bluuebunny/crossref_metadata_2025_split huggingface dataset:
HIGH AFFINITY ALDOSTERONE BINDING SITES (TYPE I RECEPTORS) IN RAT HEART
Authors: Pearce Paul , Funder John W. 
Published: June 2007

SUMMARY1. The use of the receptor stabilizing agent sodium molybdate, and of RU26988 to exclude [3H]‐aldosterone binding from Type II glucocorticoid receptors, has enabled the characterization of high affinity Type I aldosterone binding sites in rat atrial and ventricular cytosols.2. In adult male and female rats the affinity of binding (Kd 4°C) is ∼ 1–2 nmol/l for both atria and ventricles; specificity of binding is similar to that for Type I sites in classical aldosterone target tissues (aldosterone = corticosterone≫dexamethasone).3. Levels of atrial Type I sites are higher than the corresponding levels in ventricle in both males and females, whereas for Type II (classical glucocorticoid) receptors the reverse is the case; levels of both Type I and Type II sites fall over the age range examined (40 days‐6 months).4. The physiological function(s) of cardiac Type I sites, and their in vivo mineralo‐corticoid or glucocorticoid selectivity, remain to be explored.
EFFECT OF 3 DAY INFUSION OF ACTH OR CRF ON THE PITUITARY‐ADRENAL AXIS
Authors: Silberberg Suzanne , Funder John W. 
Published: June 2007

SUMMARY1. The effects of 72 h subcutaneous infusion of graded doses of rat CRF and ACTH(1–24) were studied in rats of initial weight 150–170 g. Rat CRF was infused at 30, 100 or 300 ng/h, and ACTH(1–24) at 125, 250 or 500 ng/h.2. There was a progressive though modest increase in adrenal weight for all CRF doses, and an associated reduction of thymus weight. Circulating ir‐ACTH, ir‐β‐endorphin and corticosterone levels, and adrenal DN A content, were not increased after 3 days. Adrenal RNA and protein content were increased at the highest CRF dose used.3. ACTH infusion caused a progressive increase in adrenal weight and thymie involution which was marked at the higher doses; circulating corticosterone levels were not significantly altered by the lowest dose but were significantly raised by the higher doses. As expected, plasma ir‐β‐endorphin was suppressed to low levels with all doses. Adrenal DNA did not alter but there were progressive increases in adrenal protein and RNA.4. There was a marked difference in gain between the two infusion regimens in terms of all parameters measured, suggesting that potent mechanisms exist to temper the pituitary‐adrenal response to markedly different levels of peripheral CRF input. The damped effect of CRF infusion compared with that of ACTH may represent desensitization of CRF receptors at the pituitary; alternatively, it may reflect binding and substantial inactivation of CRF in peripheral blood.
CARDIOVASCULAR RESPONSES TO ACUTE MYOCARDIAL ISCHAEMIA IN MORPHINE‐DEPENDENT RATS
Authors: Ko Wendy W‐W. , Dai Soter , Chan Mo‐Yin 
Published: June 2007

SUMMARY1. The cardiovascular responses to acute myocardial ischaemia were studied in opiate‐dependent animals before and after 2 weeks morphine withdrawal.2. Rats were treated with morphine sulphate in drinking water for 2, 3 or 5 weeks. The development of morphine tolerance and dependence was verified by the tailimmersion test for analgesia and the naloxone‐precipitated withdrawal syndrome, respectively.3. Acute left coronary artery ligation induced a decrease in blood pressure, a slight increase in heart rate and ventricular tachycardia or fibrillation in anaesthetized naive rats.4. Chronic morphine treatment did not alter the haemodynamic responses to coronary artery ligation. However, a significantly lowered incidence, and prolonged time of onset, of ventricular arrhythmias was found in 3 and 5 week morphine‐treated rats. This phenomenon did not occur in animals receiving morphine for 2 weeks and in a 3 week morphine‐treated group which was subsequently withdrawn for 2 weeks.5. It is suggested that the decreased occurrence of early ventricular arrhythmias resulting from acute myocardial ischaemia in chronic morphine‐treated rats may be related to the degree of opiate tolerance and dependence.
RAPID HAEMODYNAMIC RESPONSES TO ATRIAL NATRIURETIC FACTOR (99–126) IN CONSCIOUS SHEEP
Authors: Parkes D. G. , Coghlan J. P. , McDougall J. G. , Scoggins B. A. 
Published: June 2007

