bluuebunny/crossref_metadata_2025_split huggingface dataset:
MECHANISMS OF LIDOCAINE ACTIONS ON NORMAL AND ABNORMAL RHYTHMS IN CANINE CARDIAC TISSUES IN VIVO AND IN VITRO
Authors: Abete P. , Ferrara N. , Rengo F. , Vassalle M. 
Published: June 2007

SUMMARY1. The actions of lidocaine on cardiac pacemaker rhythms were studied in anaesthetized dogs and in Purkinje fibres from hearts of the same animals.2. In vivo, lidocaine (1 mg/ kg, intravenously) slowed the sino‐atrial (SA) node rhythm (– 5.0%), and (during vagal stimulation) prolonged ventricular standstill by + 25.1% and slowed the idioventricular rhythm (– 16.7%). A higher dose (4 mg/kg) had more pronounced effects.3. Propranolol also slowed sinus (– 26.2%) and idioventricular (– 27.2%) rhythms, and prolonged ventricular standstill (+ 36.8%). In the presence of propranolol, the effects of lidocaine on idioventricular rhythm were exaggerated.4. In Purkinje fibres driven in vitro, lidocaine (10 μmol/L) decreased contractile force (– 47.9%) and (during the interruption of drive) prolonged the suppression of (+ 53.2%) and slowed the escape rhythm (– 67.0%).5. In the presence of lidocaine the threshold potential was shifted to less negative values and diastolic depolarization slope was decreased (– 23.6%).6. Lidocaine slowed spontaneously active Purkinje fibres, abolished early afterdepolarizations in low [K]0 and slow responses in high [K]0 (by shifting the threshold to less negative values), and antagonized strophanthidin arrhythmias.7. TTX reduced the hyperpolarization by lidocaine in low [K]0 and vice versa.8. We conclude that lidocaine enhances vagally‐induced ventricular standstill by depressing the idioventricular rhythm far more than the sinus rhythm, an action enhanced by beta‐blockade. Furthermore, lidocaine depresses normal and different types of abnormal automaticity through direct and indirect effects of the blockade of the fast sodium channel.
ROLE OF THE SYMPATHETIC NERVOUS SYSTEM IN THE ONSET OF HYPERTENSION IN THE RAT: THE EFFECT OF 6‐OH‐DOPAMINE
Authors: Li Ming , Whitworth Judith A. 
Published: June 2007

SUMMARY1. The effect of chemical sympathectomy with 6‐OH‐dopamine (6‐OHDA) on the onset of adrenocorticotrophin (ACTH)‐induced hypertension was examined in Sprague–Dawley rats (n= 23).2. 6‐OHDA injection produced a fall in systolic blood pressure (SBP) from 100±5 mmHg control to 74±4 mmHg post‐6‐OHDA Treatment Day 1 (P<0.001), but did not alter food or water intake, urine volume or electrolyte excretion.3. Compared with sham injection, ACTH‐treated rats showed an increase in blood pressure (sham: 98±7 mmHg; ACTH: 123±9 mmHg on Treatment Day 10; P<0.01), loss of bodyweight, and increases in water intake and urine volume.4. The magnitude of the blood pressure rise on ACTH was greater in 6‐OHDA‐treated rats than in intact control rats. Metabolic changes were similar.5. Chemical sympathectomy with 6‐OHDA did not delay or block the onset of ACTH hypertension in the rat.
REPERFUSION ARRHYTHMIAS IN CLOSED‐CHEST RATS: THE EFFECT OF MYOCARDIAL NORADRENALINE DEPLETION AND Ca2+‐ANTAGONISM
Authors: Kirchengast Michael , Hergenröder Stefan 
Published: June 2007

