bluuebunny/crossref_metadata_2025_split huggingface dataset:
DUAL MODES OF ACTION FOR DISODIUM CROMOGLYCATE IN INHIBITION OF ANTIGEN‐INDUCED CONTRACTIONS OF GUINEA‐PIG ISOLATED AIRWAYS SMOOTH MUSCLE
Authors: Stewart A. G. , Fennessy M. R. 
Published: June 2007

SUMMARY1. Disodium cromoglycate (DSCG; 10 μmol/l‐1 mmol/l) relaxed the tone induced in the guinea‐pig isolated trachea by histamine (5 μmol/l). Both isoprenaline and fenoterol were approximately 1000 times more potent than DSCG in relaxing tracheal smooth muscle.2. Ovalbumin (1 μg/ml) contracted isolated tracheal and parenchymal strips from sensitized guinea‐pigs. The sensitization procedure used was selective for eliciting IgG antibody production.3. In concentrations equieffective for relaxation of the isolated trachea, fenoterol (20 nmol/l), isoprenaline (60 nmol/l) and DSCG (100 μmol/l) inhibited ovalbumin‐induced contractions of both tracheal and parenchymal strip preparations.4. DSCG produced a significantly greater (P < 0.05) inhibition of ovalbumin‐induced contractions of isolated trachea than did isoprenaline, suggesting that at 100 μmol/l DSCG produced a greater inhibition of mediator release than that produced by isoprenaline.5. Compound 48/80 (200 μg/ml) contracted the isolated trachea whereas this concentration had no contractile effect on the parenchymal strip. The failure of DSCG to inhibit compound 48/80 induced contractions of the isolated trachea together with the lack of contractile effect of compound 48/80 on the parenchymal strip suggest that compound 48/80 is inferior to antigenic stimulation as a reliable analogue of immunological activation of mast cells and consequent mediator release.6. On the basis of DSCG‐induced relaxation of the isolated trachea and greater inhibition of ovalbumin‐induced contractions relative to that produced by isoprenaline, it is concluded that DSCG has dual modes of action in inhibition of antigen‐induced contraction of isolated airways smooth muscle, that is, DSCG produced functional antagonism of antigen‐induced mediators in addition to inhibiting mediator release.
A STUDY OF STIMULATION‐EVOKED ACTIVATION OF α2‐ADRENOCEPTORS IN THE RAT ISOLATED VAS DEFERENS
Authors: Pennefather Jocelyn N. 
Published: June 2007

SUMMARY1. Experiments were performed with prostatic and epididymal segments of rat vas deferens to determine whether α2‐adrenoceptors in this organ were activated during field stimulation of sympathetic terminals with short trains of pulses applied at low frequencies.2. In prostatic segments the magnitude of twitches evoked by trains of ten field pulses at 1 or 2 Hz declined after 2–3 s of stimulation. In contrast, facilitation of twitches and fusion of contractions occurred when similar stimulation was applied to epididymal segments.3. In prostatic segments from rats treated with reserpine (2.5 mg/kg i.p.) 24 h previously, there was no decline in the magnitude of twitches produced by successive impulses in a train of stimulating pulses. In epididymal segments from reserpine‐treated rats facilitation of twitches in response to successive impulses in each train still occurred.4. In prostatic segments cocaine (5 and 10 μmol/1) enhanced twitch fade with stimulation at 1 and 2 Hz without altering the time for onset of this effect. In epididymal segments cocaine led to enhancement and prolongation of contractile responses.5. In prostatic segments yohimbine (0.01–0.06 μmol/l) reduced or reversed the effect of cocaine in enhancing twitch fade. In preparations where the reversal of the effect of cocaine by yohimbine was incomplete, subsequent addition of phentolamine (1 μmol/l) produced complete reversal.6. In epididymal segments yohimbine (0.01 μmol/l) produced a further enhancement in the twitch responses to stimulation at 1 and 2 Hz. Subsequent addition of phentolamine (1 μmol/l) reversed the facilitatory effects of cocaine and yohimbine.7. Propranolol (10 μmol/l) was without effect upon responses to stimulation in either segment of rat vasa deferentia.8. These experiments indicate that noradrenaline, released by short trains of impulses applied at low frequency to hypogastric nerve terminals activates prejuctional α2‐adrenoceptors in the prostatic segment of the vas deferens. In the epididymal portion the effects arising from activation of prejunctional α2‐adrenoceptors are outweighed by the consequences of activation of extrajunctional α1‐adrenoceptors located on longitudinally arranged muscle.
SECRETORY AND VASCULAR EFFECTS OF THE OPTICAL ISOMERS OF NICARDIPINE
Authors: Iwatsuki K. , Iijima F. , Chiba S. 
Published: June 2007

