bluuebunny/crossref_metadata_2025_split huggingface dataset:
INAPPROPRIATELY ELEVATED LEVELS OF ATRIAL NATRIURETIC PEPTIDE MAY CONTRIBUTE TO THE PATHOPHYSIOLOGY OF ORTHOSTATIC HYPOTENSION
Authors: Tunny Terry J. , Gordon Richard D. , Klemm Shelley A. , Bachmann Anthony W. , Finn Wendy L. 
Published: June 2007

SUMMARY1. Overnight recumbent and upright plasma atrial natriuretic peptide (ANP) levels were markedly elevated (P < 0.001) in patients with orthostatic hypotension (OH).2. Overnight urinary clearance of ANP was significantly lower (P < 0.01) in patients with OH, and was inversely correlated with plasma ANP levels (r=–0.94, P < 0.01). The same negative correlation (r=–0.87, P < 0.01) was seen in normal subjects.3. Reduced urinary clearance of ANP may be associated with reduced filtered load and increased binding of ANP to the neutral endopeptidase 24.11 receptor binding sites in the proximal renal tubule.4. ANP may be involved in the pathophysiology of orthostatic hypotension.
EFFECTS OF REPEATED DOSES OF PSEUDOEPHEDRINE ON BLOOD PRESSURE AND PLASMA CATECHOLAMINES IN NORMAL SUBJECTS AND IN PATIENTS WITH PHAEOCHROMOCYTOMA
Authors: Gordon Richard D. , Ballantine Donna M. , Bachmann Anthony W. 
Published: June 2007

SUMMARY1. Increases in blood pressure (BP) and in plasma noradrenaline concentration (NA) were observed after two doses of a non‐prescription decongestant containing pseudoephedrine (PE) in two of three patients with phaeochromocytoma, before but not after removal of the tumour. The pressor response was terminated by oral phenoxybenzamine, and modified by prior exposure to this drug.2. In eight normal subjects administration of the same two doses prevented falls in BP and in NA usually seen with prolonged recumbency, but neither BP nor NA increased. However, a pressor response was observed in a normal subject with a strong family history of hypertension.3. Exposure to PE in non‐prescription decongestants is not without risk in hypertension.
SUBPRESSOR CALCIUM INFUSION INCREASES ISOVOLUMIC LEFT VENTRICULAR RELAXATION TIME AND ATRIAL NATRIURETIC PEPTIDE IN HUMANS
Authors: Finn Wendy L. , Gordon Richard D. , Seneviratne Basil I. , Tunny Terry J. , Klemm Shelley A. 
Published: June 2007

SUMMARY1. Subpressor calcium infusion for 1 h, which raised calcium levels to the upper limit of normal in normal subjects, increased plasma and urinary levels of atrial natriuretic peptide (ANP).2. Heart rate fell, presumably due to carotid baroreflex stimulation (supported by the fall in noradrenaline) and the resultant fall in cardiac output prevented the expected rise in blood pressure due to the rise in total peripheral resistance (TPR). Thus the increase in ANP was not explained by an increase in blood pressure or noradrenaline.3. There was no evidence for increased atrial stretch (no increase in atrial area or early velocity of left ventricular filling) as a mechanism for increased ANP.4. Isovolumic left ventricular relaxation time increased, early velocity of ventricular filling decreased and TPR increased, consistent with increased tone in left ventricular and arteriolar muscle.5. This suggests a direct effect of calcium on the atrial myocyte, stimulating ANP either through contractile or secretory mechanisms.
POLYMORPHISMS OF CANDIDATE GENES IN ESSENTIAL HYPERTENSION
Authors: West M. J. , Summers K. M. , Huggard P. R. 
Published: June 2007