SUMMARY1. The influence of myocardial noradrenaline depletion on the incidence and severity of reperfusion arrhythmias in closed‐chest anaesthetized rats was investigated. Five‐minute left coronary artery occlusion was carried out via an implanted occluder. Four groups of rats were studied: controls, rats treated with reserpine (5 mg/kg, intraperitoneally) 24 h before occlusion, and rats receiving 0.2 mg/kg gallopamil intravenously 5 min before occlusion either with or without reserpine pretreatment.2. In the control group all animals had ventricular tachycardia (VT) and fibrillation (VF) immediately after reperfusion. Gallopamil reduced VT to 50% and VF to 25% (P<0.05 versus control). In the reserpine group all had VT, and 67% had VF, this being not significantly different from controls. Additional treatment with gallopamil markedly reduced VT and totally prevented VF (P<0.05 versus control).3. Thus, total depletion of myocardial noradrenaline stores neither prevented the occurrence nor reduced the severity of reperfusion arrhythmia in rats, while gallopamil treatment was effective.
INVESTIGATIONS INTO INTERACTIONS BETWEEN DOXAZOSIN AND ENALAPRILAT AT α1‐ADRENOCEPTORS IN ANAESTHETIZED RATS
Authors: Marwood John , Tierney Garth , Stokes Gordon 
Published: June 2007

SUMMARY1. In anaesthetized intact Sprague‐Dawley rats, the angiotensin‐converting enzyme inhibitor enalaprilat, 1 mg/kg, had no significant effect on the pressor responses to the α1‐adrenoceptor agonist phenylephrine (PE). Doxazosin 1 mg/kg was found to be a potent α1‐adrenoceptor antagonist.2. The combination of enalaprilat 1 mg/kg plus doxazosin 1 mg/kg was 3.3‐fold more potent in antagonizing α1‐adrenoceptors than doxazosin 1 mg/kg alone.3. After treatment of rats with deoxycorticosterone acetate (DOCA) twice weekly for 5 weeks, the α1‐adrenoceptor antagonist action of doxazosin in anaesthetized rats was not potentiated by enalaprilat 1 mg/kg.4. Since DOCA treatment suppresses renin activity, these findings strongly support the hypothesis that angiotensin II can modulate the functional activity of α1‐adrenoceptor in vascular smooth muscle.
EFFECTS OF DIETARY SODIUM RESTRICTION AND FISH OIL SUPPLEMENTS ON BLOOD PRESSURE IN THE ELDERLY
Authors: Cobiac Lynne , Nestel Paul J. , Wing Lindon M. H. , Howe Peter R. C. 
Published: June 2007

SUMMARY1. The effects on blood pressure of dietary fish oil, sodium restriction and a combination of both strategies were examined in a short‐term dietary intervention study of 50 healthy elderly subjects (average age 67 years) with mean initial systolic and diastolic blood pressures of 133 and 77 mmHg, respectively.2. Subjects were allocated to one of four treatment groups: fish oil with normal sodium, fish oil with low sodium, sunflower oil with normal sodium and sunflower oil with low sodium for 4 weeks. They then crossed over to the alternative sodium treatment for a further 4 weeks whilst remaining on the same oil.3. The combination of fish oil supplementation with dietary sodium restriction caused significant reductions of blood pressure in the first 4 weeks: systolic blood pressure (SBP) fell by 8.9 mmHg, mean arterial pressure (MAP) by 7.4 mmHg and diastolic blood pressure (DBP) by 6.0 mmHg.4. Fish oil enhanced the effect of sodium restriction on blood pressure. In the crossover protocol, a change in sodium excretion of 92 mmol/day was accompanied by changes of 6.4, 3.3 and 2.2 mmHg for SBP, MAP and DBP, respectively, in the subjects taking fish oil. However in those taking sunflower oil, blood pressure did not change significantly.5. The results indicate beneficial interactive effect of dietary fish oil and sodium intake on blood pressure.
POTASSIUM, GLUCOSE, INSULIN INTERRELATIONSHIPS DURING ADRENALINE INFUSION IN NORMOTENSIVE AND HYPERTENSIVE HUMANS
Authors: Gordon Richard D. , Bachmann Anthony W. , Ballantine Donna M. , Thompson Robyn E. 
Published: June 2007

