bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF RESERPINE ON THE CONTENT AND UPTAKE OF DOPAMINE AND NORADRENALINE IN RABBIT ARTERIES
Authors: Okada Keiji , Shinozuka Kazumasa , Shimoura Keiko , Kobayashi Yuta , Hattori Keisuke , Nakase Akira 
Published: June 2007

SUMMARY1. Change with time of the content and uptake of dopamine (DA) and noradrenaline (NA) in the renal, superior mesenteric and femoral arteries and abdominal aorta of rabbit after reserpine administration was examined. Endogenous DA and NA were measured by high performance liquid chromatography coupled with electrochemical detector.2. A single dose of reserpine (3 mg/kg, i.p.) maximally depleted the endogenous DA and NA contents in the four blood vessels 24 h after the administration; the ratios of reductions were 70–90% and approximately 90% of the normal levels, respectively. The DA contents in all four vessels recovered to the normal level within 4 days after reserpine. However, NA content did not recover to the normal levels within 30 days after reserpine except in the mesenteric artery.3. The activity of dopamine β‐hydroxylase (DBH) significantly increased in all four blood vessels 1 h after reserpine. Although the DBH activity returned to the normal level after 3 days in the mesenteric artery, it returned within 24 h in the other three vessels.4. [3H]‐Dopamine and [3H]‐NA uptake were almost completely depressed 1 h after reserpine. The [3H]‐NA uptake in four vessels recovered to the normal level 2–14 days after reserpine, and [3H]‐DA uptake recovered after 30–45 days. Thus, the endogenous DA content in blood vessels was completely restored although DA uptake and NA content were still affected.5. These results suggested that the recovery of stored DA after reserpine was faster than that of stored NA and the recovery of DA uptake after reserpine was slower than NA uptake. This indicates a possibility that a part of DA pool may be different from NA pool in adrenergic nerve terminals in the blood vessels.
CHROMOSOME 17q23: A LOCUS FOR CARDIOVASCULAR DISEASE
Authors: Morris Brian J. 
Published: June 2007

SUMMARY1. The gene for dipeptidyl carboxypeptidase 1 (angiotensin I‐converting enzyme, kininase II; DCP1), located on chromosome 17q23, has been implicated in hypertension in rats. In humans associations have been found for the insertion allele of a bi‐allelic insertion/deletion polymorphism of DCP1 with hypertension and the deletion allele with myocardial infarction. Other hypertension studies have, however, failed to find a relationship.2. Mathematical predictions based on DCP1 association data suggest that high sib‐pair numbers may be needed to achieve statistical significance by this approach, although differences in the severity of hypertension in different study groups could account for the disparate findings.3. No association was found between DCP1 allele or genotype frequencies and obesity in essential hypertensives.
METABOLISM OF URIDINE IN EXPANDED EXTRACELLULAR VOLUME STATES
Authors: Hasnain Quloobul , Macdonald Graham , Haupert Garner T. 
Published: June 2007

SUMMARY1. Uridine and uridine monophosphate (UMP) are natriuretic and a vasopressor in intact rats. In deoxycorticosterone acetate (DOCA)‐salt hypertensive rats metabolic clearance rate (MCR) of uridine is raised and basal plasma uridine diminished, suggesting that metabolism of uridine is linked to changes in extracellular space.2. Plasma uridine concentration was raised in 38 patients with chronic renal failure compared with age‐ and sex‐matched healthy controls (8.49 μmol/L, 4.37–13.74 μmol/L median, interquartile range, and 2.64 μmol/L 2.51–2.74 μmol/L, respectively, P < 0.001). Plasma uridine was significantly diminished after isotonic fluid removal by ultrafiltration (UF) from 7.25 μmol/L (3.7–11.08) to 5.07 μmol/L (3.3–8.3), P < 0.001, whereas concentration of marker solutes urea and creatinine remained unchanged. During haemodialysis (HD), plasma uridine fell significantly from its pre‐HD level.3. In an animal model of expanded extracellular space the one‐kidney, one‐clip rat, plasma uridine was significantly higher (20.56±1.19 μmol/L, P < 0.01) and MCR diminished (34.93 ± 3.44 mL/kg per min, P < 0.01) compared with sham‐operated animals (plasma uridine 12.14 ± 1.07 and MCR 53.59 ± 4.11 mL/ kg per min). Uridine or UMP did not inhibit Na+, K+‐ATPase in either of the two assay systems.4. It was concluded that catabolism of uridine is reduced by extracellular expansion and probably increased by volume reduction by UF. Such a function may be due to the presence of a hypertensive natriuretic factor postulated by Dahl and de Wardener (1980), but would not be consistent with the ouabain‐like factor postulated by other workers in this situation because it has no inhibitory effect on Na+, K+‐ATPase.
STIMULATION OF PHOSPHATIDYLINOSITOL TURNOVER IN ADULT RAT LEFT ATRIA DOES NOT INVOLVE RELEASE OF INOSITOL (1,4,5) TRI SPHOSPHATE
Authors: Anderson Karen E. , Myers Damian , Woodcock Elizabeth A. 
Published: June 2007

