bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF ARGININE VASOPRESSIN, ANGIOTENSIN II AND ENDOTHELIN‐1 ON THE RELEASE OF BRAIN NATRIURETIC PEPTIDE IN VIVO AND IN VITRO
Authors: Horio Takeshi , Kohno Masakazu , Takeda Tadanao 
Published: June 2007

SUMMARY1. The stimulatory effects of the vasoactive peptides arginine vasopressin (AVP), angiotensin II (AII) and endothelin‐1 (ET‐1) on the release of brain natriuretic peptide (BNP) were investigated in anaesthetized rats and in cultured rat atrial and ventricular cardiocytes.2. A bolus injection of AVP induced a dose‐dependent increase in plasma immunoreactive (ir)‐BNP concentration in rats. AII induced a rapid and transient elevation in the ir‐BNP level, while the increase produced by ET‐1 was long‐lasting. The elevation of the plasma ir‐BNP concentration after stimulation by these three vasoconstrictors appeared to be paralleled by the elevation in mean blood pressure.3. In the in vitro study, the rat atrial and ventricular cardiocytes both secreted ir‐BNP into the medium in a time‐dependent manner. ET‐1 clearly stimulated the secretion of ir‐BNP in both atrial and ventricular cardiocytes. In contrast, AVP and AII had no stimulatory effect in vitro.4. Reverse‐phase high performance liquid chromatography of the rat plasma and culture medium revealed a single major ir‐BNP component that corresponded to synthetic rat BNP‐45.5. These observations indicate that AVP, AII and ET‐1 stimulate the release of ir‐BNP (probably rat BNP‐45) through a change in blood pressure. In addition, ET‐1 may also induce ir‐BNP release through direct stimulation. As a cardiac hormone secreted from ventricles as well as atria, rat BNP may play a role in the regulation of blood pressure against the pressor effects of AVP, AII and ET–1.
DIETARY Ng‐NITR0‐l‐ARGININE INDUCES SUSTAINED HYPERTENSION IN NORMOTENSIVE WISTAR‐KYOTO RATS
Authors: Ikeda K. , Jr O. G. Gutierrez , Yamori Y. 
Published: June 2007

SUMMARY1. Prolonged oral administration of NG‐nitro‐l‐arginine (l‐NNA) for a period of 5 weeks in 8 week old male normotensive Wistar‐Kyoto (WKY) rats n= 10), induced hypertension in all animals. Hypertension was characterized by a sharp initial increase in both systolic blood pressure (SBP) and mean blood pressure (MBP) until the third day (from 126 ± 3 mmHg to 160 ± 6 mmHg and from 95 ± 3 mmHg to 133 ± 6 mmHg, respectively). This was followed by a gradual and steady increase until the fourth week (163 ± 4, 171 ± 3 and 189 ± 8 mmHg for SBP in weeks 1, 2 and 4, respectively; and 135 ± 4, 143 ± 3and 157 ±5 mmHg for MBP in weeks 1, 2 and 4, respectively).2. Intravenously L‐arginine‐HCl (500 mg/kg) administered on the last day of the 5th week abolished the effect of dietary l‐NNA on the arterial blood pressure.3. Dietary l‐NNA‐induced hypertension in WKY rats is easily obtainable and free of any surgical operation, and can be utilized as a new experimental model to further understand the importance of endothelium‐dependent relaxing factor/nitric oxide in blood pressure regulation and to clarify the pathological significance in intact animals where endothelium‐dependent relaxing factor/nitric oxide is functionally involved.
ENHANCEMENT BY ENDOTHELIN‐1 OF THE RELEASE OF CATECHOLAMINES FROM THE CANINE ADRENAL GLAND IN RESPONSE TO SPLANCHNIC NERVE STIMULATION
Authors: Takeuchi Akihiko , Kimura Tomohiko , Satoh Susumu 
Published: June 2007

