bluuebunny/crossref_metadata_2025_split huggingface dataset:
BUPRENORPHINE AND GASTROINTESTINAL TRANSIT IN RATS: EFFECT OF NALOXONE ON THE BIPHASIC DOSE‐RESPONSE CURVE
Authors: Cowan Alan 
Published: June 2007

SUMMARY1. Buprenorphine (0.01–10 mg/kg, subcutaneous [s.c.]) slowed the passage of a charcoal meal along the gastrointestinal tract in rats. The dose‐response relationship was U‐shaped.2. When rats were pretreated with naloxone (0.30 mg/kg, s.c), both the descending and ascending components of the buprenorphine dose‐response curve were displaced to the right.3. Buprenorphine‐induced delay of transit was maximal at a dose of 0.10 mg/kg. In rats pretreated with naloxone, a 30‐fold higher dose of buprenorphine was required for a comparable peak effect.4. Moderate‐high doses of buprenorphine may be acting on a functionally related binding site which non‐competitively inhibits the usual buprenorphine‐μ opioid receptor interaction.
AMRAD: THE FIRST 4 YEARS
Authors: Grace John P. 
Published: June 2007

SUMMARY1. AMRAD (Australian Medical Research and Development) Corporation is a Melbourne biomedical research and development based pharmaceutical company that has successfully completed the first 4 years of its activities.2. The success of the company is a result of a number of factors including the association with world class medical research institutes, adequate seed capital and sound management skills.
INHIBITION OF NO SYNTHESIS HAS AN ADDITIVE EFFECT ON HYPERTENSION INDUCED BY ACTH IN CONSCIOUS RATS
Authors: Li Ming , Dusting G. J. , Whitworth Judith A. 
Published: June 2007

SUMMARY1. The haemodynamic and metabolic effects of oral intake of ∼30 mg/kg per day N‐nitro‐l‐arginine (NOLA) were examined in sham and adrenocorticotrophin (ACTH, 0.5 mg/kg per day) treated conscious Sprague‐Dawley rats (n= 33).2. NOLA administration produced an increase in systolic blood pressure of 24±6 mmHg (P < 0.001), but did not alter food or water intake, urine volume or electrolyte excretion in rats not treated with ACTH.3. Compared with sham injection, ACTH‐treated rats demonstrated an increase in systolic blood pressure (water + sham, 3±1 mmHg; water + ACTH, 16±3 mmHg; P < 0.001), loss of bodyweight, and increases in water intake and urine volume.4. The magnitude of the blood pressure rise in ACTH‐treated rats was greater in those receiving NOLA than in those drinking water only (water + ACTH, 16±3 mmHg; NOLA + ACTH, 37±3 mmHg; P < 0.05). Metabolic changes were similar.5. Inhibition of nitric oxide is unlikely to be a major determinant of ACTH‐induced hypertension in the rat, since NOLA increased blood pressure whether or not ACTH was administered, indicating an additive effect of ACTH and NOLA administration.
ANGIOTENSIN‐CONVERTING ENZYME INHIBITION CAUSES DETERIORATION IN RENAL FUNCTION IN ONE‐KIDNEY GOLDBLATT HYPERTENSIVE RATS WITH AND WITHOUT RENAL ARTERIAL STENOSIS
Authors: Huang Wann‐Chu , Wu Jian‐Nan , Jin Jong‐Shiaw 
Published: June 2007