SUMMARY1. The turnover rate of inositol (1,4,5) tris phosphate (Ins(1,4,5)P3) in noradrenaline‐stimulated adult rat left atria was calculated from changes in specific activity and was found to equal 110 ct/min per mg tissue. In contrast, the isomers of inositol mono‐ and bis phosphates accumulated at a rate of 508 ct/min per mg.2. Neomycin, which inhibits release of Ins (1,4,5)P3, inhibited the accumulation of inositol phosphates in noradrenaline‐stimulated isolated neonatal cardiomyocytes but did not inhibit accumulation in left atria.3. These data demonstrate that most of the inositol phosphates which accumulate in adult rat left atria do not derive from Ins (1,4,5) P3.4. These data are best explained by a model in which noradrenaline stimulation results mainly in the breakdown of phosphatidylinositol(4)mono phosphate (PtIns(4)P1) to inositol(1,4)bis phosphate (Ins(1, 4)P2). Thus, heart tissue avoids the generation of Ins(1,4,5)P3.
SINGLE POINT ESTIMATION OF PLATELET ANGIOTENSIN II RECEPTOR NUMBER MAY NOT BE VALID SCREENING TEST FOR PREGNANCY‐INDUCED HYPERTENSION
Authors: Yang Y. , Pawlak M. A. , Macdonald G. J. , Duggan K. A. 
Published: June 2007

SUMMARY1. Quantification of platelet angiotensin II (AII) receptors has been suggested as a screening test for pregnancy‐induced hypertension (PIH). Saturation analysis is too technically demanding to screen the requisite numbers and although a simplified method has been proposed, it has not been validated against saturation. This study sought to compare the two methods.2. Platelet AII receptor number was determined by saturation analysis and from the specific binding at each of three radioligand concentrations. The two methods were compared by correlation and by plotting their differences against their means to determine limits of agreement.3. Significant correlations were observed at all three radioligand concentrations; however, none of the regression lines approached the line of equality. There was increasing scatter as receptor number increased and 95% confidence intervals were too large to be clinically useful.4. From this study it is concluded that the simplified method for estimating platelet AII receptor number is inaccurate and caution is urged in its use as a screening test for PIH.
ALTERED BLOOD PRESSURE, RENAL TUBULAR FUNCTION AND LEVELS OF CIRCULATING INHIBITORS OF Na‐K‐ATPase IN MATURE SHR EXPOSED TO LOW SALT DIET IN THE PERINATAL PERIOD
Authors: Nicolantonio R. Di , Walker L. L. , Harris P. J. , Amhian A. , Adam W. R. , Morgan T. O. 
Published: June 2007

SUMMARY1. It has been shown previously that low salt diet, confined to the perinatal period only, reduces blood pressure (BP) and sodium retention in spontaneously hypertensive rat (SHR) offspring at maturity when compared with those given high salt diet.2. In this study it is shown that such high salt diets are associated with an increased level of circulating Na‐K‐ATPase inhibitor (CINK) activity.3. Animals given perinatal high salt diet have a significantly greater tubular reabsorptive capacity when compared with those given low salt diet.4. The finding of a high level of circulating Na‐K‐ATPase inhibitory material in the face of increased renal tubular capacity and blood pressure suggests that while this inhibitory material may play a role in the elevated blood pressure of animals given high salt diet, it cannot cause the elevated rate of fluid reabsorption.
STEREOLOGICAL STUDIES ON MESENTERIC RESISTANCE ARTERY STRUCTURE IN NEW ZEALAND GENETICALLY HYPERTENSIVE AND CONTROL RATS
Authors: Ledingham J. M. , Millar J. A. 
Published: June 2007

