bluuebunny/crossref_metadata_2025_split huggingface dataset:
RENAL VASOCONSTRICTION IS MODULATED BY NITRIC OXIDE
Authors: Reid Julianne J. , Rand Michael J. 
Published: June 2007

SUMMARY1. The effect of the nitric oxide synthesis inhibitor, NG‐nitro‐L‐arginine (NOLA), has been examined on vascular reactivity in the rat isolated perfused kidney.2. NOLA (10 jμmol/L) had no effect on basal perfusion pressure, but significantly enhanced the vasoconstrictor responses to sympathetic nerve stimulation (1–16 Hz, 10 s) and noradrenaline (10–300 pmol). The enhancements were greater with the lower frequencies of stimulation and lower doses of noradrenaline.3. The enhancing effect of 10 /μmol/L NOLA on vasoconstrictor responses to nerve stimulation was partially prevented by 100 μmol/L L‐arginine while 100 μmol/ L D‐arginine had no effect.4. The results suggest that nitric oxide attenuates vasoconstrictor responses in the rat kidney, and provide evidence that nitric oxide has a physiological role in the modulation of vascular reactivity.
LONG‐TERM ANGIOTENSIN II ANTAGONISM IN SPONTANEOUSLY HYPERTENSIVE RATS: EFFECTS ON BLOOD PRESSURE AND CARDIOVASCULAR AMPLIFIERS
Authors: Oddie Catherine J. , Dilley Rodney J. , Bobik Alex 
Published: June 2007

SUMMARY1. The angiotensin II type 1 receptor antagonist, losartan, prevented the development of hypertension in spontaneously hypertensive rats (SHR).2. Losartan also prevented the development of left ventricular hypertrophy and vascular amplifier abnormalities.3. Part of the hypotensive effect induced by long‐term treatment with losartan persisted for a long time after the withdrawal of treatment.4. The results support the hypothesis that angiotensin II contributes to the development of hypertension and cardiovascular hypertrophy in SHR.
DIFFERENTIAL REGULATION BY TRANSFORMING GROWTH FACTOR‐β1 OF PLATELET‐DERIVED GROWTH FACTOR‐ STIMULATED PROLIFERATION OF VASCULAR SMOOTH MUSCLE CELLS FROM SHR AND WKY RATS
Authors: Saltis John , Agrotis Alex , Bobik Alex 
Published: June 2007

SUMMARY1. This study has examined and compared the time‐course of action of transforming growth factor‐β1 (TGF‐β1) on platelet‐derived growth factor‐BB‐stimulated proliferation of vascular smooth muscle cells isolated from normotensive Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).2. Transforming growth factor‐β1 inhibited vascular smooth muscle cell proliferation stimulated by platelet‐derived growth factor‐BB in WKY rats by approximately 60–75%.3. In contrast, transforming growth factor‐β1 potentiated an 8–35% growth factor action on cell proliferation in the SHR.4. Defects in transforming growth factor‐β1 action may be part of the molecular mechanism responsible for the development of vascular hypertrophy in the SHR.
Platelet‐activating factor in bronchoalveolar lavage fluid of patients with adult respiratory distress syndrome
Authors: Matsumoto Kohei , Taki Fumio , Kondoh Yasuhiro , Taniguchi Hiroyuki , Takagi Kenzo 
Published: June 2007

SUMMARY1. To clarify the role of platelet‐activating factor (PAF) in the development of adult respiratory distress syndrome (ARDS), we performed bronchoalveolar lavage (BAL) in 19 patients with ARDS and examined cell populations, albumin concentrations and PAF levels. PAF levels were measured by a newly developed radioimmunoassay.2. In the BAL fluid of ARDS patients, neutrophil percentages and albumin concentrations markedly increased compared with control subjects.3. PAF was detected in 14 of 19 patients with ARDS, whereas it did not exist in the control subjects.4. Furthermore, we investigated the priming effect of recombinant human tumour necrosis factor‐α (TNFα), which is known to be one of the most important mediators in the development of ARDS, on PAF production induced by the calcium ionophore in neutrophils.5. Pre‐incubation with TNFα dose‐dependently increased both extracellular and intracellular PAF production in neutrophils.6. These results suggest that PAF might play an important role in the development of ARDS.
INTERACTION OF THE NON‐STEROIDAL ANTIINFLAMMATORY DRUG FLUFENAMIC ACID WITH GASTRIC ACID SECRETION AND H+/K+ ‐ATPase
Authors: Beil W. , Greite C. , Sewing K‐F. 
Published: June 2007

