (200 mg), a non‐selective β‐blocking drug with vasodilator properties, were compared with placebo in six normal men on constant sodium intake.2. Control and treatment blood pressures were lower with dilevalol than placebo, although the pattern of blood pressure fall was similar in both.3. Plasma active renin and aldosterone concentrations were lower on dilevalol than placebo after 4 h of recumbency (P < 0.05).4. Total plasma renin, renin substrate, cortisol and atrial natriuretic peptide concentrations were similar on dilevalol and placebo.5. There were no differences in glomerular filtration rate and no deleterious biochemical or haematological changes on dilevalol or placebo.
IN VITRO TIME COURSE STUDIES ON TRAIN‐OF‐FOUR FADE INDUCED BY HEXAMETHONIUM, PANCURONIUM AND DECAMETHONIUM IN THE RAT HEMIDIAPHRAGM
Authors: Gwee M. C. E. , Cheah L. S. 
Published: June 2007

SUMMARY1. In vitro time course studies on the effects of hexamethonium (7 mmol/L), pancuronium (5 μmol/L) and decamethonium (220 μmol/L) on nerve‐evoked (2 Hz for 2 s every 20 s) maximal twitches (T1, T2, T3, T4) of the rat hemidiaphragm were conducted. All three drugs progressively depressed all four twitches in a given train but at different rates (T4 > T3 > T2≫ T1).2. The response‐time profiles for T1 and T4 varied widely for the three drugs such that, for the same degree of T1‐block, each drug produced a different magnitude of T4‐block during the onset of and recovery from neuromuscular blockade.3. Analysis of the T1 versus T4/T1 plot showed that, at 50% T1‐block, the corresponding T4/T1 (i.e. train‐of‐four ratios) during the onset (and recovery) phase were 0.16 (0.29), 0.46 (0.40) and 0.66 (0.53) for hexamethonium, pancuronium and decamethonium, respectively. Thus, for the same degree (i.e. 50%) of twitch (T1) tension depression, the three drugs differed widely in their ability (hexamethonium ≫ pancuronium > decamethonium) to produce fade as reflected in the respective train‐of‐four ratio.4. Our results therefore show that the train‐of‐four ratio (T4/T1) at 50% T1‐block obtained from such in vitro time course studies is a useful quantitative index of the potential of various drugs to cause train‐of‐four fade. Based on this index a classification of various compounds already studied is proposed as follows: hexamethonium ≫ pancuronium ∼ (+)‐tubocurarine > decamethonium ∼ succinylcholine ≫α‐bungarotoxin.
STIMULATION OF β1‐ADRENOCEPTORS ENHANCES ELECTRICALLY EVOKED [3H]‐ACETYLCHOLINE RELEASE FROM RAT PHRENIC NERVE
Authors: Wessler I. , Holzer G. , Künster A. 
Published: June 2007

SUMMARY1. The effects of isoprenaline, noradrenaline and fenoterol on the electrically evoked release of [3H]‐acetylcholine from the rat phrenic nerve were investigated.2. Isoprenaline (0.1 μmol/L) and noradrenaline (1 μmol/L) enhanced evoked [3H]‐acetylcholine release by about 90%, an effect which was abolished by CGP 20712A (0.1 μmol/L), a specific antagonist at β1‐adrenoceptors. Noradrenaline still enhanced [3H]‐acetylcholine release in the presence of phentolamine (1 μmol/L).3. The enhancing effect of both isoprenaline and noradrenaline decreased at prolonged exposure times (24–32 min). A pre‐exposure of the tissue to a low concentration (0.01 μmol/L) of isoprenaline prevented the enhancing effect of 0.1 μmol/L isoprenaline.4. Fenoterol, a specific agonist at β2‐adrenoceptors, did not modify evoked [3H]‐acetylcholine release.5. The present results indicate the existence of facilitatory β1‐adrenoceptors on the motor nerve. These receptors appear to be desensitized either by a high concentration of, or by a long exposure to, agonists. Under the present conditions noradrenaline enhances the release of newly synthesized transmitter mainly by stimulation of β‐adrenoceptors.
SYSTEMIC AND REGIONAL EFFECTS OF ENDOTHELIN IN RABBITS: EFFECTS OF ENDOTHELIN ANTIBODY
Authors: Miyamori I. , Itoh Y. , Matsubara T. , Koshida H. , Takeda R. 
Published: June 2007