SUMMARY1. The renal and hypotensive effects of a new angiotensin‐converting enzyme (ACE) inhibitor, cilazapril, were evaluated in 18 one‐kidney, one‐clip Goldblatt hypertensive rats (1K1C), 10 one‐kidney normotensive rats (1K) and eight 1K1C rats with acute unclipping (1KU). Cilazapril was infused intravenously (25 μg/kg per min) into anaesthetized rats, and the arterial blood pressure (BP) and renal clearance of rats were measured.2. In 1K rats, cilazapril reduced BP from 123 ± 4 to 117 ± 4 mmHg (P < 0.05), and produced diuresis, natriuresis and kaliuresis without significantly changing glomerular filtration rate (GFR).3. In 1K1C rats, cilazapril significantly reduced BP (from 157 ± 5 to 143 ± 6 mmHg; P < 0.05), GFR (14.4 ± 6.7%), urine flow (27.1 ± 8.5%) and sodium excretion (39.4 ± 7.4%). Mechanically graded reductions of renal arterial pressure alone also produced parallel decreases in GFR and renal excretory function.4. In 1KU rats, removal of the renal arterial clip significantly decreased BP and increased renal function. Subsequent infusion of cilazapril further reduced BP and urinary excretions of sodium and water but did not significantly change GFR.5. These results suggest that the renal function of the 1K1C hypertensive model is pressure‐dependent, and that ACE inhibitor exerts a mild antihypertensive effect but causes a pressure associated reduction in renal function. Furthermore, the detrimental effect of ACE inhibitor on the residual kidney persists after acute surgical correction of the stenosis.
RESPONSE OF PLASMA RENIN‐ANGIOTENSIN SYSTEM TO A SINGLE CAPTOPRIL ADMINISTRATION IN PATIENTS RECEIVING LONG‐TERM TREATMENT WITH CAPTOPRIL
Authors: Iwata Takeru , Dazai Yasunobu , Kitami Yutaka , Muneta Shinjiro , Imamura Yoichi , Murakami Eiki , Hiwada Kunio 
Published: June 2007

SUMMARY1. The responses of angiotensin II (AII), AIII, aldosterone and plasma renin activity (PRA) to a single dose of captopril were investigated in hypertensive patients receiving long‐term (more than I year) captopril therapy (CT patients) and compared with those of non‐treated hypertensive patients (NT patients).2. Baseline levels of AII and aldosterone were significantly lower in CT patients than in NT patients. AM tended to be lower and PRA was slightly higher in CT than in NT patients, but these differences were not significant.3. A single administration of captopril (50 mg orally) significantly decreased plasma levels of AII, AIII and aldosterone as well as blood pressure in both CT and NT patients.4. These results demonstrate that chronically repeated administration of captopril to hypertensive patients effectively reduces the daily blood pressure and concomitantly the plasma AII level to acceptable levels in patients with no experience of ACE inhibition.
IN VIVO AND IN VITRO EFFECTS OF ATRIAL NATRIURETIC PEPTIDE ON RENIN RELEASE
Authors: Ishimitsu Toshihiko , Hirata Yasunobu , Matsuoka Hiroaki , Ishii Masao , Sugimoto Tsuneaki , Kangawa Kenji , Matsuo Hisayuki 
Published: June 2007

SUMMARY1. This study investigated the effect of atrial natriuretic peptide on renin release from the kidney. The in vitro direct effect was examined in the animal experiment using renal cortical slices of rat, and the in vivo effect was observed in the human infusion study.2. In the in vitro experiments, α‐human atrial natriuretic peptide (α‐hANP) ranging 10−9 to 10−6 mol/L did not change the basal renin release rate from the renal cortical slices (∼9% at 10−6 mol/L, NS). Isoproterenol (10−6 mol/L) increased renin release by 40% (P < 0.001), whereas angiotensin II (10−6 mol/L) suppressed it by 48% (P < 0.001). However, α‐hANP did not affect the stimulative effect of isoproterenol or the inhibitory effect of angiotensin II.3. Also in the human study, infusion of 25 ng/kg per min α ‐hANP failed to change the plasma renin activity in normotensive subjects (–4%) or patients with essential hypertension (+5%), or even in patients with raised renin levels such as renovascular hypertension (+ 10%) or congestive heart failure (‐13%).4. These results put forth negative views on the direct involvement of atrial natriuretic peptide in renin release from the juxtaglomerular apparatus.
DIFFERENT BIVENTRICULAR REMODELLING OF MYOSIN AND COLLAGEN IN PULMONARY HYPERTENSION
Authors: Ishikawa Shigenori , Honda Masaaki , Yamada Sachiko , Goto Yasutoshi , Morioka Shigefumi , Ishinaga Yuji , Murakami You , Masumura Sumio , Moriyama Katsutoshi 
Published: June 2007