SUMMARY1. Stereological methods were used to quantitate and compare the structure of mesenteric resistance arteries (MRA) in New Zealand genetically hypertensive (GH) rats aged 4, 10 and 16 weeks and their normotensive control strain (N).2. Blood pressure (BP) (tail‐cuff and intra‐arterial) were recorded before the vessels were fixed by perfusion and embedded in Technovit Kulzer GmbH D‐6393, Wehrheim, Germany).3. Media and lumen volumes were measured on transverse sections (TS), by the Cavalieri method, and numbers of smooth muscle (SM) cells were estimated by the optical disector method.4. There were no significant differences in lumen volume per unit vessel length between GH and age‐matched N groups at any age. However, at 10 and 16 weeks volume in GH groups was 9–10% lower than their respective N groups.5. Media volume per unit vessel length increased in GH rats at all ages. The media/lumen ratio also increased in GH at all ages.6. Smooth muscle cell density (SM cell number per unit volume of media) decreased in GH rats at all ages, i.e. there was no evidence of hyperplasia.7. Blood pressure (tail‐cuff and intra‐arterial) significantly increased in GH rats at 4 weeks of age and also at 10 and 16 weeks.8. These results show that media volume is increased in GH early in life, is not due to hyperplasia, but may be due to hypertrophy of the SM cells, an increase in the amount of extracellular matrix or a combination of both. However, since hypertension is also present at an early age, structural abnormalities cannot be said to be a primary cause of GH hypertension.
EFFECTS OF ENALAPRILAT ON SYMPATHETIC ACTIVITY AND METABOLISM OF EXERCISING MUSCLES IN RABBIT
Authors: Shimizu Kazumasa , Wang Zhi‐Qin , Way Diana J. , Palmos Jenny , McGrath Barry P. 
Published: June 2007

SUMMARY1. To investigate the effects of angiotensin‐converting enzyme inhibition (ACEI) on exercise performance, the following were measured in eight normal rabbits performing graded treadmill exercise during intravenous vehicle saline or enalaprilat infusion: haemodynamics, noradrenaline (NA) spillover, hindlimb oxygen consumption and lactate release.2. Blood pressure, heart rate (HR), femoral blood flow (FBF), hindlimb lactate release, hindlimb oxygen consumption and hindlimb NA spillover rate were all significantly increased during exercise and the changes during enalaprilat infusion were similar to control responses.3. At submaximal exercise (6 m/min), ACEI did not significantly alter the responses of hindlimb lactate release, NA spillover rate or oxygen consumption. At the higher exercise load (12 m/min), ACEI reduced hindlimb NA spillover rate (33.1 ± 4.2 vs 61.3 ± 17.1 ng/min) and significantly increased oxygen consumption (241 ± 53.4 vs 133 ± 23.396, P < 0.05). The ratio of hindlimb NA spillover rate to total NA spillover rate was markedly increased during exercise, with similar changes being observed in ACEI and control experiments.4. This study indicates that acute ACEI has a favourable effect on oxygen utilization in exercising muscle in the normal rabbit. Suppression of local sympathetic activation during exercising stress, as reflected in a reduced NA spillover response, may benefit the microcirculation in exercising muscles.
STRUCTURAL INFLUENCES ON RESISTANCE IN THE HINDLIMB VASCULAR BED OF THE RENAL HYPERTENSIVE RABBIT
Authors: Neilson J. A. , West M. J. 
Published: June 2007