SUMMARY1. The effects of the non‐steroidal anti‐inflammatory drug (NSAID) flufenamic acid on H+production in isolated and enriched guinea‐pig parietal cells and on H+/K+‐ATPase activity in ion‐tight inside‐out membrane vesicles from pig gastric mucosa were studied.2. At low concentrations (0.1 and 1.0 μmol/L), flufenamic acid increased the secretory response of parietal cells to dibutyryl cyclic AMP (dbcAMP). At higher concentrations (10 and 100 μmol/L) it progressively inhibited basal and dbcAMP‐stimulated acid production.3. Flufenamic acid (10 μmol/L) increased K+ (0.5–10.0 mmol/L) and K+ (0.5–1.0 mmol/L) plus gramicidin‐stimulated ATPase activity in gastric membrane vesicles. The Km value for K+ (1.6 and 1.0 mmol/L in the absence and presence of gramicidin, respectively) was decreased to 0.8 and 0.5 mmol/L, respectively. At higher concentrations (≥ 50 μmol/L), flufenamic acid inhibited K+ plus gramicidin‐stimulated ATPase activity (inhibited concentration at 50% [IC50] = 186 μmol/L) and reduced the proton concentration (IC50= 50 μmol/L).4. It is concluded that flufenamic acid‐induced enhancement of dibutyryl cyclic AMP‐stimulated H+ production in the parietal cell reflects the stimulation of H+/K+‐ATPase. We suggest that activation of the enzyme involves increased affinity of K+ towards the K+‐binding site of the enzyme and/ or increased KC1 permeability at the vesicle membrane. The inhibitory action of the drug on H+production in parietal cells results from a detergent and/or protonophoric‐like action at the apical parietal cell membrane, and from inhibition of H+/K+‐ATPase activity.
PLASMA ADENOSINE CONCENTRATIONS ARE ELEVATED IN CONSCIOUS SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Yamada K. , Goto A. , Ishii M. , Yoshioka M. , Matsuoka H. , Sugimoto T. 
Published: June 2007

SUMMARY1. Plasma levels of adenosine were measured in unrestrained, conscious spontaneously hypertensive rats (SHR) to examine the potential role of adenosine, a naturally occurring substance with profound cardiovascular actions, in cardiovascular regulation in these genetically hypertensive rats.2. We employed a specific and sensitive assay for adenosine based on fluorescent determination of adenine compounds by high performance liquid chromatography.3. Plasma adenosine concentrations were significantly higher in 13 week old SHR with hypertension than in Wistar‐Kyoto rats (0.165±0.022 vs 0.096±0.008 μmol/L; P < 0.05).4. These observations indicate that plasma adenosine levels are increased in conscious SHR with established hypertension, and also suggest that adenosine may be at least partly involved in the pathophysiology of high blood pressure in SHR.
INTRACORONARY PGE2 AND VERATRINE INHIBITS RENIN RELEASE IN CONSCIOUS DOGS VIA CHEMOSENSITIVE VENTRICULAR AFFERENTS
Authors: Gorman A. J. , Chen J‐S. , Foster S. , Snyder R. G. , Lams S. G. 
Published: June 2007