SUMMARY1. The effect of endothelin‐1 on the release of adrenal catecholamines was examined in anaesthetized dogs.2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz was applied before and after the intravenous injection of endothelin‐1.3. Endothelin‐1 (0.1 and 0.3 μg/kg) significantly enhanced the release of adrenal catecholamines induced by 3 Hz SNS, but did not affect basal release and the release of adrenal catecholamines induced by 1 Hz SNS.4. Endothelin‐1 produced a slight and short‐lasting fall in arterial blood pressure and decreases in adrenal and renal blood flow rates.5. These results indicate that endothelin‐1 enhances the release of adrenal catecholamines from the canine adrenal gland in response to relatively high frequency SNS.
THE CLINICAL PHARMACOLOGY OF ACE INHIBITORS: EVIDENCE FOR CLINICALLY RELEVANT DIFFERENCES?
Authors: Lees Kennedy R. , Squire Iain B. , Reid John L. 
Published: June 2007

SUMMARY1. Potential differences among ACE inhibitors include pharmacokinetic and pharmacodynamic factors. The presence of a sulfhydryl group conferring antioxidant properties, the administration as a pro‐drug to delay the onset and prolong the duration of haemodynamic effects, and the route of elimination are examples of possible differences.2. Adverse effects of ACE inhibitors may be mediated by effects on bradykinin metabolism at tissue sites, which may be separable from haemodynamic responses mediated largely by angiotensin II withdrawal.3. Clinically important differences between ACE inhibitors in their adverse event profile have yet to be proven. Evidence is emerging that plasma ACE inhibition and haemodynamic responses are separable, and this may indicate the potential for other organ‐specific effects to differ among ACE inhibitors.4. At present, however, the greatest distinguishing features for one compound vs another are the time to onset and the duration of action, which determine the frequency of administration.
CEREBROVASCULAR PROTECTION BY SEQUENTIAL BILATERAL CAROTID ARTERY LIGATION IN AGED SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Horie R. , Mano M. , Omura K. 
Published: June 2007

SUMMARY1. Sequential bilateral carotid artery ligation (BCL) separated by a 1 week interval was performed on 5 month spontaneously hypertensive rats (SHR) (i.e. SHRSR‐B1/Izm) and the developmental course of hypertension and cerebrovascular lesions in advanced age were analysed as compared with those in age‐matched sham‐operated controls.2. Behavioural activity and behavioural reaction to light were also investigated in the above‐mentioned SHR, young and adult stroke‐prone SHR (i.e. SHRSP‐A3/Izm), SHR (i.e. B1/Izm) and Wistar‐Kyoto rats (i.e. WKY/Izm).3. All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth.4. SHR usually die within a few days of BCL. In the present study, however, they successfully survived without cerebrovascular damage for a long time, although they developed a similar severe hypertension in a significantly shorter period of time (P < 0.05) and showed behavioural abnormalities that were probably due to severe cerebral ischaemia.5. These experimental results suggest an ischaemic tolerance phenomenon in a hypertensive model that was exposed to mild ischaemic stress by unilateral carotid artery ligation (UCL) before the subsequent induction of severe ischaemia by BCL. The results also suggest that an aggravation of hypertensive cerebrovascular changes due to long‐lasting ischaemia after BCL was prevented through a possible cumulative effect of ischaemic stress.
CIRCULATING LEVELS OF ACTIVE, TOTAL AND INACTIVE RENIN (PRORENIN), ANGIOTENSIN I AND ANGIOTENSINOGEN IN CARBON TETRACHLORIDE‐TREATED RATS
Authors: Cruz Cristino , Ibarra‐Rubio Maria Elena , Pedraza‐Chaverrí José 
Published: June 2007