SUMMARY1. Family and population studies have reported that blood pressure has a heritability of 30–50%, but simple genetic models do not readily explain the patterns of inheritance of hypertension.2. Restriction fragment length polymorphisms were used to study allele frequencies of a selection of candidate genes that may be important in determining the genetic component of hypertension. These included the genes for renin, haptoglobin, neuropeptide Y and cardiac myosin β heavy chain.3. There was no significant association between alleles at any of these loci and the presence of hypertension in this population, suggesting that the contribution of variation at these loci to the genetic component of the variance in hypertension may be quite small.
AXONAL PROJECTIONS FROM RESPIRATORY CENTRES TOWARDS THE ROSTRAL VENTROLATERAL MEDULLA IN THE RAT
Authors: Pilowsky Paul , Wakefield Bruce , Minson Jane , Llewellyn‐Smith Ida , Chalmers John 
Published: June 2007

SUMMARY1. Efferent pathways from brainstem respiratory centres towards bulbospinal tyrosine hydroxylase immunoreactive neurons were identified in the rat using a combination of electrophysiology, retrograde and anterograde tract‐tracing, and immunohistoehemistry.2. Varicose axons originating from respiratory centres were found in close apposition to bulbospinal tyrosine hydroxylase immunoreactive neurons in the ventrolateral medulla.3. These findings support the idea that respiratory rhythms in sympathetic nerves may be due to a synaptic connection between brainstem respiratory neurons and bulbospinal tyrosine hydroxylase immunoreactive neurons of the CI cell group.
MESENTERIC VASCULAR ANGIOTENSIN‐CONVERTING ENZYME IS INCREASED IN EXPERIMENTAL DIABETES MELLITUS
Authors: Jandeleit Karin , Rumble Jon , Jackson Bruce , Cooper Mark E. 
Published: June 2007

SUMMARY1. Diabetes mellitus was induced by streptozotocin in male Wistar rats, and angiotensin‐converting enzyme measured in plasma and mesenteric vessels 3 weeks later.2. Diabetes was associated with increased mesenteric wet weight/ bodyweight ratio (control 0.2 s.e.m. 0.02 mg/g, n= 21, vs diabetes 1.0 s.e.m. 0.3 mg/g, n= 27, P < 0.01, ANOVA).3. Plasma angiotensin‐converting enzyme activity was increased in diabetic rats (98 s.e.m. 3 nmol HL/mL per min) compared with controls (64 s.e.m. 6 nmol HL/mL per min, P < 0.01, ANOVA).4. Mesenteric vessel angiotensin‐converting enzyme was increased in diabetes mellitus estimated by radioligand binding site density (fmol/mg protein; 1407 s.e.m. 166 fmol/mg protein) compared with controls (890 s.e.m. 56 fmol/mg protein, P < 0.05, ANOVA) and by enzyme kinetic assay (diabetes, 15.5 s.e.m. 1.5 nmol HL/mg protein per min, controls, 8.3 s.e.m. 0.7 nmol HL/mg protein per min, P < 0.01, ANOVA). The equilibrium dissociation constant of ligand‐angiotensin‐converting enzyme interaction was unchanged.5. Increased vascular angiotensin‐converting enzyme concentration may contribute to vascular hypertrophy and diabetic vasculopathy by increased local synthesis of angiotensin II.
MESENTERIC RESISTANCE AND BRAIN MICROVASCULAR ANGIOTENSIN‐CONVERTING ENZYME IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Jandeleit Karin , Perich Rose , Jackson Bruce , Johnston Colin I. 
Published: June 2007