SUMMARY1. The contribution of arteriolar structural change to hindlimb vascular resistance was examined in the renal wrap hypertensive rabbit.2. Haemodynamic variables were recorded at rest and after maximal vascular dilation using sodium nitroprusside and peripheral autonomic effector blockade. In the same animals at the end of experiments, morphometric measurements of hindlimb muscle arterioles were made.3. Mean arterial pressure (MAP) and hindlimb vascular resistance were elevated in hypertensive animals compared with normotensive animals at rest and after maximal dilation.4. Lumen area and lumen diameter were reduced whereas wall area and wall area to lumen area ratio were increased in hypertensive animals compared with normotensive animals.5. In the renal wrap model of hypertension, the reduction in lumen area of arterioles, < 200 pm in diameter, is sufficient to explain the increase in haemodynamic resistance.
EFFECTS OF AN ORALLY ACTIVE VASOPRESSIN V1 RECEPTOR ANTAGONIST
Authors: Burrell L. M. , Phillips P. A. , Stephenson J. , Risvanis J. , Hutchins A‐M. , Johnston C. I. 
Published: June 2007

SUMMARY1. This paper reports on the in vitro and in vivo characteristics of a non‐peptide vasopressin V1 receptor antagonist 1‐{1‐[4‐(3‐acetylaminopropoxy)benzoyl]‐4‐piperidyl}‐3,4‐dihydro‐2(1H)‐quinolinone (OPC‐21268).2. OPC‐21268 caused a concentration‐dependent displacement of the selective V1 receptor antagonist radioligand, [125I]‐[d(CH2)5, sarcosine7]AVP from vasopressin V1 receptors in rat liver and kidney membranes, inhibitory concentration of 50% (IC50) 4 ± 10‐8, 0.3 mol/L liver and 1.5 ± 10‐8, 0.2 mol/L kidney. OPC‐21268 had little effect on the selective V2 antagonist radioligand [3H]desGly‐NH29‐d(CH2)5[d‐Ileu2, Ileu4]AVP binding to V2 receptors in renal membranes (IC50 > 10‐4 mol/L).3. After oral administration to rats, OPC‐21268 was an effective V1 antagonist to both liver and kidney V1 receptors, in a dose‐dependent manner.4. These studies confirm that OPC‐21268 is a potent non‐peptide, orally effective V1 vasopressin receptor antagonist.
EFFECT OF POSITIVE FAMILY HISTORY OF HYPERTENSION ON THE BLOOD PRESSURE AND CATECHOLAMINE RESPONSES TO A 6 HOUR ADRENALINE INFUSION
Authors: Bachmann Anthony W. , Ballantine Donna M. , Gordon Richard D. 
Published: June 2007

SUMMARY1. The effects of 6 h infusions of adrenaline (INF‐A) or dextrose (INF‐D) and of post‐infusion cold pressor test (CPT) were compared in normal subjects, with (FH +) and without (FH ‐) a family history of hypertension.2. Increased urinary excretion rates suggested facilitated noradrenaline (NA) release during and after INF‐A in both FH + and FH ‐.3. Urinary adrenaline (U ADR) excretion increased during INF‐A, as expected, and was also slightly higher after INF‐A than INF‐D.4. The effect of INF‐A on systolic blood pressure (SBP) was greater in FH — than in FH S but diastolic blood pressure (DBP) did not fall as quickly with nocturnal recumbency after INF‐A in FH +.5. A significantly greater response in plasma NA to CPT was seen in FH + than in FH — after INF‐A. A similar trend was also seen after INF‐D.6. Increases in DBP due to CPT were higher in FH + than in FH ‐ after both infusions.7. This study provides evidence of increased noradrenergic activity during and after INF‐A, and also of a difference in response to sympathetic stimulation between FH + and FH ‐.
EFFECTS OF NITRO‐l‐ARGININE ON ENDOTHELIUM‐DEPENDENT RELAXATION OF CANINE CEREBRAL ARTERIES
Authors: Ohta Fumihito , Kobayashi Yuta , Shinozuka Kazumasa , Shimoura Keiko , Hattori Keisuke , Moritake Kouzo 
Published: June 2007