SUMMARY1. Significant increases in arterial noradrenaline (NA) of similar magnitude were seen in normotensive (NT) and hypertensive humans (HT) during adrenaline (ADR) infusion.2. Significant falls in plasma potassium (K+) were observed in both NT and HT during ADR infusion, even at rates equivalent to minor stress. Levels achieved were significantly lower in HT than in NT.3. Plasma glucose increased significantly in HT at all ADR infusion rates but only at higher rates of infusion in NT.4. Basal insulin levels were significantly higher in NT than in HT. After cessation of infusion, insulin increased three‐fold in HT and two‐fold in NT.5. Infusion of ADR to produce levels seen during mild to moderate stress resulted in significant increases in plasma NA, falls in plasma K+ and increases in plasma glucose. The expected large insulin response to rising glucose was not seen until after ADR was ceased, confirming the inhibitory effect of ADR on glucose stimulated insulin release.
DOES URINARY ATRIAL NATRIURETIC PEPTIDE REFLECT PLASMA LEVELS IN HUMANS?
Authors: Tunny Terry J. , Finn Wendy L. , Klemm Shelley A. , Gordon Richard D. 
Published: June 2007

SUMMARY1. Saline infusion produced concurrent mean increases over basal in plasma and urinary atrial natriuretic peptide (ANP) of approximately 100%.2. Subpressor calcium infusion also produced concurrent increases in plasma and urinary ANP of 38 and 60% respectively.3. Urinary ANP appeared to be as responsive to the dynamic stimulation of saline and calcium infusion as plasma levels.4. Urinary ANP may be useful when an integrated estimation of ANP secretion and metabolism is required. Further studies are required to assess clinical utility in a variety of settings, for example during endopeptidase 3.4.24.11 inhibition.
HAEMODYNAMIC AND HORMONAL EFFECTS OF N‐NITRO‐l‐ARGININE, AN INHIBITOR OF NITRIC OXIDE BIOSYNTHESIS, IN SHEEP
Authors: Tresham J. J. , Dusting G. J. , Coghlan J. P. , Whitworth J. A. 
Published: June 2007

SUMMARY1. The haemodynamic and hormonal responses to N‐nitro‐l‐arginine (NOLA), a potent inhibitor of nitric oxide biosynthesis in endothelial cells, were investigated in conscious sheep.2. Mean arterial blood pressure (MAP), heart rate (HR) and cardiac output by thermodilution (CO) were measured in four oophrectomized ewes. Two other ewes were surgically implanted with aortic electromagnetic flow probes and an indwelling carotid arterial line for monitoring CO and MAP over 40 h.3. After a control period, NOLA (10 mg/kg) was injected intravenously and MAP, HR and CO monitored and blood samples taken at intervals over the following 24 h.4. NOLA increased blood pressure within minutes, from 76 ± 4 to a maximum of 99 ± 4 mmHg (P<0.001) at 6 h after injection. It remained elevated 24 h after injection. CO and HR fell but these falls were not sustained longer than 6 h. Calculated total peripheral resistance increased to a maximum of 2 h, but had returned to control levels 24 h after injection. There were no significant changes in plasma concentrations of renin, atrial natriuretic factor, vasopressin, noradrenaline or endothelin during the first hour.5. NOLA may be a useful tool in understanding the role of the endothelium and nitric oxide in the control of blood pressure.
EFFECTS OF V2 RECEPTOR ACTIVITY ON THE PRESSOR RESPONSE TO VASOPRESSIN IN THE RAT
Authors: Shimizu Keishi , Schwartz Jeffrey , McGrath Barry P. 
Published: June 2007

SUMMARY1. To determine the contribution of V1 and V2 receptor activity on the enhancement of reflex buffering of the pressor response to arginine‐vasopressin (AVP), mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of phenylephrine, AVP, or Phe2Orn8OT, a potent, selective V1‐receptor agonist in the absence and presence of Val4DArg8VP, a potent, selective V2‐receptor agonist.2. There were no significant differences in MAP responses to the V1 agonist in the absence and presence of the V2 agonist in either conscious intact or autonomic‐blocked rats.3. Autonomic blockade with methscopolamine and hexamethonium increased the pressor sensitivity to phenylephrine threefold. In contrast, the pressor sensitivities to AVP and Phe2Orn8OT were increased 14‐fold and 11‐fold, respectively, by autonomic blockade.4. V2‐receptor activity does not have any inherent vasocative action or synergistic vasoactive action with V1‐receptor activity.5. V2 receptors do not play a role in enhancing reflex buffering of the pressor response to AVP; V1 receptors are suggested to play the role.
PRESYNAPTIC REGULATION OF NEUROTRANSMITTER RELEASE IN HYPERTENSION
Authors: Tsuda Kazushi , Masuyama Yoshiaki 
Published: June 2007