SUMMARY1. Angiotensin‐converting enzyme (ACE) concentration was measured in mesenteric and brain microvessels from spontaneously hypertensive rats (SHR) and compared with normotensive controls using a specific radioligand binding assay.2. Plasma angiotensin‐converting enzyme activity was similar in SHR (n= 15) and normotensive controls (n= 21; 58 ± 1 nmol HL/mL per min, vs 64 ± 6 nmol HL/mL per min).3. There was no significant difference between the mesenteric vascular angiotensin‐converting enzyme radioligand binding site density (Bmax, fmol/ mg protein) of SHR and normotensive controls (954 ±77 vs 890 ±56, P= 0.5, unpaired Student's t‐test), despite significant differences in systolic blood pressure (220 ± 8 mmHg vs 120 ± 6 mmHg respectively, P < 0.01) and increased mesenteric wet weight to body weight ratio in the hypertensive rats (0.28 ± 0.02 mg/g, n= 5 vs 0.16 ± 0.02 mg/g, n= 7, P < 0.01).4. Brain vascular angiotensin‐converting enzyme radioligand binding site density (Bmax, fmol/ mg protein) was also similar in SHR and normotensive controls (467 ±62, n= 5 vs 497 ± 64, n= 5, P= 0.7, unpaired Student's t‐test).5. These results demonstrate that vascular angiotensin‐converting enzyme concentration is not altered in the SHR and that vascular ACE is not increased in this form of vascular hypertrophy or regulated by the blood pressure level.
VARIATION IN ANGIOTENSIN‐CONVERTING ENZYME (ACE) INHIBITOR AFFINITY AT TWO BINDING SITES ON RAT PULMONARY ACE: INFLUENCE ON BRADYKININ HYDROLYSIS
Authors: Perich Rose B. , Jackson Bruce , Johnston Colin I. 
Published: June 2007

SUMMARY1. ACE from rat lung and testis was characterized by radioligand binding studies using [125I]‐Ro 31‐8472, the radioiodinated hydroxy derivative of the potent ACE inhibitor cilazaprilat.2. Analysis of the displacement of [125I]‐Ro 31‐8472 from ACE by ACE inhibitors of different structure by the ligand program was best fitted by a two binding site model for lung ACE and a one binding site model for testis ACE.3. There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/ L) for site one vs site two: cilazaprilat 40 ± 3 vs 430 ± 92*; lisinopril 25±1 vs 848 ± 107**; and quinaprilat 4 ± 1 vs 1869 ± 720; **P < 0.05; **P < 0.005, t‐test, n= 3). Reduction in binding affinity at site two of lung ACE was related to an increase in ACE inhibitor side chain length or complexity of carboxyl terminal moiety. ACE inhibitor binding affinity at the testis ACE binding site resembled site one of lung ACE.4. Inhibition of bradykinin hydrolysis by lung ACE in the presence of increasing concentrations of cilazaprilat or quinaprilat was similar (F= 0.64; P>0.05), suggesting that bradykinin cleavage predominates at ACE active site one.5. The differences in ACE inhibitor affinity at the two ACE active sites has implications in physiological substrate selectivity, and may influence the pharmacodynamic effects of different ACE inhibitors.
DEVELOPMENT AND VALIDATION OF ECHOCARDIOGRAPHY METHODS FOR ESTIMATING LEFT VENTRICULAR MASS IN RATS
Authors: Jones Elizabeth F. , Harrap Stephen B. , Calafiore Paul , Tonkin Andrew M. 
Published: June 2007

SUMMARY1. The aim of this study was to develop non‐invasive echocardiography methods of measuring left ventricular mass (LVM) in rats, and to determine their usefulness in detecting left ventricular hypertrophy.2. After initial studies to identify the optimum transducer and to ascertain the resolution limits of echocardiography, the repeatability of LVM estimates was studied. The average difference between two independent estimates in 86 male rats (average LVM = 674.7 mg) was 5.4 mg, and the standard deviation of the difference was 107.6 mg.3. To determine agreement between direct and indirect methods, LVM was measured in 38 male rats by echocardiography and compared with direct measurement of the left ventricular weight at sacrifice. The mean difference between the two methods was 9.14 ± 56.6 mg. The limits of agreement were from ‐ 122.4 to +104.1 mg.4. Echocardiography was then used to measure LVM in eight male spontaneously hypertensive rats and eight male normotensive Donryu rats at 9 weeks of age. The mean LVM of SHR was 768.2 mg ± 152.6, which was significantly (2P < 0.001) greater than the LVM of DRY (435.4 mg ± 32.2).5. We conclude that echocardiography provides a non‐invasive, repeatable and relatively accurate estimate of LVM in rats. The method is a potentially useful tool for studying the development or regression of cardiac hypertrophy in longitudinal experiments.
EFFECT OF NEUTRAL ENDOPEPTIDASE INHIBITOR IN RATS WITH CONGESTIVE HEART FAILURE
Authors: Murohara Yoshiharu , Johnston Colin I. 
Published: June 2007