SUMMARY1. Haemodynamic effects of 20 μg and 100 μg injection of atrial natriuretic factor 99–126 (ANF) were studied in conscious sheep.2. ANF injection rapidly decreased blood pressure associated with a fall in total peripheral resistance, increased heart rate and cardiac output. These parameters returned to normal within 5 min of injection.3. This study shows that ANF has an initial vasodilatory action to decrease blood pressure, which is different from the hypotensive mechanism seen with short‐term infusion (60 min) of ANF in sheep.
INFLUENCE OF ACUTE MYOCARDIAL ISCHAEMIA ON VENTRICULAR CYCLIC AMP CONCENTRATIONS IN NAIVE AND MORPHINE‐TREATED RATS
Authors: Ko Wendy W. W. , Dai Soter , Chan Mo‐Yin 
Published: June 2007

SUMMARY1. Ventricular cyclic AMP (cAMP) concentrations of naive and morphine‐treated rats subjected to acute myocardial ischaemia were examined.2. In naive rats, ventricular cAMP levels were increased at 3 min but decreased 5 and 10 min after left coronary artery ligation. Statistically significant changes were observed in the right ventricle after 3 min and in the left ventricle after 10 min.3. Acute morphine treatment did not significantly alter ventricular cAMP content in rats subjected to either sham operation or acute left coronary artery ligation.4. Ventricular cAMP concentrations were significantly lower in sham‐operated rats after 5 weeks of chronic morphine treatment while after 3 weeks of chronic morphine treatment, this phenomenon was seen only after acute coronary ligation. The reductions were reversed by opiate withdrawal.5. These observations support the theory that elevated cAMP levels may contribute to the production of early ventricular arrhythmias during acute myocardial ischaemia. It is suggested that the reduction in ventricular cAMP concentrations may partly account for the previously reported decreased occurrence of early ventricular arrhythmias in chronic morphine‐treated rats subjected to acute left coronary artery ligation.
RELATIONSHIP BETWEEN THE DOSE‐RESPONSE EFFECTS OF DIAZEPAM AND CLOBAZAM ON ELECTROENCEPHALOGRAPHIC PARAMETERS AND ON KINDLED AMYGDALOID SEIZURE ACTIVITY IN RATS
Authors: Harris Q. L. G. , Lewis S. J. , Young N. A. , Vajda F. J. E. , Jarrott B. 
Published: June 2007

SUMMARY1. The possibility that the anticonvulsant activity of the benzodiazepines, diazepam and clobazam, is related to changes in EEG parameters, particularly β activity, was investigated in amygdaloid kindled rats.2. The effects of diazepam (1, 2, 4, 8 and 16 μmol/kg), administered intraperitoneally (i.p.), clobazam (1, 2, 4, 8, 16 and 32 μmol/kg, i.p.) or vehicle (dimethyl sulfoxide) on the cortical EEG of amygdaloid kindled rats were quantitated for 15 min using computerized period amplitude analysis. Immediately afterwards, the amygdala was stimulated and the after‐discharge duration (AD) and the seizures stage (SS) were determined.3. The equivalent percentage time (EPT) of the diazepam‐treated group was decreased in the θ band (4–8 Hz) and increased in the α (8–12 Hz) and first six β (12–36 Hz) bands. The mean peak amplitude (MPA) was increased in the α (8–12 Hz) and all seven β bands (12–40 Hz). Clobazam increased the EPT and MPA in the α (8–12 Hz) and all seven β (12–40 Hz) bands. The MPA was also increased by clobazam in the θ (4–8 Hz) band.4. Diazepam reduced both the AD and SS of the kindled seizures at doses of 4, 8 and 16 μmol/kg, whereas clobazam was anticonvulsant at doses of 16 and 32 μmol/kg. The reduction in both AD and SS correlated with increases in the EPT and MPA in the first β (12–16 Hz) band in the diazepam‐treated group and in the first four β (12–28 Hz) bands in the clobazam‐treated group.
RILMENIDINE ACTS AS A PARTIAL AGONIST AT PREJUNCTIONAL α2‐ADRENOCEPTORS IN GUINEA‐PIG ATRIA
Authors: Li C. G. , Rand M. J. 
Published: June 2007