SUMMARY1. Prostaglandins (PG) and veratrum alkaloids stimulate ventricular sensory receptors with non‐myelinated vagal afferents and mediate inhibitory circulatory responses.2. The present study in conscious instrumented dogs was carried out to determine the effects of intracoronary artery infusions of veratrine (Ver‐IC) and PGE2 (PGE2‐IC) on plasma renin activity (PRA).3. A 15‐20 mmHg decrease in arterial pressure was produced during Ver‐IC (0.2–0.8 μg/kg per min) and PGE2‐IC (10‐50 ng/kg per min), but there was no change in PRA or heart rate.4. In contrast, significant increases in PRA (+ 3.51 ± 0.37 ng angiotensin 1/mL per h; P < 0.01) and heart rate (+ 38.5 ± 6.2 beats/min; P < 0.001) were elicited in response to a 15–20 mmHg decrease in arterial pressure produced by intravenous infusions of nitroprusside.5. Pharmacological blockade of afferent fibres in the pericoronary region of the left main coronary artery during Ver‐IC resulted in significant hypotension‐induced increases in PRA (P < 0.001) and heart rate (P < 0.001), thus removing the inhibitory influence of chemosensitive ventricular afferents.6. Therefore, intracoronary veratrum alkaloids and prostaglandins inhibit hypotension‐induced increases in PRA and heart rate in the conscious dog. This is mediated by chemosensitive receptors located in the left ventricular myocardium along with afferent nerves in the pericoronary region and cervical vagi.
A DEVELOPMENTAL GENETIC MECHANISM INVOLVING ANGIOTENSIN IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Harrap Stephen B. 
Published: June 2007

SUMMARY1. Certain genes drive the blood pressure of young spontaneously hypertensive rats (SHR) to stable hypertensive levels in adulthood.2. Relatively brief blockade of the renin‐angiotensin system in young SHR can reset the track of SHR pressure to a lower level for the life of the animal. This effect appears to be a characteristic of the SHR strain.3. It is proposed that the expression of a particular SHR hypertensive gene depends on angiotensin and is limited to young animals. This hypothesis explains some of the phenotypic abnormalities observed in young SHR and the decremental long‐term blood pressure effects following ACE inhibitor treatment.4. The identity of the gene is unclear, but information from biochemical, physiological and pharmacological studies may direct attention to distinct candidate genes within specific chromosomal regions of interest.5. Understanding these genetic mechanisms may have important implications for future preventive strategies.
DIABETIC RENAL MICROVASCULAR DISEASE: THE ROLE OF HYPERTENSION AND ACE INHIBITORS
Authors: Cooper Mark E. , Rumble Jonathan R. , Gin Trevor , Lim‐Joon Troy 
Published: June 2007

SUMMARY1. It has been suggested that hypertension may be an important determinant of the rate of progression of diabetic microangiopathy.2. Renal microvascular disease as assessed by urinary albumin excretion and glomerular ultra‐structure was evaluated in a model in which streptozotocin diabetes was induced in spontaneously hypertensive rats (SHR).3. Diabetes was associated with increases in urinary albumin excretion, and hypertension resulted in a further increase in albuminuria.4. Various antihypertensive regimens were administered to diabetic SHR, with the angiotensin‐converting enzyme inhibitor perindopril and triple therapy (hydralazine, reserpine and hydrochlorothiazide) being more effective than the calcium antagonist (lacidipine) in retarding the increase in albuminuria in diabetic SHR.5. Antihypertensive therapy appears to ameliorate the development of diabetic renal disease.
THE EFFECT OF HYPERTENSION AND ACE INHIBITION ON ARTERIAL STRUCTURE AND COMPLIANCE
Authors: Safar M. E. , Levy B. I. 
Published: June 2007

SUMMARY1. Large artery dilatation may be produced by angiotensin‐converting enzyme inhibition in hypertensive subjects independently of blood pressure reduction. The resulting increase in arterial compliance may be due to both blood pressure reduction and to arterial smooth muscle relaxation.2. In healthy volunteers and in hypertensive subjects, dosages producing large artery dilatation seem to be even higher than those causing arteriole dilatation with the resulting blood pressure reduction.3. It may be important to consider such findings for the remodelling of the cardiovascular system produced by angiotensin‐converting enzyme inhibition.
CLINICAL EFFICACY OF PERINDOPRIL IN HYPERTENSION
Authors: Morgan Trefor , Anderson Adrianne 
Published: June 2007