SUMMARY1. To clarify the metabolism of contractile and non‐contractile proteins of the ventricles during the development of right ventricular hypertrophy (RVH) and accompanying congestive heart failure (CHF) in response to a pressure overload, monocrotaline was injected subcutaneously into Sprague‐Dawley (SD) rats. Myosin isoenzymes (MIE) were analysed by pyrophosphate gel electrophoresis under non‐dissociating conditions. Acid‐soluble collagens were analysed by an improved, non‐interrupted sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS‐PAGE). Tissue collagen content was also measured after the estimation of hydroxyproline concentration in tissues.2. Monocrotaline induced RVH, but not left ventricular hypertrophy, at 2 weeks after the injection of monocrotaline, with severe RVH with CHF present at 4 weeks. In the right ventricles (RV) treated with monocrotaline, MIE shifted significantly from V1 to V3 at 2 weeks. The shift of MIE was more pronounced at 4 weeks. The proportion of type III collagen increased significantly compared with controls at 2 weeks. At 4 weeks, the proportion of types III and V collagens increased significantly compared with controls.3. In left ventricles (LV) treated with monocrotaline, a similar but less remarkable shift of MIE was observed without remodelling of collagen types at 2 and 4 weeks. The concentration of collagen in either the RV or LV treated with monocrotaline showed no significant changes at 2 and 4 weeks compared with controls.4. These results demonstrate a remodelling of the contractile and non‐contractile proteins during the development of RVH and accompanying CHF, and provide evidence for changes in protein metabolism of the counterpart of RV (i.e. the LV). These results may provide important insights into the pathophysiology of adaptive or non‐adaptive cardiac hypertrophy in response to a pressure overload.
AFFERENT CONTROL OF VASOPRESSIN AND RENIN RELEASE DURING HAEMORRHAGE IN NORMAL AND AUTONOMICALLY BLOCKED RABBITS
Authors: Courneya Carol‐Ann , Korner Paul I. , Oliver Judith R. , Woods Robyn L. 
Published: June 2007

SUMMARY1. The role of the arterial and cardiac baroreceptors on the arginine vasopressin (AVP) and plasma renin activity (PRA) responses to haemorrhage was studied in conscious rabbits. They were bled at a rate of approximately 3% of their blood volume (BV)/min, both when the autonomic nervous system (ANS) was intact and during ANS blockade, which markedly enhances the AVP response due to the much greater haemodynamic disturbance. Under each condition of ANS function 2×2 factorial analysis was performed, each with four groups of rabbits, including animals with both sets of baroreceptors working, one or other set working and neither set working.2. With intact ANS, haemorrhage had to be terminated at different times in the four groups. This presents problems for factorial analysis due to differences in the relationship between plasma AVP (or PRA) and release rate. A method for overcoming this was developed by extrapolating the BV‐log AVP curves to a common time from the start of bleeding.3. Under both conditions of ANS function the arterial and cardiac baroreceptors together accounted for 90‐95% of the rise in AVP during haemorrhage. With normal ANS function, the rise in AVP was about 70% through cardiac (probably ventricular) baroreceptors (P= 0.01) and about 30% through arterial baroreceptors (P= 0.08). This compares with an earlier study at a rate of bleeding of 1.8% BV/min, where the entire drive came from the cardiac receptors. During ANS blockade, plasma AVP was enhanced approximately five‐fold, which was mostly mediated through the arterial baroreceptors, but the cardiac baroreceptor component was also greater; arterial/cardiac baroreceptor drive was 2/1.4. Baroreflexes played no role in renin release during haemorrhage, but the experiments with ANS blockade suggest that a hormonal factor, which was related to the cardiac innervation, may limit the rise in PRA in the latter part of haemorrhage.
CARDIAC β‐ADRENOCEPTOR CHANGES IN EXPERIMENTAL HYPERTHYROIDISM IN DOGS
Authors: Hoey Andrew , Brown Lindsay , Marchant Catherine , Atwell Rick , Sernia Conrad 
Published: June 2007