SUMMARY1. The acute hormonal, renal and haemodynamic effects of SCH 39370, a new neutral endopeptidase (NEP) inhibitor, were evaluated in rats with congestive heart failure (CHF) produced by coronary ligation.2. Left ventricular systolic pressure and left ventricular end diastolic pressure were significantly decreased by SCH 39370 treatment.3. SCH 39370 improved cardiac function by increasing cardiac index and decreasing total peripheral resistance.4. SCH 39370 induced a transient but significant diuresis and natriuresis.5. These effects were associated with significant increases in urinary atrial natriuretic peptide (ANP) and cyclic GMP excretion, but not with an increase in plasma ANP levels.6. The results suggest that NEP inhibition may be a new therapeutic method for treating CHF possibly by potentiating the biological activities of endogenous ANP.
INTERACTION BETWEEN VASOPRESSIN AND ENDOTHELIN IN RENAL PAPILLARY TUBULES: UNCOUPLING FOLLOWING CELL ISOLATION AND CULTURE
Authors: Woodcock Elizabeth A. , Land Sarah 
Published: June 2007

SUMMARY1. In freshly prepared rat renal papillary tubules, endothelin‐related peptides inhibited the vasopressin‐stimulated accumulation of cAMP. No inhibition was observed when tubules were cultured overnight ex vivo.2. Endothelin‐1, endothelin‐3 and sarafatoxin S6b had similar potencies as inhibitors of cAMP accumulation, indicating an endothelin (ETb) receptor.3. These results demonstrate an interaction between ETb receptors and vasopressin receptors at the level of their signal transduction pathways, and show that this relationship is lost following cell culture.
ENDOTHELIUM‐DEPENDENT AND‐INDEPENDENT RELAXATION BY DOPAMINE IN THE RABBIT PULMONARY ARTERY
Authors: Yamauchi Masanobu , Kobayashi Yuta , Shimoura Keiko , Hattori Keisuke , Nakase Akira 
Published: June 2007

SUMMARY1. The relaxing response of dopamine (DA) was studied in the rabbit pulmonary artery. DA caused concentration‐related relaxation in helically cut strips of the artery contracted with prostaglandin F2α in the presence of prazosin.2. The DA‐induced relaxation in endothelium‐denuded strips was reduced to about 40% compared with that in endothelium‐intact strips.3. Methylene blue and haemoglobin, inhibitors of endothelium‐dependent relaxation, reduced the DA‐induced relaxations in endothelium‐intact strips to the level of endothelium‐denuded strips. These results indicate that the DA‐induced relaxation is partially mediated or modified by the release of endothelium‐derived relaxing factor (EDRF).4. Apomorphine, as a DA agonist, caused concentration‐dependent relaxation in endothelium‐intact strips. Bromocriptine, a DA2 agonist, produced only a little relaxation at higher concentration.5. In endothelium‐intact strips, haloperidol, a DA antagonist, and the DA1 antagonists, fluphenazine and SCH 23390 inhibited DA‐induced relaxations. On the other hand spiperone and domperidone, DA2 antagonists, were inactive.6. In endothelium‐denuded strips, fluphenazine and SCH 23390 inhibited DA‐induced relaxations, but domperidone was inactive.7. These results indicate that the DA‐induced relaxation is mediated by DA receptors, and that DA1 receptors are involved in both endothelium‐dependent and‐independent relaxation in the rabbit pulmonary artery.
RANITIDINE INHIBITS ADRENERGIC TRANSMISSION IN THE RAT ISOLATED ANOCOCCYGEUS MUSCLE
Authors: Gwee M. C. E. , Cheah L. S. 
Published: June 2007