SUMMARY1. The present study was carried out to determine whether rilmenidine, a recently introduced antihypertensive agent which acts on α2‐adrenoceptors, has partial agonist activity on prejunctional α2‐adrenoceptors in guinea‐pig atria.2. Isolated preparations of guinea‐pig atria were incubated with [3H]‐noradrenaline and the efflux of radioactivity induced by stimulation of intramural sympathetic nerves was used as an index of release of transmitter noradrenaline.3. Rilmenidine (1 μmol/1) inhibited noradrenaline release evoked by short trains (five, 20 and 50 pulses) of sympathetic nerve stimulation and this inhibitory effect of rilmenidine was antagonized by the α2‐adrenoceptor antagonists, idazoxan (0.1 and 0.3 umol/1) and rauwolscine (0.3 umol/1) whereas it was not affected by the α1‐adrenoceptor antagonist prazosin (0.1 μmol/1).4. On the other hand, rilmenidine (1 μmol/1) enhanced noradrenaline release evoked by long trains (150 and 300 pulses) of stimulation and this effect was also abolished by idazoxan (0.1 μmol/1).5. These findings suggest that the effects of rilmenidine on transmitter release depend on the degree of auto‐inhibition: when the concentration of noradrenaline in the biophase of the prejunctional α2‐adrenoceptors is low, rilmenidine acts as an agonist, but when the concentration is high it acts as an antagonist. Thus, rilmenidine, like clonidine, is a partial agonist on prejunctional α2‐adrenoceptors in guinea‐pig atria.
INVOLVEMENT OF HYPOTHALAMIC ADRENALINE IN THE CLONIDINE WITHDRAWAL SYNDROME IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Lewis Stephen J. , Rowe Peter , Jarrott Bevyn 
Published: June 2007

SUMMARY1. The concentrations of adrenaline and other catecholamines (noradrenaline and its major metabolite DHPG, dopamine and its major metabolite DOPAC) were measured in the hypothalamus and medulla oblongata of normotensive Wistar‐Kyoto (WKY) and spontaneously hypertensive rats (SHR) which had received a continuous subcutaneous infusion of clonidine (10 μg/kg per h) for 10 days, and also in WKY and SHR rats which were killed 15–18 h after the cessation of the 10‐day infusion.2. The concentrations of adrenaline in the hypothalamus and medulla oblongata/pons of the clonidine treated WKY and SHR rats were not different from their respective controls. However, the adrenaline concentrations in the hypothalamus (but not the medulla oblongata) were significantly decreased in the post‐infusion WKY and SHR.3. These results suggest that hypothalamic adrenergic mechanisms may have a common involvement in the post‐clonidine infusion syndromes displayed by the WKY and SHR strains.
SHORT COMMUNICATION: LONG‐LASTING DEPOLARIZATION OF THE CENTRAL TERMINALS OF CUTANEOUS AFFERENTS IN L7 SEGMENT EVOKED BY VOLLEYS ASCENDING FROM THE SACRAL CORD IN THE CAT
Authors: Lupa K. , Wójcik G. , Tarnecki R. , Niechaj A. 
Published: June 2007

SUMMARY1. In 72% of non‐anaesthetized spinal cats, single volleys ascending from the sacral cord evoke long‐lasting primary afferent depolarization in L7 segment. It occurs in the central terminals of cutaneous but not in Ia muscle afferents.2. Volleys descending to L7 segment evoke only short‐lasting presynaptic depolarization.3. It is concluded that presynaptic inhibition in L7 segment produced by ascending volleys is more effective than that evoked by descending volleys.
SHORT COMMUNICATION: EFFECT OF OESTRADIOL REPLACEMENT ON SWIM‐INDUCED ANTINOCICEPTION IN OVARIECTOMIZED MICE
Authors: Wong Chak‐Lam 
Published: June 2007