SUMMARY1. Triiodothyronine (T3; 1.0 mg/kg per day subcutaneously) was administered to 10 dogs for 14 days; 10 saline‐treated dogs served as controls. T3‐treated dogs showed the expected physiological responses of hyperthyroidism; further, chronotropic responses to isoprenaline in vivo were significantly increased in T3‐treated dogs.2. β‐Adrenoceptor subtype density was measured in membrane preparations by displacement of l25I‐iodocyanopindolol binding by the selective β2‐adrenoceptor antagonist, ICI 118, 551. T3 treatment led to a 93% increase in right atrial β1‐adrenoceptor density and a 141% increase in left ventricular β1‐adrenoceptor density; β2‐adrenoceptor densities in right atrial, left ventricular and lung membranes were unchanged.3. T3‐treatment did not change basal or maximally stimulated adenylate cyclase activities in left ventricular membranes.4. Thus, the cardiovascular changes in experimental hyperthyroidism in dogs were accompanied by an increased chronotropic response in vivo to isoprenaline and an increased β1‐adrenoceptor density in atrial and ventricular membranes. However, there was no corresponding change in basal or maximal responsiveness of adenylate cyclase in ventricular membranes.
EPITHELIAL DISRUPTION BY PROTEASES AUGMENTS THE RESPONSIVENESS OF PORCINE BRONCHIAL SEGMENTS
Authors: Taher I , Sparrow Malcolm P. 
Published: June 2007

SUMMARY1. The effect of disruption to the epithelium of intact porcine bronchi was examined by comparing the responsiveness to agonists applied to the adventitial and luminal surfaces. The development of smooth muscle tone was measured as an increase in pressure in an isovolumic bronchial segment of approximately 2 mm i.d. The reactivity and sensitivity to acetylcholine (ACh) introduced intraluminally was greatly attenuated when compared with adventitial addition.2. Luminal exposure to K+ and vanadate (VO3) had little effect compared with strong responses obtained by adventitial application.3. Intraluminal exposure to trypsin, chymotrypsin and elastase (1 mg/mL) selectively augmented both the sensitivity and the reactivity to the luminal addition of ACh, K+ and carbachol.4. Mechanical removal of the epithelium produced a 716‐fold increase in sensitivity to ACh introduced luminally but had no effect on ACh applied adventitially.5. The inhibitory effects of luminally introduced isoprenaline on electrical field stimulation responses were also significantly potentiated in segments stripped of epithelium.6. The evidence presented here indicates that the responsiveness of in vitro airways segments is highly influenced by the epithelial layer, which acts most prominently as a barrier inhibiting the penetration of luminally introduced agonists.
INFLUENCE OF CIMETIDINE ON GALLAMINE‐INDUCED NEUROMUSCULAR PARALYSIS IN RATS
Authors: Mishra Yogendra , Ramzan Iqbal 
Published: June 2007

SUMMARY1. The effect of cimetidine on gallamine‐induced neuromuscular paralysis was evaluated in urethane‐anaesthetized and mechanically ventilated rats.2. Intravenous cimetidine (between 3.2 and 100 mg/kg) produced an immediate and sustained potentiation of gallamine‐induced neuromuscular paralysis.3. Intravenous calcium (0.35 mmol/kg) completely reversed the cimetidine‐induced potentiation of gallamine's effect.4. Cimetidine alone did not produce neuromuscular paralysis.5. Cimetidine did not alter either the serum concentration or the total serum clearance of gallamine.6. Cimetidine thus potentiates the action of gallamine via a pharmacodynamic and not a pharmacokinetic mechanism.
DIRECT RENAL EFFECTS OF ENDOTHELIN IN CHRONIC HYPOXIC SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Chen C. F. , Chien C. T. , Wu M. S. 
Published: June 2007

SUMMARY1. The direct renal effects of endothelin (ET) were studied in eight chronic hypoxic rats (HA) and eight sea level (SL) spontaneously hypertensive rats (SHR).2. After 4 weeks of exposure to simulated 5486 m (18000 ft) hypoxia, all HA rats were in apparently good health, and baseline renal function, except effective renal blood flow, was not significantly different from SL rats.3. Intrarenal arterial administration of ET (600 ng/ kg per h) reduced ipsilateral renal excretion of water, sodium and potassium, glomerular filtration rate and effective renal plasma flow in both SL and HA rats to almost the same extent.4. Administration of ET antiserum, however, increased the renal excretion of water in HA rats.5. It is concluded that ET may play a role in the renal regulation of chronic hypoxic SHR.
EFFECTS OF NOISE ON BLOOD PRESSURE AND VASCULAR REACTIVITIES
Authors: Wu Chin‐Chen , Chen Shiu‐Jen , Yen Mao‐Hsiung 
Published: June 2007