SUMMARY1. The effects of ranitidine on adrenergic transmission in the rat isolated anococcygeus muscle were investigated.2. Cumulative doses (2–8 mmol/ L) of ranitidine produced a concentration‐dependent inhibition of motor responses of the rat isolated anococcygeus muscle evoked by field stimulation (20–25 V, 10 Hz for 10 s, 1 ms pulse width) every 2 min, but also potentiated the contractile response to exogenous noradrenaline (5 μmol/L). The inhibited motor responses recovered rapidly and completely after washing out ranitidine.3. 4‐Aminopyridine (100 μmol/L) effectively reversed the partially inhibited (55% or greater) motor responses.4. The results strongly suggest that ranitidine can inhibit adrenergic transmission in the anococcygeus muscle by a prejunctional mechanism with, presumably, consequent development of supersensitivity of the effector cells to noradrenaline.
CARDIAC EFFECTS OF LOCAL ANGIOTENSIN‐CONVERTING ENZYME INHIBITION IN HYPERTENSIVE PATIENTS
Authors: Nakashima Yoshiyuki , Nii Takanobu , Tashiro Eiichiro , Ikeda Masaharu , Arakawa Kikuo 
Published: June 2007

SUMMARY1. The direct cardiac effects of angiotensin‐converting enzyme (ACE) inhibitor in 22 hypertensive patients were investigated. Radionuclide ventriculography and echocardiography were performed to measure left ventricular function before and 60 min after administration of a subdepressor dose of captopril.2. Since the response to ACE inhibitor is not uniform, patients were classified into 12 patients without significant blood pressure change following captopril (group I) and 10 patients with reduction of blood pressure (group II).3. Clinical and baseline haemodynamic characteristics were similar for the two groups.4. Ejection fraction (EF) increased without changes of heart rate and end‐diastolic dimension after ACE inhibitor in group I as well as group II. The change of EF was not different for the two groups. No correlation was found between changes in EF and blood pressure in group I patients.5. This study indicates that ACE inhibitor might directly influence left ventricular function independent of systemic haemodynamic changes.
MODELLING OF FREQUENCY‐DEPENDENT EFFECTS OF LIGNOCAINE HOMOLOGUES ON THE MAXIMUM UPSTROKE VELOCITY OF ACTION POTENTIALS IN GUINEA‐PIG PAPILLARY MUSCLES
Authors: Hamamoto Takuyuki , Ichiyama Masashi , Takahashi Yoshihiro , Ban Takashi 
Published: June 2007

SUMMARY1. The effects of 14 lignocaine homologues on the maximum upstroke velocity (Vmax) of the action potentials (AP) were studied in guinea‐pig papillary muscles. These drugs possess one, two or three methyl groups in different positions: an ortho‐chloro,‐carbomethoxy or‐ethyl group instead of an ortho‐methyl group; or an N‐butyl group instead of an N‐diethyl group in lignocaine molecules.2. At 50–100 μol/L, six drugs possessing two ortho substituents (but not the other eight) reduced Vmax more prominently at 2‐4 Hz than at 1 Hz, and slowed the time courses of recovery of the premature responses. None of the drugs affected resting potential.3. Besides the two‐state piecewise exponential model (models I and II) frequently used, a time‐dependent and time‐independent, two‐state model (model III) was formulated and applied to these experimental data. The above two groups were effectively distinguished by the difference of the estimated association and dissociation rate constants (model II) and equilibrium constants for phasic state (model III) and for resting (model II) or tonic (model III) states.4. The equilibrium constants for resting or tonic state correlated well with log P (where P = the n‐octanol: water partition coefficients), but correlated better with an indicator variable that denotes the existence of two ortho substituents, suggesting the importance of the contribution of steric factors to the activity.
COMPARATIVE EFFECTS OF DOPAMINE AND DOBUTAMINE ON THE PULMONARY HAEMODYNAMIC RESPONSE TO HYPOXIA IN DOGS VENTILATED WITH A HYPOXIC GAS MIXTURE
Authors: Tanaka Hiroyuki , Tajimi Kimitaka , Kasai Takeshi , Kobayashi Kunio 
Published: June 2007