SUMMARY1. The effects of optical isomers of nicardipine on the secretion of pancreatic juice and blood flow were investigated in the dog‐isolated, blood‐perfused pancreas.2. Intra‐arterial administration of (‐)‐nicardipine (10–300 μg) caused a dosedependent increase in pancreatic secretion. However, the (+)‐isomer was much less potent than the (‐)‐isomer and even in 300 μg of (+)‐isomer caused only a slight secretion.3. (+)‐ And (‐)‐nicardipine increased perfusion blood flow in a dose‐dependent manner, and (+)‐nicardipine was approximately five times as potent as the (‐)‐isomers. The maximum increase in a flow rate was produced by 30 μg of (+)‐isomer and 100 μg of (‐)‐isomer.4. Bicarbonate concentration in pancreatic juice induced by (‐)‐ and (+)‐nicardipine was increased in a dose‐dependent manner, but the protein concentration was only increased slightly.5. From these results, it is concluded that there is a stereoselectivity in the secretory and vascular actions of optical isomers of nicardipine.
EFFECTS OF Δ1 AND Δ6‐TETRAHYDROCANNABINOL ON THE ADENYLATE CYCLASE ACTIVITY IN VENTRICULAR TISSUE OF THE RAT HEART
Authors: Li D. M. F. , Ng Camay K. M. 
Published: June 2007

SUMMARY1. Adrenaline 1 μg markedly elevated the activity of adenylate cyclase in ventricular tissue of rat hearts.2. Δ1‐THC 25, 50 and 100 μg significantly reduced the adenylate cyclase activity with the maximum effect observed with the dose or 25 μg. Doses below or above this range did not produce any significant effect on the enzyme activity.3. Neither Δ6‐THC 25 and 100 μg nor PVP 400 μg had any significant action on adenylate cyclase.4. The Δ1‐THC‐induced lowering of the cyclic AMP concentration in ventricular tissue of rat hearts can be explained, at least partly, by its ability to reduce the activity of adenylate cyclase in these tissues. It is suggested that this enzyme inhibition underlies the cardiac depressant action of Δ1‐THC.
CARDIAC HYPERTROPHY IN THE ABSENCE OF PRESSURE OVERLOAD: AN EXPERIMENTAL AND CLINICAL REPORT
Authors: Genovese Arturo , Latte Salvatore , Betocchi Sandro , Bozzaotre Mariano , Giunta Anna , Chiariello Massimo 
Published: June 2007

SUMMARY1. A simulated altitude of 7000 m was applied in rats chronically exposed to hypoxia in a hypobaric chamber. In these experimental conditions the contralateral ventricle not exposed to pressure overload (that is, the left) showed a significant degree of hypertrophy. The hypoxic stimulus did not affect systemic artery pressure or the heart rate.2. Chronic adrenergic stimulation performed in the rat treated with low doses of isoprenaline (a direct stimulating adrenergic drug) or with tyramine (primarily a releaser of endogenous catecholamines) induced hypertrophy of the right ventricle, left ventricle, and interventricular septum without modifying the haemodynamic parameters mentioned above.3. The development of ventricular hypertrophy in the absence of pressure overload is stressed.4. A role for neurohumoral factors (that is, adrenergic stimulation and catecholamines) in the development of ventricular hypertrophy is suggested.
STUDIES ON THE MECHANISM OF ACTION OF THE HYPOTENSIVE EFFECT OF KETANSERIN
Authors: Marwood John F. , Stokes Gordon S. 
Published: June 2007