SUMMARY1. The present study investigated the effects of noise stress (100 dB, 1 kHz, 4 h/day, 6 days/ week) on both systolic blood pressure and vascular reactivities in rats exposed to noise for 2 and 4 weeks. The systolic blood pressure was significantly increased after rats were exposed to noise for 4 weeks but not 2 weeks.2. In isolated thoracic aortic rings, the responses to serotonin were enhanced in noise‐treated rats while there were no changes in response to phenylephrine and high K4between noise‐treated and control rats.3. The relaxant responses to endothelium‐dependent vasodilators (A23187 and acetylcholine) in noise‐treated rats were less than those in control rats. The vasodilator responses to acetylcholine were completely abolished by methylene blue or Nω‐nitro‐L‐arginine.4. Responses to the endothelium‐independent vasodilator, nitroglycerin, were not significantly changed after rats were exposed to noise.5. The enhanced response to vasoconstrictors and the attenuation to endothelium‐dependent vasodilators may account for elevations in blood pressure during noise stress. This indicates that the elevation in blood pressure by noise stress may be partly due to the deterioration of endothelial function.
THE EFFECTS OF THYROXINE TREATMENT ON SLOW‐ AND FAST‐CONTRACTING SKELETAL MUSCLE CONTRACTIONS OF THE CAT AND THEIR CYCLIC AMP LEVEL
Authors: Merican Zainuddin , Sukumaran S. , Raj Vijaya Lechimi , Rajikin Mohd Hamim , Khalid B. A. K. 
Published: June 2007

SUMMARY1. The effects of thyroxine treatment on soleus and extensor digitorum longus (EDL) muscle contractions and their cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) levels were examined in anaesthetized cats.2. Thyroxine treatment decreased the tension of incomplete tetanic contractions of the soleus as well as the EDL muscles. The effect on tension of these muscles was not associated with an increase in the cyclic AMP level of the muscle as is the case with a β2‐adrenoceptor agonist effect.3. The results do not support the involvement of cyclic AMP in the tension depressant effect of thyroxine on contractions of skeletal muscle.4. It is suggested that the muscle weakness and tremor observed in thyrotoxicosis and during administration of β‐adrenoceptor agonists are mediated by different mechanisms.
INCREASED Na+/H+ EXCHANGE ACTIVITY IN VASCULAR SMOOTH MUSCLE CELLS OF SPONTANEOUSLY HYPERTENSIVE RATS AND POSSIBLE INVOLVEMENT OF PROTEIN KINASE C
Authors: Inariba Hiromi , Kanayama Yoshiharu , Takaori Kazuo , Negoro Nobuo , Inoue Takatoshi , Takeda Tadanao 
Published: June 2007

SUMMARY1. Na+ influx into cultured vascular smooth muscle cells (VSMC) obtained from spontaneously hypertensive rats (SHR) and from Wistar‐Kyoto rats (WKY) was measured. Na+ influx via the Na+/H+ exchange system was measured as the rate of 22Na+ influx into cultured VSMC sensitive to ethylisopropylamiloride (EIPA), a specific inhibitor of the exchange system.2. The total 22Na+ influx rate in SHR was significantly higher than in WKY (6.08 ±0.16 vs 4.13±0.09 nmol/min per mg protein; P < 0.001; n= 14). The EIPA (1 × 104 mol/L)‐sensitive 22Na+ influx rate in SHR was significantly higher than that in WKY (4.32 ± 0.27 vs 2.17 ± 0.14 nmol/min per mg protein; P < 0.001; n= 14). There was no difference in EIPA‐insensitive 22Na+influx between SHR and WKY. The EIPA‐sensitive 22Na+ influx rate into VSMC was significantly decreased in SHR but not in WKY by the addition of 1 × 10 ‐4 mol/L 1‐(5‐isoquinoline‐sulfonyl)‐methylpiperazine (H‐7), an inhibitor of protein kinase C (PK‐C).3. These results suggest that the increase in Na+ influx in SHR may be due to elevation of the Na+/H+ exchange activity, and possible involvement of PK‐C in the increased Na+/H+ exchange activity in VSMC from SHR.
CARDIOVASCULAR HABITUATION TO EMOTIONAL STRESS IN LYON HYPERTENSIVE RATS
Authors: Julien Claude , Sacquet Joëlle , Kandza Patrice , Su Ding‐Feng , Vincent Madeleine , Barrés Christian 
Published: June 2007