SUMMARY1. Plasma renin activity (PRA), plasma angiotensin I concentration (ANG I), plasma angiotensinogen concentration (PAC) and the plasma levels of active, total and inactive renin (prorenin) were measured in rats with carbon tetrachloride (CCl4)‐induced acute renal failure. Rats were treated with a single oral dose of CCl4 (2.5 mL/kg) and killed 1, 2, 3 and 7 days later.2. On days 1–3 PRA, ANG I and PAC decreased and increased on day 7. Active renin fell on days 2 and 3, total renin (trypsin treatment) augmented on day 1 and diminished on day 3, prorenin and per cent prorenin increased on days 1 and 2. Angiotensin I concentration paralleled PRA and PAC. The CCl4‐induced decrease in PRA was secondary to the fall in active renin and in PAC. Total renin augmented as a consequence of the elevation of prorenin. Renal function, evaluated by serum urea, serum creatinine and creatinine clearance, decreased on days 1 and 2 when PRA was low and plasma prorenin was high.3. These data do not support the involvement of the circulating active renin‐angiotensin system (RAS) in the pathophysiology of acute renal failure induced by CCl4, however, increased prorenin levels were associated with the decrease in renal function.
EFFECTS OF ADENOSINE AND ITS ANALOGUES ON ACTIN POLYMERIZATION IN HUMAN POLYMORPHONUCLEAR LEUCOCYTES
Authors: Tsuruta Satoru , Ito Setsuko , Mikawa Haruki 
Published: June 2007

SUMMARY1. The effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes (PMN) induced by three different chemotactic stimulants, platelet‐activating factor (PAF), N‐formyl‐methionyl‐leucyl‐phenylalanine (FMLP) and an activated fragment of C5 (C5a) were investigated.2. Adenosine and its analogues inhibited the actin polymerization induced by these three agents in a concentration‐dependent manner and theophylline, a competitive antagonist at adenosine receptors, abolished these inhibitory effects.3. The adenosine analogue 5′‐N‐ethylcarboxamideadenosine (NECA) was a more potent inhibitor of actin polymerization than either l‐N6‐phenylisopropyladenosine (PIA) or adenosine itself; the rank order of potency of these agonists was characteristic of adenosine A2 receptors.4. Adenosine deaminase (ADA) abolished the inhibitory effect of adenosine and augmented PAF‐induced actin polymerization.5. It was concluded that, at physiological concentrations, adenosine inhibits actin polymerization in PMN via activation of PMN surface membrane adenosine A2 receptors and thus modulates chemotactic stimulus‐induced PMN motility.
MORPHINE AND MORPHICEPTIN INCREASE THE THRESHOLD FOR EPINEPHRINE‐INDUCED CARDIAC ARRHYTHMIAS IN THE RAT THROUGH BRAIN MU OPIOID RECEPTORS
Authors: Rabkin Simon W. 
Published: June 2007

SUMMARY1. To determine whether morphine modulates the development of cardiac arrhythmias through mu opioid receptors by an action within the central nervous system (CNS). Catecholamine‐induced ventricular arrhythmias were produced, in the rat, by continuous infusion of epinephrine at incremental doses until the development of fatal arrhythmias, usually ventricular fibrillation.2. Morphine, 0.1 mg/kg i.v., significantly suppressed (P < 0.05) the development of epinephrine‐induced arrhythmias compared with the control group. This was opposed by the mu opioid antagonist naloxone (1 or 2 mg/kg) in a dose‐dependent manner.3. To determine whether these effects were operative in the brain, rats received an injection of either morphine 50 μg/kg or its diluent (control) into the lateral cerebral ventricle intracerebroventricularly (i.c.v.). Morphine significantly increased (P < 0.05) the threshold for the development of arrhythmias.4. To further explore whether this effect was operative at the mu opioid receptor, a more specific mu opioid receptor agonist morphiceptin (50 mUg/kg) was administered i.c.v. and produced a significant increase (P < 0.05) in the threshold for cardiac arrhythmias compared with controls.5. The action of morphine was further established to be operating through mu opioid receptors from experiments with the i.c.v. administration of naloxone (+) and naloxone (—) followed by morphine showing that the action of morphine in the brain was prevented by the opioid antagonist naloxone but not by its stereo‐isomer that is not a mu opioid receptor antagonist.6. These data suggest a role for morphine to modulate cardiac arrhythmias, specifically to increase arrhythmia threshold, through an action within the CNS at mu opioid receptors.
EFFECTS OF CORTISOL ON BLOOD PRESSURE AND SALT PREFERENCE IN NORMAL HUMANS
Authors: Wong K. S. , Williamson P. M. , Brown M. A. , Zammit V. C. , Denton D. A. , Whitworth J. A. 
Published: June 2007