SUMMARY1. The effects of porcine endothelin‐1 (10‐12‐5 × 10‐10mol/kg) on arterial blood pressure (BP) and the renal, mesenteric and carotid blood flow (BF), and the effects of endothelin‐1 antibody were studied in rabbits.2. Endothelin‐1 caused a sustained increase in BP. The renal, mesenteric and carotid BF were decreased dose‐dependently by endothelin‐1. The approximate half‐maximal effective values (ED50) were 5.5 × 10‐11, 8.6 × 10‐11 and 2.0 × 10‐10 mol/kg for renal, mesenteric and carotid BF respectively. Compared with carotid BF, the renal and mesenteric BF responses were significantly more sensitive to endothelin‐1.3. Combined administration of endothelin‐1 and its antibody showed a significant inhibition of the BP and renal BF responses. However, endothelin‐1 antibody alone did not change either BP, renal BF, mesenteric BF or carotid BF in vivo.4. The present results demonstrate that endothelin is a potent vasoconstrictor in vivo. However, circulating endothelin may not contribute to the control of BF and BP. The role of endothelin as a local modulator of the vascular tone remains to be investigated.
EFFECTS OF THE α2‐ADRENOCEPTOR AGONIST UK14304 ON PRESSOR RESPONSES IN PITHED RATS
Authors: Xiao X‐H. , Rand M. J. 
Published: June 2007

SUMMARY1. Intravenous infusions of UK14304 (0.3–10 μg/kg per min) in pithed rat produced dose‐dependent pressor responses which were not affected by prazosin (10 μg/kg) but were reduced by yohimbine (0.3 mg/kg).2. Pressor responses to noradrenaline (0.1 μg/kg), phenylephrine (1 μg/kg) and vasopressin (10 mU/kg) were enhanced during infusions of UK14304 (0.03–1 μg/kg per min). Likewise, pressor responses to spinal sympathetic stimulation were enhanced during infusions of low concentrations of UK14304 (0.03–0.3 μg/kg per min) but were reduced during infusion of a higher concentration of UK14304 (10 μg/kg per min).3. After administration of yohimbine (0.3 mg/kg) or the calcium channel blocking drug diltiazem (infused at 50 μg/kg per min), pressor responses to noradrenaline and UK14304 were reduced, and responses to noradrenaline during infusion of UK14304 were not enhanced.4. Prazosin (10 μg/kg) revealed a secondary depressor component in the response to sympathetic stimulation which is due to β‐adrenoceptor activation, since it was abolished by ICI 118551 (0.3 mg/kg). In the presence of ICI 118551 plus prazosin, pressor responses to sympathetic stimulation were enhanced during infusions of UK14304.5. The depressor response to nitroprusside and the depressor component of responses to sympathetic stimulation after prazosin were enhanced during infusions of UK14304 at concentrations that increased the blood pressure.6. The findings show that α2‐adrenoceptor activation enhanced the pressor responses to sympathetic nerve stimulation, noradrenaline, phenylephrine and vasopressin in the pithed rat and α‐adrenoceptor activation produced depressor responses which increased with increasing blood pressure.
THE EFFECT OF IVERMECTIN ON SOME HAEMATOLOGICAL INDICES IN RABBITS: INFLUENCE OF VITAMIN K TREATMENT
Authors: Ali B. H. 
Published: June 2007

SUMMARY1. Rabbits were treated with the antiparasitic drug ivermectin at subcutaneous doses of 0.2, 1 and 2.5 mg/kg and blood collected weekly for 4 weeks thereafter for measuring some blood parameters. At a dose of 0.2 or 1 mg/kg the drug had no significant effect on any of the parameters measured. At a dose of 2.5 mg/kg, the drug reduced significantly the erythrocyte counts, haemoglobin concentration, haematocrit, mean corpuscular haemoglobin concentration and mean corpuscular haemoglobin on weeks 1, 2, 3 and 4. Platelet counts were not significantly affected.2. In another trial, ivermectin was injected subcutaneously at a dose of 2.5 mg/kg, after pre‐treatment with either saline or vitamin K (30 μg/kg for 30 days), and prothrombin time, bleeding time and platelet counts measured at weekly intervals for 4 weeks. Bleeding time and thrombin time were significantly increased 1 week after treatment, and remained higher than the control for 4 weeks.
PROGNOSIS OF MALE PATIENTS WITH TREATED HYPERTENSION FOLLOWED OVER 15 YEARS
Authors: Morgan Trefor O. , Anderson Adrianne , Hopper John , Maskill Greg 
Published: June 2007

SUMMARY1. Male patients aged 50–75 years on treatment for hypertension in 1973 have been followed for 15 years.2. Overall mortality in the 271 patients was 63% and 41% died of vascular disease.3. Coronary artery disease or sudden death occurred in 44% of the patients who died and was between 2 and 6 times more common than in the general population.4. Treatment of hypertension has improved overall prognosis but mortality from coronary artery disease is more common than in the general population.
HIGH SALT DIET AMELIORATES EFFECTS OF ANGIOTENSIN CONVERTING ENZYME INHIBITION IN SPONTANEOUSLY HYPERTENSIVE STREPTOZOTOCIN DIABETIC RATS
Authors: Jackson Bruce , Fabris Bruno , Paxton Donna , Franze Linda , Johnston Colin I. 
Published: June 2007