SUMMARY1. Ketanserin, 0.01–3.0 mg/kg i.v., was found to cause a dose‐related fall in blood pressure in anaesthetized rats. However, these decreases were only significant after 1 and 3 mg/kg doses. Subsequent administration of prazosin, 0.2 mg/kg i.v., had no significant effect on blood pressure.2. In the presence of ketanserin 3 mg/kg, plus prazosin 0.2 mg/kg, adenosine caused a significant dose‐dependent fall in blood pressure in anaesthetized rats.3. Methysergide, 1 mg/kg i.v., significantly attenuated the blood pressure responses to serotonin in anaesthetized rats whereas ketanserin (1 and 3 mg/kg) had no overall effect on serotonin responses.4. Ketanserin, 1 and 3 mg/kg i.v., was found to antagonize the pressor effects of phenylephrine and reverse the pressor effects of adrenaline in anaesthetized rats. Responses to angiotensin II were not significantly affected by ketanserin.5. These results suggest that ketanserin lowers blood pressure in anaesthetized rats by blockade of α‐adrenoceptors.
EFFERENT MECHANISMS RESPONSIBLE FOR THE BRADYCARDIA PRODUCED BY LESIONS COINCIDING WITH THE A1 GROUP OF CENTRAL CATECHOLAMINE NEURONS IN THE CONSCIOUS RABBIT
Authors: Denoroy Luc , West Malcolm J. , Chalmers John 
Published: June 2007

SUMMARY1. The effector mechanisms responsible for the bradycardia evoked by bilateral lesions of the brainstem coinciding with the A1 catecholamine cells were analyzed in four groups of rabbits. Sham or lesion operations were carried out in animals with intact cardiac effectors, with cardiac sympathetic block induced by propranolol, with cardiac vagal block induced by methylscopolamine and with total cardiac autonomic block induced by the use of both drugs together.2. Lesions produced a transient increase in blood pressure of 25 (s.e.m. =4) mmHg and a transient bradycardia, or increase in heart period of 141 (s.e.m. =18) ms. The bradycardia had both baroreflex‐independent and baroreflex‐dependent components as determined from analysis of stimulus response curves relating heart period to mean arterial pressure.3. The ‘baroindependent’ component of the bradycardia, measured as a lengthening in heart period, ranged from 35–49 ms in the four groups of animals and was unaffected by administration of propranolol alone, methylscopolamine alone, or of both together. These findings suggest that the baroindependent slowing of the heart is not mediated through changes in activity of either the cardiac sympathetic nerves or of the vagal fibres innervating the heart.4. The ‘baroreceptor’ component of the bradycardia reflects that portion of the decrease in heart rate resulting directly from the increase in blood pressure. This component was found to account for a lengthening in the heart period of 81 (s.e.m. =23) ms in animals with intact effector mechanisms: it was virtually abolished by methylscopolamine (0 ms, s.e.m. =13) but not significantly affected by propranolol (54 ms, s.e.m. =25), indicating that this barodependent component is predominantly mediated through the vagus.
HAEMODYNAMIC AND HORMONAL EFFECTS OF PRAZOSIN ON HEAD‐UP TILT IN ESSENTIAL HYPERTENSIVE PATIENTS: COMPARISON WITH THOSE OF PROPRANOLOL
Authors: Kida Osamu , Morotomi Yasuyuki , Higa Toshinobu , Kodama Kenji , Someya Noriyuki , Tanaka Kenjiro 
Published: June 2007