SUMMARY1. A 30 s swim in water at 30°C reduced the number of abdominal constrictions produced in female mice by intraperitoneally administered acetic acid and this antinociceptive effect was antagonized by naloxone.2. Oophorectomy abolished the development of antinociceptive activity in response to swim.3. The development of antinociceptive activity and naloxone antagonism were restored in oophorectomized mice maintained on daily oestradiol injection.4. The present study indicates that the increase in abdominal constriction response to acetic acid in oophorectomized mice was due to the removal of the source of female sex hormone.
INHIBITION OF α‐TOCOPHEROL AND CALCIUM CALMODULIN‐STIMULATED PHOSPHODIESTERASE ACTIVITY IN VITRO BY ANTHRACYCLINES
Authors: Nwankwoala Reginald N. P. , West William L. 
Published: June 2007

b1. The inhibition of α‐tocopherol and calmodulin‐stimulated phosphodiesterase activities was investigated in vitro.2. Anthracyclines—doxorubicin, daunorubicin and aclacinomycin—inhibited calcium calmodulin‐stimulated cyclic 3′,5′‐AMP (cAMP) nucleotide phosphodiesterase (EC. 3.1.4–17) activity (IC50= 33.00 ± 3.50–36.50 ± 2.75 μmol/l). The stimulation of this enzyme by α‐tocopherol was also inhibited by doxorubicin (IC50= 18.50 ± 4.00 μmol/l).3. The anthracycline‐induced inhibition of the calcium calmodulin and α‐tocopherol‐stimulated phosphodiesterase activity was competitive with calmodulin and α‐tocopherol respectively. Increasing the concentration of the substrate, cAMP or calcium ions did not attenuate the drug‐induced inhibition. The basal activity of the enzyme was not inhibited by concentration of doxorubicin up to 50 μmol/l.4. In vivo, single dose drug distribution studies of the fluorescence of doxorubicin indicate that in the heart after a cardiotoxic dose (20 mg/kg), myocardial concentrations were achieved which could cause 70–80% inhibition of this phosphodiesterase enzyme.5. Inhibition of calmodulin function by anthracyclines via direct interaction with calmodulin may contribute significantly to the effects of anthracyclines, such as disturbance in calcium homeostasis as well as acute and chronic deleterious effects on the myocardium. The action of α‐tocopherol to bind or complex anthracycline may in part contribute to its protection against anthracycline‐induced membrane damage and cardiotoxicity.
EFFECT OF ATRIAL PEPTIDE ON COLLECTING DUCT FUNCTION
Authors: Fitzgibbon Wayne , Morgan Trefor 
Published: June 2007

b1. The effects of synthetic rat atrial natriuretic peptides (ANP) on diffusional 22Na+, 36Cl− and tritiated water (THO) permeability of in vitro microperfused rat papillary collecting ducts and the effect in vivo of ANP on stop‐flow sodium concentrations in the terminal segment of rabbit nephrons were studied.2. The addition of 4 ± 10−8 or 4 ± 10−7 mol/l ANP to the medium or perfusion solution did not alter diffusional 22Na+ or 36Cl− permeability of microperfused rat papillary collecting ducts.3. The basal diffusional THO permeability of papillary collecting ducts was not altered when 4 ± 10−7 mol/l ANP was present in the medium and did not inhibit the increment in diffusional THO permeability induced by vasopressin or reduce the permeability to water in a duct previously stimulated by vasopressin.4. The administration of ANP (2 μg/kg bodyweight) to rabbits in water diuresis did not alter systemic blood pressure but induced a marked natriuresis and increases in urine flow and potassium excretion. This natriuresis was not associated with alterations in stop‐flow sodium reabsorptive capacity or sodium permeability of the collecting tubules and ducts.5. Previously reported in vivo clearance data suggest that ANP causes, at least in part, a natriuresis by altering sodium transport in the medullary collecting ducts. In this study, however, a direct effect could not be demonstrated and it is possible that the medulla needs to be functioning in its normal environment for such effects to be demonstrated.
EFFECT OF pH ON VASOPRESSIN‐INDUCED WATER PERMEABILITY IN COLLECTING DUCTS OF ISOLATED RAT PAPILLAE
Authors: Fitzgibbon Wayne , Morgan Trefor 
Published: June 2007