SUMMARY1. To dissociate the effects on the development of diabetic renal injury of angiotensin converting enzyme (ACE) inhibition per se, and a reduction in systemic blood pressure, we have studied the effects of chronic ramapril treatment in streptozotocin diabetic spontaneously hypertensive rats, with modulation of the hypotensive effect by a high salt diet.2. Three weeks following uninephrectomy and induction of diabetes with streptozotocin, spontaneously hypertensive rats were allocated to three treatment groups. Groups 1 and 2 received 1% sodium chloride and Group 3 water as drinking solution. Groups 2 and 3 received 0.4 mg/kg per day ramapril in drinking solution over the subsequent 2 month study period.3. Sodium chloride drinking solution (1%) completely prevented any hypotensive effect of ramapril. Blood pressure was reduced in Group 3 rats over the entire period of study, when compared with Group 2 rats (P<0.001).4. Urinary protein excretion progressively increased in Group 1 and 2 rats, and was significantly reduced (P<0.001) in Group 3. After 2 months treatment, urinary protein (expressed as mean and s.e.m.) was 160±30 mg/day in Group 1, 240±50 mg/day in Group 2, and 60±11 mg/day in Group 3.5. Angiotensin converting enzyme inhibition per se was not associated with a reduced protein excretion in diabetic nephropathy, requiring concomitant control of systemic blood pressure to become renoprotective.
URIDINE KINASE INHIBITION IS INVOLVED IN THE VASODILATOR EFFECTS OF MINOXIDIL IN THE RAT
Authors: Macdonald Graham , Walker Therese , Assef Rhonda , Duggan Karen 
Published: June 2007

SUMMARY1. Since minoxidil is a pyrimidine derivative, its actions on vascular smooth muscle may derive from structural relationships to the uridine nucleotides, which have been shown to be vasoconstrictive in the rat.2. Minoxidil at a low vasodepressor dose of 0.03 mg/kg per min abolished the pressor response to uridine at doses from 2 to 8 μmol/kg per min, but did not reduce the responses to uridine monophosphate or uridine diphosphate in similar pressor doses, suggesting an action on either transport of uridine into cells or on uridine kinase which catalyses phosphorylation of uridine to uridine monophosphate, the mediator of uridine's vascular actions.3. The active metabolite of minoxidil was found to inhibit rat liver uridine kinase in vivo using an HPLC technique.4. Plasma uridine concentration was significantly higher in 11 hypertensive patients on minoxidil compared with pretreatment values, suggesting that uridine kinase inhibition is of a degree sufficient to increase the circulating pool of uridine.5. The data is consistent with uridine kinase inhibition being a mechanism for the vasodilator actions of minoxidil.
LACK OF PRESSOR RESPONSE TO INTRACEREBROVENTRICULAR INFUSION OF ALDOSTERONE IN SHEEP
Authors: Tresham Janette J. , Coghlan John P. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. Studies in the rat and the dog have shown that infusion of aldosterone for several weeks into the cerebral ventricles (ICV) can produce hypertension at doses that do not have an effect when infused systemically. We have previously shown that a high physiological dose of aldosterone infused intravenously at 10 μg/h in sheep produces an increase in blood pressure of 7 mmHg within 2 days.2. In this paper we report the effects of ICV infusion of aldosterone at 2 μg/h for 6 days in conscious sheep.3. Neither blood pressure nor heart rate were altered, and there were no consistent changes in any of the metabolic parameters measured.4. These results do not support a role for central effects of aldosterone in the hypertension produced by systemic infusion of the steroid in sheep.
PLASMA AND PITUITARY THYROID‐STIMULATING HORMONE LEVELS IN BROMOCRIPTINE‐TREATED NEW ZEALAND GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Tan B. K. H. , Hutchinson J. S. 
Published: June 2007

ABSTRACT1. The effects of a 13‐day intraperitoneal (i.p.) infusion of bromocriptine, delivered by osmotic pump, on plasma and pituitary thyroid‐stimulating hormone (TSH) levels were investigated in New Zealand genetically hypertensive (GH) rats and their normotensive (NT) controls.2. In both the GH and NT rats, bromocriptine significantly reduced plasma TSH level but did not have any significant effect on pituitary TSH content.3. No significant difference was found in the plasma TSH level and pituitary TSH content between the vehicle‐treated GH and NT rats.4. These results suggest that there are no differences between the GH and NT rats with regard to the activity of the central dopaminergic system influencing TSH release and also that TSH does not play a role in the hypertension of the GH rats.