SUMMARY1. To evaluate the haemodynamic and hormonal effects of prazosin, head‐up tilt was performed in 10 essential hypertensive patients, and these effects of prazosin on the tilt were compared with those of propranolol. The tilts were performed in control phase and the last days of treatment for two weeks with propranolol (90 mg/day) or prazosin (3–6 mg/day).2. Each drug significantly lowered the mean blood pressure at rest, and also suppressed its rise on the tilt. Heart rates were significantly increased by the tilt in the control phase, in the propranolol phase and in the prazosin phase. Cardiac index was significantly reduced by the tilt from 2.66 (s.e.m. =0.22) 1/min per m2 to 2.08 (s.e.m. =0.20) in the propranolol phase. However, there were not significant changes in other phases. Total peripheral resistance indices were significantly increased by the tilt in all three phases. Plasma renin activity and plasma aldosterone were significantly increased by the tilt from 2.14 (s.e.m. =0.47) ng/ml per h to 2.46 (s.e.m. =0.54) and from 50.6 (s.e.m. =12.9) pg/ml to 74.9 (s.e.m. =14.9) respectively, in the control phase. And they were also significantly increased from 1.06 (s.e.m. =0.29) to 1.65 (s.e.m. =0.45) and from 41.4 (s.e.m. =16.3) to 54.0 (s.e.m. =17.4) in the prazosin phase. There were no significant increases during the administration of propranolol.3. We observed that prazosin did not alter heart rate and cardiac index, but suppressed the renin‐angiotensin system at rest. It is suggested that prazosin did not influence haemodynamic and hormonal responses to the tilt.
ACUTE EFFECTS OF COLD ON BLOOD PRESSURE, RENIN‐ANGIOTENSINALDOSTERONE SYSTEM, CATECHOLAMINES AND ADRENAL STEROIDS IN MAN
Authors: Hiramatsu Kunihide , Yamada Takashi , Katakura Masafumi 
Published: June 2007

SUMMARY1. In an attempt to study effects of cold on blood pressure and the reninangiotensin‐aldosterone system, 34 healthy young subjects with or without a family history of essential hypertension were exposed to moderate cold (4°C for 1 h) or severe cold (immersion of the hands to 0°C for 10 min). Moderate cold elevated blood pressure, aldosterone, cortisol and noradrenaline when the subjects wore summer clothing but not when the subjects wore winter clothing. Regardless of the clothing worn, skin blood flow and plasma renin activity decreased significantly in response to moderate cold but angiotensin II decreased insignificantly.2. Severe cold elevated blood pressure, cortisol, aldosterone and noradrenaline. Administration of dexamethasone significantly depressed an increase of aldosterone and cortisol in response to cold but failed to effect an elevation of blood pressure and noradrenaline. Plasma renin activity and angiotensin II concentration were not affected at all during and after cold exposure.3. It is suggested that, among the various hormones studied, noradrenaline is the only hormone responsible for an elevation of blood pressure in response to cold.
AN IMPORTANT EFFECT OF TSH ON PROSTACYCLIN CONCENTRATION IN PORCINE THYROID CELLS
Authors: Takasu N. , Takahashi K. , Ishigami T. , Shimizu Y. , Yamada T. , Sato S. 
Published: June 2007

SUMMARY1. Fresh thyroid slices obtained from normal pigs contained prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α) and prostacyclin (PGI2, measured as the end metabolite, 6‐keto PGF1α), but the concentrations of PGI2 exceeded those of PGE2 and PGF2α. A preferential increase of PGI2 was produced when the slices were exposed to a large dose of TSH (thyroid‐stimulating hormone).2. When thyroid cells were isolated and cultured in the absence of TSH, thyroidal concentrations of PGI2, PGE2 and PGF2α were about equal. When the cells were acutely exposed to a large dose of TSH, intrathyroidal concentration of prostaglandin increased significantly, but the relative concentrations of prostaglandins were not markedly altered.3. When thyroid cells were cultured in the presence of a small dose of TSH, relative concentrations of thyroidal prostaglandins were comparable to those of fresh thyroid slices, as a result of a preferential increase of PGI2 and decreases of PGE2 and PGF2α. Further increase of PGI2 was induced when the cells cultured with TSH were acutely exposed to a large dose of TSH.4. It is concluded that although cells contain PGE2, PGF2α and PGI2, a preferential accumulation of PGI2 is found only when thyroid cells are chronically stimulated by TSH.
ACTIVITIES OF NAD+‐DEPENDENT ALDEHYDE DEHYDROGENASE AND ALCOHOL DEHYDROGENASE IN THE LIVER OF SPONTANEOUSLY HYPERTENSIVE RATS IN THE PROCESS OF DEVELOPMENT
Authors: Shiohara E. , Tsukada M. , Iwatsuki K. , Iijima F. , Chiba S. 
Published: June 2007