b1. The effects of basolateral and luminal pH on diffusional water permeability of microperfused collecting ducts of isolated rat papillae were examined in the presence and absence of vasopressin at two concentrations.2. In the absence of vasopressin, collecting duct diffusional water permeabilities did not differ when the pH of the luminal fluid was varied. Similarly, in the absence of vasopressin, collecting duct diffusional water permeabilities did not differ when the bath pH was varied.3. In the presence of 50 μU/ml vasopressin, increases in diffusional water permeability of collecting ducts perfused with solutions at pH 5.0, 7.4 or 9.0 did not differ significantly. Similarly, increases in diffusional water permeability induced by 200 μU/ml vasopressin were not different when collecting ducts were perfused with solutions at pH 5.0, 7.4 or 9.0.4. The presence of vasopressin (50 μU/ml) in the bathing medium at pH 6.4, 7.4 and 8.4 induced increments in diffusional water permeability of 0.40 ± 0.21 (n= 14, P > 0.05), 1.56 ± 0.27 (n= 27, P < 0.001) and 1.67 ± 0.24 (n= 12, P < 0.001) μm/s, respectively. The increment in water permeability at pH 6.4 was significantly less than that at pH 7.4 (P < 0.001).5. The presence of vasopressin (200 μU/ml) in the bathing medium at pH 6.4, 7.4 and 8.4 induced increments in diffusional water permeability of 2.16 ± 0.54 (n= 9, P < 0.01), 2.55 ± 0.51 (n= 17, P < 0.001) and 0.98 ± 0.34 (n= 11, P < 0.05) μm/s respectively. The increment in diffusional water permeability induced by 200 μU/ml vasopressin at pH 8.4 was significantly less than that at pH 7.4 (P < 0.025).6. These findings indicate that vasopressin‐induced increases in diffusional water permeability across papillary collecting ducts are modified by changes in basolateral pH but not by changes in luminal pH. It is proposed that the interaction between vasopressin action and basolateral pH is due to alteration of different pre‐and post‐cAMP events by different basolateral pH.
MET‐ENKEPHALIN AND THE ENKEPHALIN ANALOGUE FK‐33824 CENTRALLY INHIBIT ADRENOCORTICOTROPHIC HORMONE SECRETION IN SHEEP
Authors: Wang Xiaoming , Tresham Janette J. , Scoggins Bruce A. , Coghlan John P. 
Published: June 2007