SUMMARY1. Intra‐aortic blood pressure was recorded continuously in freely moving genetically hypertensive (LH), normotensive (LN) and low blood pressure (LL) rats of the Lyon strain during two 11 h periods (08:00‐19:00 h). During the first period (control), the animals were left undisturbed and during the second period (stress), a jet of air was applied for 20 min every hour. Urine was collected simultaneously and analysed for its content in norepinephrine and epinephrine.2. The first exposure to the stressor induced larger increases in blood pressure and heart rate in LH than in LN and LL rats. However blood pressure and heart rate responses to the 10 following stressors decreased in LH rats while they remained stable in LN and LL animals.3. Repeated stress exposure induced significant increases in epinephrine excretion in both LN and LL but not in LH rats.4. It is concluded that LH rats exhibit marked cardiovascular habituation to repeated stress. Taken together with the lack of stress‐induced sympathoadrenal activation, this suggests a reduced level of emotional responsiveness in Lyon hypertensive rats.
INCREASED SENSITIVITY TO ENDOTHELIN‐1 IN ISOLATED KREBS‐PERFUSED KIDNEYS OF STREPTOZOTOCIN‐DIABETIC RATS
Authors: Tammesild Paul J. , Hodgson Wayne C. , King Roger G. 
Published: June 2007

SUMMARY1. Vascular responses to endothelin‐1 (ET‐1) and noradrenaline (NA) were measured in isolated Krebs'‐perfused kidneys of 2 week old streptozotocin‐diabetic and non‐diabetic rats.2. Bolus injections of either ET‐1 or NA caused dose‐dependent increases in perfusion pressure. Responses to ET‐1 (10–60 ng/g kidney), but not to NA (0.001–10 μg/g kidney), were significantly potentiated in kidneys of diabetic rats compared with non‐diabetics.3. Indomethacin significantly attenuated responses to NA (0.3–10 μg/g kidney) in kidneys of both diabetic and non‐diabetic rats.4. Neither indomethacin (1 μmol/L) nor the cyclo‐oxygenase/lipoxygenase inhibitor BW755C (1 μmol/L) had any significant effect on the log dose‐response curve to ET‐1 in either group of kidneys.5. Perfusion with N‐nitro‐L‐arginine (NOLA; 10 μmol/L) had no effect on basal perfusion pressures, but potentiated responses to ET‐1 in both groups of kidneys. However, the difference in responses to ET‐1 between kidneys from diabetic and non‐diabetic rats remained significant in the presence of NOLA.6. ET‐1 responses were inhibited in Ca2+‐free Krebs’ solution (plus 1 mmol/L EGTA).7. The results of the present study indicate an increased sensitivity to ET‐1 in isolated Krebs'‐perfused kidneys of diabetic rats. Responses to ET‐1 were unaffected by cyclo‐oxygenase and/ or lipoxygenase inhibitors, but were potentiated by an endothelium‐derived relaxing factor (EDRF) synthesis inhibitor.
ENALAPRIL DECREASES PLASMA NORADRENALINE LEVELS DURING THE COLD PRESSOR TEST IN HUMAN HYPERTENSIVES
Authors: Minatoguchi Shinya , Ito Hiroyasu , Koshiji Masatoshi , Masao Kakami , Hirakawa Senri , Majewski Henryk 
Published: June 2007

SUMMARY1. The effects of the angiotensin‐converting enzyme (ACE) inhibitor enalapril on the responses of blood pressure and plasma catecholamine levels to the cold pressor test in human hypertensives were examined.2. Systolic and diastolic blood pressure decreased significantly after treatment with enalapril (5 mg/ day for 4 weeks) as did the resting level of plasma noradrenaline.3. The cold pressor test induced a rise in blood pressure and plasma noradrenaline levels. After 2 and 4 weeks enalapril treatment, the rises in the plasma noradrenaline level and systolic and diastolic pressure due to cold pressor test were reduced significantly.4. These results suggest that ACE inhibition has a sympatho‐inhibitory effect. One possible explanation is that enalapril reduces angiotensin II formation thus decreasing the activation of release‐enhancing angiotensin II receptors on postganglionic sympathetic nerve endings.