SUMMARY1. The difference in the basal activities of NAD+‐dependent aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) was investigated in the liver of age‐matched spontaneously hypertensive (SH) and normotensive Wistar Kyoto (WK) rats.2. A significant difference between the SH and WK rats in the basal ALDH activity, ADH activity and the protein content of subcellular fractions was observed. The activities of mitochondrial low Km‐ and high Km‐ALDH in the SH rats at 5–8 weeks of age were higher than those in the WK rats. The microsomal high Km‐ALDH activity in the SH rats at 5 and 11 weeks of age was higher than that in the WK rats. The ADH activities in the SH rats at 5–14 weeks of age were lower than those in the WK rats. The mitochondrial protein content in the SH rats at 5–14 weeks of age was higher than those in the WK rats.3. At 14 weeks of age, an increase in the blood acetaldehyde level was observed after an intraperitoneal injection of 1.5 g/kg of ethanol in the SH rats. No difference in blood ethanol level was observed between the SH and WK rats.
EFFECTS OF BROMOCRIPTINE ON PANCREATIC SECRETION IN THE ISOLATED, BLOOD‐PERFUSED PANCREAS OF THE DOG
Authors: Iwatsuki K. , Iijima F. , Chiba S. 
Published: June 2007

SUMMARY1. Effects of bromocriptine on the secretion of pancreatic juice were investigated with dog isolated, blood‐perfused pancreas.2. Bromocriptine (1–10 mg) caused dose‐dependent increases in the secretion of pancreatic juice. However, bromocriptine did not affect the perfusion blood flow rate. The secretory response to bromocriptine was inhibited by pretreatment with a dopamine antagonist, sulpiride, but not by phentolamine, propranolol, atropine, metiamide, indomethacin or tetrodotoxin.3. Bromocriptine caused a dopamine‐like secretion of the pancreatic juice containing a high concentration of bicarbonate but had little effect on protein output.4. These results suggest that bromocriptine increases pancreatic secretion stimulating directly on pancreatic dopamine receptors.
COMPARISON OF THE REFLEX EFFECTS OF ARTERIAL BARORECEPTORS AND CARDIAC RECEPTORS ON THE HEART RATE OF CONSCIOUS RABBITS
Authors: Ludbrook John 
Published: June 2007

SUMMARY1. The reflex effects on heart rate (HR) of presumptive cardiac receptors have been differentiated from those of the arterial baroreceptors in conscious rabbits by inflating cuffs on the ascending aorta, descending aorta, inferior vena cava and pulmonary artery.2. When the outflow from the right ventricle was progressively impeded the accompanying increase in HR was entirely explicable by unloading of the arterial baroreceptors.3. As the outflow from the left ventricle was progressively impeded there was an initial increase in HR due to unloading of the arterial baroreceptors, followed by a progressive decline. This decline was attributed to a reflex arising from vagallyinnervated receptors in the left side of the heart. The threshold of this cardiac receptor‐HR reflex occurred at a higher level of mean aortic pressure than that at which the effects of the arterial baroreceptors on HR were maximal. Cholinergic (vagal) efferent nerves were responsible for two‐thirds of the decline in HR caused by the reflex.4. The properties of the cardiac receptor‐HR reflex were altered by drugs that affect myocardial contractility. Isoprenaline raised the mean aortic pressure at which the threshold occurred, but lowered the corresponding level of left ventricular end‐diastolic pressure. Propranolol virtually abolished the reflex, even though left ventricular end‐diastolic pressure reached a high level.5. It is concluded that in the conscious rabbit the arterial baroreceptor reflexes normally prevent the threshold of the cardiac receptor‐HR reflex from being attained.
COMPARISON OF THE EFFECTS OF d‐AMPHETAMINE ON FI AND DRL SCHEDULE PERFORMANCE OF SELF‐STIMULATING RATS
Authors: Nalwa V. , Rao P. S. 
Published: June 2007