SUMMARY1. Adrenocorticotrophic hormone (ACTH) and corticosteroids stimulate salt appetite in laboratory animals. The hypothesis tested was that cortisol administration increases salt preference in humans.2. Sodium taste studies (detection and recognition thresholds, taste intensity and preference tests) were conducted before, during and after cortisol administration (200 mg/day for 5 days) in normal men on a free diet.3. Cortisol significantly increased systolic blood pressure (SBP), 113 ± 3–130±4 mmHg, P < 0.05; diastolic blood pressure (DBP), 65±3–81±2 mmHg, P < 0.05; mean arterial pressure (MAP), 81± 2–97± 3 mmHg, P < 0.05; and bodyweight, 72.9±3.0–75.4±3.3 kg, P < 0.05.4. Salt detection and recognition thresholds, taste intensity and preference for sodium chloride were unchanged following cortisol.
α‐AND β‐ADRENOCEPTOR AGONIST ACTIVITY IN THE VENOM OF THE AUSTRALIAN HUNTSMAN SPIDERS, DELENA CANCERIDES AND ISOPEDA MONTANA
Authors: Korszniak N. V. , Story D. F. 
Published: June 2007

SUMMARY1. Crude venom gland extracts (VGE) were prepared from female Delena cancerides and Isopeda montana spiders. The VGE were tested in isolated rat atrial, caudal artery and pithed rat preparations for pharmacological activity.2. In rat isolated atrial preparations, D. cancerides and I. montana VGE, each in a concentration of 2 glands/mL, produced increases in atrial rate which were abolished by propranolol (1 μmol/L) but not by ketanserin (0.1 μmol/L) or reserpine pretreatment (2.5 mg/kg s.c. 24 h prior to experimentation) indicating a direct action on atrial β‐adrenoceptors.3. In rat caudal artery preparations each VGE produced an increase in perfusion pressure, which was taken as an index of vasoconstriction. Pressor responses to D. cancerides VGE (1 gland/mL) were abolished in the presence of prazosin (1 mol/L) but not by reserpine pretreatment, indicating an action of the VGE on vascular α1‐adrenoceptors. Neither prazosin nor reserpine pretreatment had any effect on pressor responses of rat caudal artery preparations to I. montana VGE. Ketanserin (6 nmol/L) produced a small reduction in the degree of vasoconstriction produced by the VGE. This demonstrates a lack of α1‐adrenoceptor agonist activity of the VGE.4. Both VGE produced dose‐dependent increases in mean arterial pressure and heart rate in pithed rat preparations. The use of relatively selective receptor antagonists indicated that the increases in mean arterial pressure (MAP) produced by both VGE were mediated by an action on α2‐adrenoceptors.
A SIMPLE METHOD FOR ESTIMATING 24 H URINARY SODIUM AND POTASSIUM EXCRETION FROM SECOND MORNING VOIDING URINE SPECIMEN IN ADULTS
Authors: Kawasaki Terukazu , Itoh Kazue , Uezono Keiko , Sasaki Haruka 
Published: June 2007