SUMMARY1. The effect of NG‐nitro‐l‐arginine (NO2Arg) on the relaxation of canine basilar artery was investigated and compared with those of middle cerebral and femoral arteries.2. NO2Arg (10−7‐3 × 10−5 mol/L) inhibited the substance‐P (Sub‐P; 10−12‐10−8 mol/L) induced relaxation in the basilar artery precontracted with prostaglandin F2α (PGF2α; 10−5 mol/L) or KCl (10−2 mol/L) in a concentration‐dependent manner and a ratio of the maximum inhibition by NO2Arg (3 × 10−5 mol/L) was more than 90%.3. The relaxation induced by A23187 (10−9‐3 × 10−6) was also abolished by NO2Arg (3 × 10−5 mol/L), but that by glyceryl trinitrate (GTN; 10−9‐3 × 10−5 mol/L) was not, in the basilar artery precontracted with PGF2α (10−5 mol/L). NG‐nitro‐d‐arginine (NO2ArgD; 3 × 10−5 mol/L) did not affect the relaxation induced by Sub‐P (10−12‐10−8 mol/L).4. l‐arginine (l‐Arg; 3 × 10−5‐10−4 mol/L) did not inhibit Sub‐P (10−12‐10−8 mol/L) induced relaxation in the basilar artery. Pretreatment of l‐Arg (10−4 mol/L) reversed the relaxation inhibited by NO2Arg (3 × 10−6 mol/L) in the arteries.5. NO2Arg (3 × 10−5 mol/L) inhibited the Sub‐P (10−12‐10−8 mol/L) induced relaxation in the canine middle cerebral artery as much as in the basilar artery. NO2Arg (3 × 10−5 mol/L) also inhibited Sub‐P (10−12‐10−8 mol/L) induced relaxation in the femoral artery, but the degree of the inhibition was less than that in the basilar artery.6. These results suggest that the endothelium‐derived relaxing factor (EDRF) of canine basilar artery is mainly l‐Arg derived nitric oxide which may play a more important role in the basilar artery than the femoral artery.
MONOCLONAL ANTIBODIES TO ARGININE VASOPRESSIN RECEPTOR BIND TO LIVER, KIDNEY AND PITUITARY MEMBRANES
Authors: Trinder Deborah , Mooser Vincent , Phillips Paddy A. , Smith A. Ian , Casley David , Johnston Colin I. 
Published: June 2007

SUMMARY1. A vasopressin binding protein purified from rat liver membranes was used to immunize Balb/c mice and, subsequently, for the screening of hybrids raised in two different cell fusions.2. Three hybrids were obtained which secreted monoclonal antibodies (MoAb) that bound to the purified solubilized receptor as detected by an enzyme‐linked immunosorbent assay technique. All three MoAb immunoprecipitated the purified receptor.3. In addition, the MoAb bound in a concentration‐dependent manner to crude liver, kidney and anterior pituitary membranes, tissues known to contain arginine vasopressin (AVP) receptors but not to cardiac ventricle membranes which lack AVP receptors.4. However, the binding of [125I]‐[d(CH2)5, Sar7]AVP (a specific radiolabelled V1 antagonist) to the membrane‐bound receptor was not inhibited by these antibodies.5. These results suggest that MoAb recognize epitopes which are common to rat liver, kidney and anterior pituitary membranes but are not at the ligand binding site.
FIVE YEAR PROSPECTIVE STUDY ON BLOOD PRESSURE AND MAXIMAL OXYGEN UPTAKE
Authors: Sawada Susumu , Tanaka Hiroaki , Funakoshi Mitu , Shindo Munehiro , Kono Suminori , Ishiko Toshihiro 
Published: June 2007

SUMMARY1. The relationship between physical fitness (maximal oxygen uptake Vo2max) and incidence of hypertension was investigated through a prospective study for a total of 16525 human‐years of observation.2. This study involved 3305 Japanese males whose blood pressure (BP) was normal when they received their first physical examination before the age of 50. They were monitored from 1983 to 1988. The BP of 425 subjects was diagnosed as hypertension in the fifth year.3. Fitness levels were divided into quintiles according to Vo2max levels, and were compared with the changes of BP and relative risk of hypertension after adjustment for age, initial percentage of body fat (PFAT), initial BP, alcohol consumption, cigarette smoking status and familial history of hypertension. The increase in BP of subjects in the least fit group was higher than in any other group. Relative risk was calculated using a multiple logistic regression and was 1.9 × higher in the least fit group compared with the fittest group.4. The subjects were classified into three groups: the improved Vo2max group, the deteriorated Vo2max group and the unchanged Vo2max group. The increase in BP of the improved Vo2max group was significantly lower than the other two groups after adjustment for changes in PFAT, age, initial PFAT, initial BP, fitness level, alcohol consumption, cigarette smoking status and familial history of hypertension.5. It is concluded that low Vo2max level is related to higher incidence of hypertension. An improved Vo2max would therefore be able to prevent hypertension.
ANTI‐ARRHYTHMIC EFFECTS OF A NEW CALCIUM ANTAGONIST, MONOTEPIL, AJ‐2615, IN EXPERIMENTAL ARRHYTHMIC MODELS
Authors: Yamamoto T. , Hosoki K. , Karasawa T. 
Published: June 2007