b1. The effects of central administration of met‐enkephalin, leu‐enkephalin, the enkephalin analogue FK‐33824 and the opiate antagonist naloxone on plasma concentration of adrenocorticotrophic hormone (ACTH) were examined in conscious sheep.2. Intracerebroventricular infusion of met‐enkephalin and FK‐33824 significantly decreased the basal plasma concentration of ACTH.3. Intracerebroventricular infusion of FK‐33824 inhibited the haemorrhage‐induced increase in plasma concentration of ACTH.4. Intracerebroventricular infusion of naloxone attenuated the central inhibition of plasma concentration of ACTH induced by FK‐33824, but intravenous infusion of naloxone had no effect on the reduction in plasma concentration of ACTH induced by FK‐33824.5. These studies suggest that in sheep met‐enkephalin may play a central inhibitory role in the control of ACTH secretion.
ENHANCEMENT OF RENAL BUT NOT HAEMODYNAMIC EFFECTS OF ATRIAL NATRIURETIC PEPTIDE (1–28) IN SHEEP TREATED WITH ACTH
Authors: Parkes David G. , Coghlan John P. , McDougall John G. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. The haemodynamic and renal effects of short‐term infusion of human atrial natriuretic peptide (ANP) (1–28) were examined in sheep treated with ACTH and compared with the responses previously observed in normotensive sheep.2. Infusion of ANP at 100 μg/h for 60 min in ACTH‐treated sheep (5 μg/kg per day for 5 days) decreased blood pressure and produced a fall in both cardiac output and stroke volume. No changes were seen in heart rate and total peripheral resistance.3. ANP produced large increases in urine volume, urinary sodium and chloride excretion, and further decreased plasma potassium concentration in the ACTH‐treated sheep. Compared with normal sheep studied previously under the same conditions, the ACTH‐treated sheep showed a much greater diuretic and natriuretic response to ANP, although the blood pressure response to ANP was similar in both states.4. The change in renal responsiveness to ANP in sheep may be related to the increased blood volume of the ACTH‐treated animals because volume expansion is known to enhance the renal effects of ANP.
PLASMA NEUROPEPTIDE Y AND ATRIAL NATRIURETIC PEPTIDE CONCENTRATIONS IN MAN
Authors: Russell A. E. , Aylward P. E. , Smith S. A. , Cain M. D. , McRitchie R. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. In order to examine the concentration of neuropeptide Y‐like immuno‐reactivity (NPY‐LI) and atrial natriuretic peptide (ANP) in the circulation in man, blood was sampled from the iliac vein, the inferior vena cava, the superior vena cava, the pulmonary artery and the femoral artery in 13 patients undergoing cardiac catheterization.2. Plasma NPY‐LI levels were similar at all points sampled and no arteriovenous differences were found. Plasma ANP concentration in the pulmonary artery was greater than in peripheral venous blood but there was a strong correlation between the two.3. The concentration of NPY‐LI and ANP in peripheral venous blood reflects central venous and arterial concentrations.
CALCIUM ANTAGONISTS AND HYPERTENSION
Authors: Nayler W. G. , Dillon J. S. , Sturrock W. J. 
Published: June 2007

SUMMARY1. Calcium antagonists, including verapamil, are now used widely in the management of patients with hypertension.2. Six weeks of chronic therapy with verapamil (50 mg/kg per day, orally) to produce a plasma level of 80–100 ng/ml in Sprague‐Dawley rats depletes cardiac noradrenaline (NA) without apparently causing β1 adrenoceptor ‘up’ regulation.3. The effect of verapamil on cardiac NA is rapidly reversed upon verapamil withdrawal.4. Chronic therapy with nisoldipine (100 mg/kg per day, orally) had no effect on cardiac NA.5. Verapamil (50 mg/kg per day, orally) and nisoldipine (100 mg/kg per day, orally) therapy for 6 weeks prevented the time‐dependent increase in systolic blood pressure in SHR rats.6. Binding studies with (—)[3H]‐D888 (desmethoxyverapamil) indicated that the affinity of the phenylalkylamine binding sites is higher in hearts of SHR relative to hearts from age‐matched (25 weeks) WKY and SD, without any change in density.
N‐METHYL‐d‐ASPARTATE RECEPTORS IN THE SPINAL CORD MEDIATE PRESSOR RESPONSES TO STIMULATION OF THE ROSTRAL VENTROLATERAL MEDULLA IN THE RAT
Authors: Mills E. H. , Minson J. B. , Pilowsky P. M. , Chalmers J. P. 
Published: June 2007

SUMMARY1. Activation of bulbospinal neurons projecting from the C1 area of the rostral ventrolateral medulla evokes a pressor response. The nature of the neurotransmitters involved in mediating this response at spinal cord level has not been established.2. Amino acid antagonists were introduced into the spinal subarachnoid space to investigate the role of spinal amino acid receptors in mediating this pressor response in the anaesthetized rat.3. Intrathecal administration of the amino acid receptor antagonists 2‐aminophosphono valeric acid (2APV), γ‐glutamyl glycine, kynurenate or glutamic acid diethylester (GDEE) attenuated the pressor responses to stimulation of the Cl area. These compounds have been shown to antagonize N‐methyl‐d‐aspartate (NMDA) sensitive receptors.4. Intrathecal administration of 2APV significantly attenuated the increase in blood pressure produced by injection of NMDA into the spinal subarachnoid space.5. These results suggest that the pressor response produced by stimulation in the area of the Cl neurons in the rostral ventrolateral medulla of the rat is mediated at least in part by NMDA receptors in the spinal cord.