SUMMARY1. Six rats bar‐pressed for intracranial self‐stimulation in a Skinner box on fixed interval and differential reinforcement of low rate schedules with an interval parameter of 1.3 s.2. After amphetamine timing efficiency was reduced immediately on both the schedules; it recovered after 60 min on the DRL schedule but not within 120 min on the FI schedule. Response rates increased on both the schedules.3. The increased response rates correlated with the low efficiency on the DRL but not on the FI schedule.4. The selective sparing of DRL performance is in line with the similarity between the effects of amphetamine and frontal cortical lesions.
EFFECT OF MEFENAMIC ACID ON PLASMA PROTEIN‐THYROID HORMONE INTERACTION, MONODEIODINATION OF THYROXINE, URINARY EXCRETION OF TRI‐IODOTHYRONINE AND THYROTROPIN REGULATION
Authors: Koizumi Y. , Sato A. , Yamada T. , Inada M. 
Published: June 2007

SUMMARY1. A single oral dose of mefenamic acid significantly depressed plasma thyroxine (T4) within 3 h in man. Similarly, mefenamic acid depressed plasma T4 within 3 h in thyroidectomized, T4‐maintained rats.2. Plasma free fractions of T4 and tri‐iodothyronine (T3) increased significantly after a single oral administration of mefenamic acid in man. In vitro addition of mefenamic acid to plasma also increased the plasma free fraction of T4.3. Three times more T3 was excreted into urine after an acute administration of mefenamic acid.4. In vitro conversion of T4 to T3 by liver homogenate was stimulated when T4 was displaced from plasma binding protein by mefenamic acid.5. Pituitary content of T3 increased when mefenamic acid displaced T4 and T3 from the binding protein. Simultaneously, thyrotropin (TSH) secretion in response to thyrotropin releasing hormone (TRH) was completely blocked by mefenamic acid.6. Prolactin release in response to TRH and luteinizing hormone (LH) and follicle stimulating hormone (FSH) release in response to luteinizing hormone releasing hormone (LH‐RH) were not affected by mefenamic acid.7. It is concluded that mefenamic acid displaces T3 and T4 from their plasma binding protein and more T4 and T3 are available to peripheral tissues for excretion, degradation and TSH regulation.
FURTHER STUDIES ON NEOMYCIN AND EXPERIMENTAL HYPERTENSION
Authors: Fraillon Danielle , Wynne Ken. N. , Funder John W. 
Published: June 2007

SUMMARY1. Acute glucocurticoid (corticosterone) hypertension in the rat is significantly attenuated by neomycin administration (Honour 1981), as is ACTH‐induced hypertension is the same species (Honour & Kent 1981) presumably by altering gut bacterial steroid metabolism.2. The effect on blood pressure of oral neomycin administration was therefore examined in hypertension resulting from administration of a variety of glucocorticoid hormones.3. Neomycin significantly attenuated the elevation of blood pressure following ACTH or corticosterone, as previously shown, or prednisolone 1 mg/day; it did not affect blood pressure in rats given dexamethasone 0.2 mg/day, or cortisol 4 mg twice daily.4. Since the differential effect of neomycin on hypertension parallels neither pressor nor glucocorticoid activity of the administered steroids we propose that it reflects different patterns of enterohepatic handling and metabolism.
VASOCONSTRICTOR EFFECTS OF URIDINE AND ITS NUCLEOTIDES AND THEIR INHIBITION BY ADENOSINE
Authors: Macdonald Graham , Assef Rhonda , Guiffre Ann , Lo Ed 
Published: June 2007

SUMMARY1. Uridine, uridine monophosphate (UMP) and uridine diphosphate (UDP) increased blood pressure when infused into intact anaesthetized rats and had similar effects on the perfusion pressure in the rat isolated perfused kidney.2. In an isolated vascular preparation, the everted rat portal vein, uridine was without effect while UMP and UDP caused log dose‐related increases in contractile work.3. Adenosine infused at a dose of 200 nmol/kg per min blocked the response to uridine in the intact rat, converting it to a depressor response at higher doses, and reduced the response to UMP.4. Uridine may need to be phosphorylated to UMP to act on blood vessels. The two compounds are effective at similar dose ranges and suppress renin secretion in the isolated kidney, while UDP, which is effective at lower doses and stimulates renin secretion, may act by a different mechanism.5. Adenosine competes for membrane transport with uridine but its inhibition of the effects of UMP is consistent with activity at intracellular sites as well.