SUMMARY1. The present review discusses evidence in support of the concept that alterations in sympathetic neurotransmitter release might contribute to the pathogenesis of hypertension.2. Studies suggest that changes in sympathetic nervous activity in both the central and peripheral nervous systems participate in blood pressure control.3. In the periphery increased release of norepinephrine from vascular adrenergic neurons might lead to the enhanced vasoconstrictor responses and thus to an elevation in systemic blood pressure.4. The amount of neurotransmitter release from sympathetic nerve endings can be regulated by autoregulatory systems by presynaptic receptors located on nerve terminals.5. It has been proposed that alterations to sympathetic nervous activity of hypertension might be partially due to abnormalities in presynaptic modulation of neurotransmitter release in central and peripheral tissues.6. This article summarizes the results of studies to evaluate presynaptic receptor functions and sympathetic neurotransmitter release in hypertension.
EVIDENCE AGAINST THE INVOLVEMENT OF VASOACTIVE INTESTINAL PEPTIDE IN OVINE PAROTID SECRETION AND BLOOD FLOW
Authors: Wright R. D. , Blair‐West J. R. , Gibson A. P. , Shulkes A. 
Published: June 2007

SUMMARY1. The proposition that stimulation of the secretomotor nerve to the ovine parotid gland might involve co‐release of vasoactive intestinal peptide (VIP) was tested by studying responses to infusion of VIP directly into the gland's arterial blood supply and by assay of VIP in parotid venous blood.2. In unstimulated glands, an arterial blood concentration of 1.5–2.5 X 10−9 mol/L VIP did not evoke fluid secretion but it increased K+ and phosphate secretion and glandular blood flow. The same blood concentration of VIP potentiated the stimulation of salivary flow rate caused by intraarterial infusion of bethanechol but nerve stimulation was not potentiated. VIP increased glandular blood flow in both conditions of stimulation.3. Atropine blocked neurally stimulated salivary secretion but an increase in glandular blood flow was still detectable. There was therefore no evidence for a non‐cholinergic neural mechanism for salivary secretion.4. Furthermore, VIP concentrations in glandular venous blood were not increased by nerve stimulation.5. The results indicate that exogenous VIP can affect the flow and composition of ovine parotid secretion but was not involved in the response to secretomotor nerve stimulation.
DIRECT AND INDIRECT STIMULATION OF PANCREATIC EXOCRINE SECRETION BY NEUROTENSIN IN ANAESTHETIZED DOGS
Authors: Iwatsuki K. , Horiuchi A. , Ren L‐M. , Chiba S. 
Published: June 2007

SUMMARY1. The effects of neurotensin on pancreatic exocrine secretion were investigated both in the intact whole pancreas and in the isolated, blood‐perfused pancreas ex vivo in anaesthetized dogs.2. Intravenous (i.v.) injections of neurotensin (0.01‐1 nmol/kg) elicited dose‐dependent increases in the secretory rate of pancreatic juice without changes in plasma levels of cholecystokinin (CCK). The concentration of bicarbonate in the pancreatic juice induced by neurotensin was increased, but the protein concentration was scarcely changed.3. The neurotensin‐induced secretion was inhibited by SCH23390, a dopamine D‐1 antagonist, but not by domperidone, phentolamine, propranolol, atropine, cimetidine, or L‐364,718, a CCK antagonist.4. Intra‐arterial (i.a.) injections of neurotensin (0.1‐3 nmol/kg) also elicited dose‐dependent increases in the secretory rate of pancreatic juice flow, but did not change bicarbonate or protein concentration. The secretory activities were less effective and 1 nmol/kg of neurotensin i.a. was approximately equal to that of 0.03 nmol/kg of neurotensin i.v.5. These results suggest that neurotensin mainly stimulates pancreatic secretion by acting indirectly. Neurotensin‐induced secretion is, at least in part, mediated by endogenously released dopamine which activates dopamine D‐1 receptors on the pancreas. In addition to its indirect action, neurotensin has a weak direct action to stimulate pancreatic secretion.
IN VITRO AUTORADIOGRAPHIC ENDOTHELIN‐1 BINDING SITES AND SARAFOTOXIN S6B BINDING SITES IN RAT TISSUES
Authors: Kohzuki Masahiro , Johnston Colin I. , Abe Keishi , Chai Siew Yeen , Casley David J. , Yasujima Minoru , Yoshinaga Kaoru , Mendelsohn Frederick A. O. 
Published: June 2007