SUMMARY1. An assessment was made of the extent sodium (Na) and potassium (K) intake can be estimated from Na, K and creatinine (Cr) content of a second morning voiding urine (SMU) specimen collected within 4 h after the first voiding upon awakening but before breakfast in 159 clinically healthy, free‐living individuals (20–79 years). The SMU and the rest of 24 h urine specimens for a 3–5 day period were collected.2. The following equations for estimating 24 h urinary Na (24HUNaV) and K (24HUKV) excretions were developed, and the accuracy and the reliability of these equations were evaluated. Estimated value of 24HUNaV (mEq/day) = 16.3 √XNa; estimated value of 24HUKV (mEq/day) = 7.2 √XK, where XNa (or XK) = SMUNa (or SMUK)/SMUCr X predicted 24 h urinary Cr excretion.3. Highly statistically significant correlations were detected between the values estimated and measured for both Na (r= 0.728, P < 0.001, n= 159) and K (r= 0.780, P < 0.001, n= 159).4. These equations were applied to Group 1 subjects, who collected the urine for a single day, and to Group 2, for 3 days. The correlation coefficients between the values estimated and measured for Na and K were 0.531 and 0.443 in Group 1, and 0.821 and 0.590 in Group 2, respectively. No statistically significant differences were observed.5. The SMU specimens provide a satisfactory alternative to both 24HUNaV and 24HUKV in adults for extensive epidemiological surveys but also for clinical application.
DISCREPANCY BETWEEN RENIN mRNA AND PLASMA RENIN LEVEL IN ANGIOTENSIN‐CONVERTING ENZYME INHIBITOR‐TREATED RATS
Authors: Morishita Ryuichi , Higaki Jitsuo , Nagano Masahiro , Nakamura Fumiaki , Tomita Naruya , Zhao Yi , Mikami Hiroshi , Miyazaki Mizuo , Ogihara Toshio 
Published: June 2007

SUMMARY1. To investigate the role of transcriptional and post‐transcriptional factors in increasing renin synthesis secondary to angiotensin‐converting enzyme (ACE) inhibitors, we studied the changes in levels of renal renin mRNA, plasma renin and other hormonal factors.2. Spontaneously hypertensive rats were orally administered 10 mg/kg spirapril or vehicle daily for 3, 14 or 28 days.3. Plasma renin activity in the spirapril‐treated group was significantly elevated compared with that in the vehicle group at any time (P<0.01). However, there was no significant change in plasma angiotensin II concentration between the two groups. The ratio of renal renin mRNA to β‐actin mRNA in the spirapril‐treated group was higher than that in the control group (P<0.01).4. At 28 days, plasma renin activity in the spirapril‐treated group was significantly elevated compared with that at 14 days (P<0.05). However, there was no change in renin mRNA between 14 and 28 days after ACE inhibitor administration.5. Plasma ACE activity in the treatment group was less than that in the control group at any time (P<0.01).6. Our study demonstrated a non‐proportional change in plasma renin and renal renin mRNA levels. It is suggested that the main determinant of the rate of renin synthesis after administration of an ACE inhibitor may be post‐transcriptional factors, and that unknown mechanisms may be involved in the increase in plasma renin level after long‐term administration of ACE inhibitor in addition to the short feedback mechanism brought about by the decrease in angiotensin II.
A POSSIBLE INTERPRETATION FOR DIFFERENCE IN NEOSTIGMINE‐INDUCED CHANGES OF SPONTANEOUS ACTIVITIES AND EVOKED MUSCLE POTENTIALS BETWEEN RAT MEDIAL GASTROCNEMIUS AND SOLEUS MUSCLES
Authors: Uramoto I. , Watanabe K. , Totsuka T. 
Published: June 2007

SUMMARY1. Under urethane‐anaesthesia, changes of spontaneous activities and evoked muscle potentials in rat medial gastrocnemius (MG) and soleus (SOL) muscles induced by the injection of neostigmine were investigated.2. Before the administration of neostigmine, spontaneous activities were rarely observed and muscle potentials evoked by single shocks were simply biphasic in both MG and SOL muscles. When the anti‐cholinesterase drug was applied, spontaneous discharges of motor units were often observed in bursts in the MG muscles, in contrast to single spikes in the SOL muscles. The biphasic wave of evoked potentials in the MG muscles was followed by one or more oscillations, which were scarcely observed in the SOL muscles. This biphasic wave also occurred even after transection of the sciatic nerve proximal to the stimulating site.3. A late component with a small amplitude could be observed in the evoked potentials of MG and SOL muscles. It was potentiated in amplitude after the administration of the drug.4. Prolonged action of acetylcholine (ACh) has been known to occur in the presence of anti‐cholinesterase drugs, and this was taken into account for the mechanism of the phenomena proposed in the present study. Contrasting changes between MG and SOL muscles were observed, which may be explained by different modes of ACh release in the MG and SOL muscles.
SHORT COMMUNICATION: EFFECTS OF NIFEDIPINE AND BAY‐K‐8644 ON THE RELEASE OF CATECHOLAMINES FROM THE DOG ADRENAL GLAND IN RESPONSE TO SPLANCHNIC NERVE STIMULATION
Authors: Takeuchi Akihiko , Kimura Tomohiko , Satob Susumu 
Published: June 2007