SUMMARY1. The effects of dopamine and dobutamine on the pulmonary haemodynamic response to hypoxia were studied in nine anaesthetized dogs under hypoxaemia induced by ventilation with hypoxic gas mixture.2. From the present study, only dopamine infusion reduced arterial oxygenation during hypoxic hypoxaemia, whereas catecholamine maintained it at the same level during normoxaemia.3. A redistribution of perfusion to the pulmonary vasculature may be related to a reduction of arterial oxygenation with dopamine infusion during hypoxic hypoxaemia.4. It is presumed that an increase in pulmonary blood flow would emphasize an inhibition of hypoxic pressor response in the pulmonary vasculature, which may not be a direct effect of dopamine.
CIRCULATING ANGIOTENSIN II LEVELS UNDER REPEATED ADMINISTRATION OF LISINOPRIL IN NORMAL SUBJECTS
Authors: Kawamura Minoru , Imanashi Masahito , Matsushima Yohkazu , Ito Keiichi , Hiramori Katsuhiko 
Published: June 2007

SUMMARY1. To examine the effect of chronic administration of angiotensin I‐converting enzyme (ACE) inhibitor on circulating angiotensin II (All) concentration, 20 mg of lisinopril was administered once daily for 7 consecutive days to eight healthy volunteers.2. Plasma ACE activity was inhibited to less than approximately 30% of the pretreatment level during the repeated administration.3. Mean arterial pressure (MAP) was slightly but significantly reduced during the administration period. Plasma All concentration measured by an established method using high performance liquid chromatography combined with a radioImmunoassay, however, was maintained at approximately the pretreatment level when it was measured at 24 h intervals after each administration of lisinopril.4. With the gradual recovery of ACE activity following discontinuation of administration, the plasma All concentration correlated with AI concentration (r= 0.46), and also with the product of AI and ACE activity (AI X ACE; r= 0.80), corresponding to the formula obtained from the kinetics of ACE activity. No correlation was observed between MAP and All levels throughout the study period.5. We conclude that in normal subjects repeatedly administered with ACE inhibitor, the All level in the circulation is still determined by an elevated level of AI and any remaining ACE activity, thus maintaining All at pretreatment levels. We confirmed that it is not necessary to achieve a decrease in plasma All concentration through the chronic administration of ACE inhibitor in order to effectively lower blood pressure.
EFFECTS OF CHRONIC ADMINISTRATION OF ANTIHYPERTENSIVE DRUGS ON VASODILATION MEDIATED BY CALCITONIN GENE‐RELATED PEPTIDE‐CONTAINING VASODILATOR NERVES IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kawasaki Hiromu 
Published: June 2007

SUMMARY1. The effects of chronic administration of antihypertensive drugs on the vasodilator response mediated by calcitonin gene‐related peptide (CGRP)‐containing nerves were investigated in spontaneously hypertensive rats (SHR).2. A 7 week period of antihypertensive treatment with captopril, nicardipine or propranolol during the developmental phase (8–15 weeks of age) significantly lowered the mean blood pressure of SHR when compared with non‐treated SHR.3. The mesenteric vascular beds isolated from SHR, which were chronically administered with captopril, propranolol or nicardipine, were perfused with Krebs’ solution containing 7/μmol/L methoxamine to produce active tone and 5 μmol/L guanethidine to block adrenergic neurotransmission.4. In the mesenteric vascular bed with active tone, perivascular nerve stimulation (PNS; 0.5–8 Hz) caused a frequency‐dependent vasodilator response that was abolished by 100 nmol/L tetrodotoxin (neurotoxin) or 1 μmol/L CGRP (8–37), a CGRP receptor antagonist.5. CGRP‐containing nerve‐mediated vasodilator responses were significantly greater in cap‐topril‐treated SHR and significantly smaller in nicardipine‐treated SHR than in non‐treated SHR. There was no difference between the response between propranolol‐treated SHR and non‐treated SHR.6. These results suggest that chronic treatment with captopril reverses the reduced neurogenic vasodilation mediated by CGRP‐containing nerves in SHR.