SUMMARY1. The distribution of binding sites for [125I]‐labelled endothelin‐1 ([125I]‐ET‐1) and [125I]‐labelled sarafotoxin S6B ([125I]‐SRT) was visualized in rat tissues using in vitro autoradiography.2. A high density of endothelin‐1 (ET‐1) binding was found in the heart. In the kidney, ET‐1 binding occurred in association with glomeruli, proximal tubules, the inner stripe and inner medulla. In the adrenal, a high density of ET‐1 binding occurred in the medulla as well as the zona glomerulosa.3. The binding affinity constant (KA) for ET‐1 binding in these sites ranged from 1 to 10 X 109/mol per litre.4. Although sarafotoxin S6B (SRT) was 10–100‐fold weaker than ET‐1 in displacing [125I]‐ET‐1 from these sites, 1 μmol/L unlabelled SRT completely abolished [125I]‐ET‐1 binding in all sites. Other venom peptides did not affect [125I]‐ET‐1 binding.5. The pattern of [125I]‐SRT receptor binding in rat tissues by in vitro autoradiography was identical to that for ET‐1 receptor binding, and both unlabelled SRT and unlabelled ET‐1 fully competed with [125I]‐SRT for binding.6. These results provide evidence that SRT binds to the ET receptor in a range of rat tissues. The results suggest that there may be subclasses of ET receptors which can be distinguished by the relative potencies of ET‐1 and SRT at various tissues.
ATRIAL NATRIURETIC PEPTIDE INHIBITS THE ALDOSTERONE RESPONSE TO METOCLOPRAMIDE IN PATIENTS WITH GLOMERULAR DISEASE AND ESSENTIAL HYPERTENSION
Authors: Matsuoka Hiroaki , Fukui Kazushige , Dan Yoshiyuki , Ishimitsu Toshihiko , Hirata Yasunobu , Kimura Kenjiro , Sugimoto Tsuneaki , Ishii Masao , Kangawa Kenji , Matsuo Hisayuki 
Published: June 2007

SUMMARY1. We examined the effects of metoclopramide (MCP: 10 mg i.v.) on plasma atrial natriuretic peptide (ANP) and aldosterone concentrations (PAC) and the effect of ANP on MCP‐induced PAC in four patients with primary glomerular diseases and seven patients with essential hypertension.2. MCP injection caused no significant changes in plasma ANP. MCP produced a marked increase in PAC without a significant change in plasma renin activity.3. The increase in PAC induced by MCP injection was markedly attenuated when preceded by the infusion of ANP (25 ng/kg per min).4. These results suggest that the dopaminergic D2 mechanism is not involved in the regulation of ANP secretion and that ANP modulates the dopaminergic regulation of aldosterone secretion.
ANTI‐ISCHAEMIC AND VASOSPASMOLYTIC EFFECTS OF A NOVEL Ca2+ CHANNEL BLOCKER, SD‐3211, IN VITRO
Authors: Miyawaki Nobuaki , Furuta Tatsuji , Shigei Tatsuro , Yamazaki Fumiko , Yamauchi Hideyasu 
Published: June 2007