SUMMARY1. To characterize the anti‐arrhythmic properties of a new calcium antagonist, monotepil, AJ‐2615, the preventive effects of AJ‐2615 were compared with those of the existing calcium antagonists, diltiazem and verapamil, in experimental models of arrhythmia.2. AJ‐2615 (0.1–3.0 mg/kg, i.v.) suppressed ventricular arrhythmias induced by adrenaline (10 μg/kg, i.v.) in rats. AJ‐2615 (0.1 mg/kg per min for 2 min, i.v.) also suppressed atrial tachycardia induced by aconitine (0.01% aconitine solution) in rats.3. In these activities, AJ‐2615 was comparable to or more potent than diltiazem and verapamil which are widely used for the treatment of arrhythmia.4. In pro‐arrhythmic activity, AJ‐2615 was less potent than diltiazem and verapamil.5. These results suggest that AJ‐2615 would be a safer anti‐arrhythmic agent, with less proarrhythmic liability than diltiazem and verapamil.
CHARACTERISTIC LOCALIZATION OF α1‐ and α2‐ADRENOCEPTORS IN THE HUMAN KIDNEY
Authors: Minamisawa Kohsuke , Umemura Satoshi , Hirawa Nobuhito , Hayashi Shuichi , Toya Yoshiyuki , Ishikawa Yoshihiro , Yasuda Gen , Ishii Masao 
Published: June 2007

SUMMARY1. The localization of α‐adrenoceptors in the plasma membranes of human kidney were investigated by radioligand binding, using an α1‐antagonist, [3H]‐bunazosin, and an α2‐antagonist, [3H]‐rauwolscine.2. Both the maximum binding (Bmax) and dissociation constant (Kd) of [3H]‐bunazosin were greater in the cortex than in the medulla. The Bmax of [3H]‐rauwolscine in the medulla was greater than in the cortex.3. Thus, α1‐adrenoceptors appeared to be localized predominantly in the cortex, while the α2‐adrenoceptors were mainly present in the medulla of the human kidney.
ATRIAL AND BRAIN NATRIURETIC PEPTIDE RESPONSE TO EXERCISE IN PATIENTS WITH ISCHAEMIC HEART DISEASE
Authors: Nicholson Sarah , Richards Mark , Espiner Eric , Nicholls Gary , Yandle Tim 
Published: June 2007

SUMMARY1. The response of venous plasma natriuretic peptides (atrial natriuretic peptide, ANP, and brain natriuretic peptide, BNP) plasma cyclic guanosine monophosphate (cGMP) and vasoactive hormones to dynamic exercise has been studied in 16 subjects undergoing diagnostic exercise tolerance for ischaemic heart disease (IHD), and in five healthy control subjects.2. In patients with IHD, plasma ANP increased 3‐fold (mean 16 ± 2.5 pmol/L pre‐exercise, 51 ± 11 pmol/L after exercise, P<0.01). Increase in plasma BNP (10.5 ± 1.6 pmol/L pre‐exercise, 13 ± 2 pmol/ L after exercise, P<0.01) was proportionately much less than ANP but more sustained. In exercising normal subjects, plasma ANP levels doubled (P<0.01) but there was no significant change in plasma BNP levels.3. In patients with IHD, there was a significant correlation between levels of plasma ANP and BNP before exercise (r = 0.97, P<0.001) as well as during exercise (r= 0.79, P<0.001).4. Hormone responses in patients with positive exercise tests did not differ significantly from those with negative tests.5. Although resting levels of plasma ANP and BNP in IHD are correlated, the findings indicate different mechanisms of secretion. The low BNP/ ANP ratio in response to acute dynamic exercise presumably reflects the predominance of ANP in pre‐secretory atrial stores.