SUMMARY1. The effects of nifedipine and Bay‐K‐8644 on the release of adrenal catecholamines were examined in anaesthetized dogs.2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz produced frequency‐dependent increases in adrenaline (ADR) and noradrenaline (NA) output determined from adrenal venous blood.3. Neither nifedipine (10 and 30 μg/kg, i.v.) nor Bay‐K‐8644 (10 and 30 μg/kg, i.v.) modified the SNS‐induced increases in catecholamine output. Basal catecholamine output tended to be increased and decreased by nifedipine and Bay‐K‐8644, respectively.4. Nifedipine produced significant decreases in arterial pressure and renal blood flow rate. Bay‐K‐8644 produced a significant increase in arterial pressure associated with a decrease in renal blood flow rate.5. These results suggest that dihydropyridine‐sensitive calcium channels do not play a major role in adrenal catecholamine release evoked by SNS.
CROSSOVER COMPARISON BETWEEN THE DEPRESSOR EFFECTS OF LOW AND HIGH WORK‐RATE EXERCISE IN MILD HYPERTENSION
Authors: Tashiro Eiichiro , Miura Shin‐ichiro , Koga Manabu , Sasaguri Manabu , Ideishi Munehito , Ikeda Masaharu , Tanaka Hiroaki , Shindo Munehiro , Arakawa Kikuo 
Published: June 2007

SUMMARY1. The relationship between work‐rate and the antihypertensive effect of exercise in hypertensives, and the mechanism of that effect, were investigated by a crossover clinical trial.2. Ten mild hypertensives were randomly divided into two groups. One group performed low work‐rate exercise (LWE) on a cycle ergometer for 10 weeks (blood lactate threshold; ∼50% of maximum oxygen consumption [V̇O2max]). After a 10 week interval without exercise training, these subjects were then switched to a high work‐rate exercise (HWE) regimen (4 mmol/ L of blood lactate; ∼75% of V̇O2max) for another 10 weeks. In the other group, the order of exercise training was reversed. Since two patients withdrew from the protocol during HWE periods, statistical analysis was performed on the data from the remaining eight patients. There were no order effects observed in any of the data from the two groups.3. During both LWE and HWE, resting blood pressure (BP) fell significantly after the initiation of exercise therapy (P<0.05). Furthermore, the overall effects of 10 weeks of LWE and HWE on BP were not significantly different.4. The work‐rate at the lactate threshold, which reflects physical fitness, had increased significantly by 16 W (P<0.01) after the LWE period and by 11 W (P<0.01) after the HWE.5. During the LWE period, changes in haemodynamic and humoral variables were not significant, except for a reduction in plasma norepinephrine at week 10 (P<0.05). In the HWE period, changes in haemodynamic and humoral variables were not significant.6. Based on these findings, LWE is recommended for mild hypertensives because of its safety.
ROLE OF SODIUM‐POTASSIUM ATPASE IN PHOSPHATE TRANSPORT BY THE EVERTED SACS OF MOUSE INTESTINE
Authors: Mary P. L. , Rao J. Prakasa 
Published: June 2007

SUMMARY1. This study investigated the uptake and release of phosphate from everted intestinal sacs of mice.2. When the activity of sodium‐potassium ATPase was altered (by changing the cationic concentrations in the medium by the addition of ouabain and the manipulation of metabolism by the use of selective inhibitors or stimulants), the release of phosphate appeared to be much more affected by the changes than the uptake of phosphate.3. A small sodium gradient allowed uptake to be maintained. The addition of ouabain in the presence of an attenuated gradient significantly reduced the uptake and release of phosphate. The inhibitory effect of ouabain on phosphate release was partly reversed by an increase in the potassium concentration in serosal fluid.4. These results indicate a role for sodium‐potassium ATPase in phosphate release from the intestine.