SUMMARY1. The present study was undertaken to determine the vasospasmolytic activity of a novel non‐dihydropyridine type of Ca2+ channel blocker, SD‐3211, in isolated canine coronary arteries and its ability to reduce myocardial ischaemic damage in isolated perfused rabbit hearts.2. The vasospasmolytic effect of SD‐3211 was investigated using 3,4‐diaminopyridine‐induced rhythmic contraction, in comparison with its enantiomer (SD‐3212), nicardipine and diltiazem. SD‐3211 was shown to reduce the peak tension and increase the contraction frequency. The order of potency for the relaxation of the peak tension was as follows: nicardipine > SD‐3211 > diltiazem > SD‐3212 and being compatible with that for the relaxant effects of these compounds on KCl‐induced contraction in the same specimen.3. Furthermore, the effect of SD‐3211 on myocardial damage due to global ischaemia for 60 min followed by 60 min of reperfusion was examined. SD‐3211 at a concentration of 2 × 10−8 mol/L was given for 40 min before and again for 60 min after the ischaemia. SD‐3211 attenuated the increase in leakage of creatine phosphokinase from the hearts and the decrease in pH of perfusate during reperfusion, while concomitantly providing a significant improvement in the post‐ischaemic recovery of developed tension.4. These results suggest that SD‐3211 has properties to reduce coronary vasospasm and to provide protection against ischaemic damage, both of which may have beneficial actions in the treatment of ischaemic heart disease.
FACTORS ASSOCIATED WITH SILENT MULTIPLE LACUNAR LESIONS ON MAGNETIC RESONANCE IMAGING IN ASYMPTOMATIC ELDERLY HYPERTENSIVE PATIENTS
Authors: Kawamoto Akiko , Shimada Kazuyuki , Matsubayashi Kozo , Nishinaga Masanori , Kimura Shigeaki , Ozawa Toshio 
Published: June 2007

SUMMARY1. Factors associated with advanced cerebrovascular damage incidentally seen on brain magnetic resonance imaging (MRI) were investigated in a population of 34 normotensive and 54 hypertensive asymptomatic elderly individuals (69±5 years).2. Four or more ‘lacunar’ lesions per subject were considered to be advanced changes, based on the distribution in normotensive subjects and were found in 11 (20%) out of 54 hypertensive subjects.3. Compared with the remaining 43 hypertensive patients with fewer or no lacunae, the proportion of subjects over 70 years of age who had electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) was significantly higher in this group of hypertensive patients. Patients with multi‐lacunar lesions also showed significantly higher ‘office’ and average ambulatory, in particular, blood pressure during sleep and less nocturnal blood pressure fall, than those with fewer or no lacunae. Furthermore, they showed a higher predicted whole blood viscosity and a lower high density lipoprotein (HDL)‐cholesterol. The predictive values of LVH on ECG for the presence of multi‐lacunar lesions in hypertensive patients were substantially high (70–90%).4. The data suggest that silent advanced cerebrovascular damages on MRI are not rare among asymptomatic elderly hypertensive patients and are associated with various cerebrovascular risk factors. A useful marker for their identification appears to be ECG‐LVH.
PATHOGENETIC ROLE OF VASCULAR ANGIOTENSIN‐CONVERTING ENZYME IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Okunishi H. , Kawamoto T. , Kurobe Y. , Oka Y. , Ishii K. , Tanaka T. , Miyazaki M. 
Published: June 2007

SUMMARY1. This study was undertaken to examine the possibility that the level of angiotensin‐converting enzyme (ACE) increases in vascular tissue, and that this may participate in the pathogenesis of hypertension in spontaneously hypertensive rat (SHR).2. In SHR, at the established hypertensive stage, the prolonged antihypertensive effect induced by a single oral dose of spirapril was closely correlated to the long‐lasting inhibition of ACE in aortae and mesenteric arteries. In contrast, ACE in plasma, lung, heart and kidney recovered from inhibition faster than in vessels.3. Prolonged daily oral treatment of SHR with spirapril, initiated at the age of 8 weeks and continued for 8 weeks, prevented the development of hypertension with concomitant decrease in aortic ACE activity. Blood pressure continued to be suppressed after the drug was withdrawn, as did the aortic ACE activity.4. Spontaneously hypertensive rats developed hypertension with age as well as with the increase in aortic ACE activity which became higher with age than that of Wistar‐Kyoto (WKY) normotensive control rats. On the contrary, ACE activity in plasma and lung of SHR was substantially lower than that of WKY at any age from 4 to 20 weeks old. Brain ACE activity of SHR did not differ from that of WKY at any age. Aged SHR showed the lower enzyme activity in the kidney compared with that of age‐matched WKY.5. Our results support the hypothesis that increased vascular ACE may play an essential role in the development and maintenance of hypertension in SHR.