SUMMARY1. Perindopril's effectiveness in mild to moderate hypertension was evaluated in three studies.2. Perindopril was more effective than sodium restriction in reducing blood pressure, and the effects were additive.3. Perindopril was as effective as atenolol in reducing blood pressure, and was well tolerated.4. Perindopril lowered blood pressure to the same extent as enalapril at peak drug levels but had a greater effect at the trough level of the drugs.5. Perindopril is an effective antihypertensive agent with an acceptable side‐effect profile in people with hypertension.
DIABETIC RAT AORTA RESPONSIVENESS TO D600 AND NIFEDIPINE
Authors: Orie N. N. , Aloamaka C. P. 
Published: June 2007

SUMMARY1. The responsiveness of aortic rings from 4 and 12 week streptozotocin‐induced diabetic rats to D600 (Gallopamil) and nifedipine was studied.2. The sensitivity and responsiveness to D600 were significantly enhanced (P < 0.05; 5‐test, ANOVA; 9 d.f.) only in the 4 week diabetic preparations precontracted with noradrenaline.3. Nifedipine‐induced relaxations were significantly enhanced (P < 0.05–0.01; t‐test, ANOVA; 8–12 d.f.) in all the diabetic (4 and 12 weeks) aortic preparations precontracted with both noradrenaline (10‐7 mol/L) and KCl (40 mmol/L) when compared with controls.4. D600, unlike nifedipine, did not produce significant relaxation of diabetic aortic preparations precontracted with KCl (40 mmol/L) at both week 4 and 12 of the disease when compared with controls.5. These results suggest that there is differential responsiveness of streptozotocin diabetic rat aorta to D600 and nifedipine.
ACUTE EFFECT OF PHYSIOLOGICAL CONCENTRATIONS OF VASOPRESSIN ON RAT RENAL FUNCTION
Authors: Carney Shane L. , Gillies Alastair H. B. , Ray Cheryl D. 
Published: June 2007

SUMMARY1. The antidiuretic, pressor and electrolyte transport effects of arginine vasopressin (AVP) were simultaneously evaluated in the anaesthetized water diuretic rat. Increasing concentrations of AVP (7.5, 75 and 750 ng/kg bolus and per h), were used to produce plasma levels which approximate the physiological range (4.8 ± 2.4, 35.7 ± 12.5, 85.2 ± 16.1 pg/mL respectively).2. Administration of a minimally effective antidiuretic dose (7.5 ng) increased mean urine osmolality (from 101 ± 7 to 312 ± 89 mosmol/kg) without altering mean arterial pressure (MAP), renal plasma flow (RPF) or glomerular filtration rate (GFR). A maximal antidiuretic dose of AVP (75 ng) increased mean urine osmolality to 2002 ± 109 mosmol/kg and was associated with significant mean increases in MAP (9 mmHg), RPF and GFR (25%) by 30–60 min. A further ten‐fold increase in AVP (750 ng) produced a greater increase in MAP (116 ± 6 to 134 ± 7 mmHg; P < 0.01) as well as increasing RPF and GFR by 35.5 and 38.9% respectively.3. Increasing concentrations of AVP also progressively increased the fractional excretion of sodium, potassium and phosphate. However, fractional calcium and magnesium excretion was significantly decreased with maximal and supramaximal concentrations.4. These studies support evidence that AVP is a pressor hormone in physiological concentrations in baroreceptor intact animals. Its role in renal electrolyte transport is unclear. Measured increases in RPF and GFR with the maximal and supramaximal AVP concentrations appear to be correlated with the increase in MAP.
SENSITIVITY OF PROPRANOLOL ELIMINATION TO HYPOXIA IN THE ISOLATED PERFUSED RAT LIVER PREPARATION
Authors: Elliott Susan L. , Morgan Denis J. , Angus Peter W. , Ghabrial Hany , Smallwood Richard A. 
Published: June 2007

SUMMARY1. The relationship between the hepatic elimination of propranolol and hepatic oxygen delivery was examined in the single‐pass isolated perfused rat liver preparation. Varying rates of oxygen delivery were produced (1.35–8.10 μmol/min per g liver) by equilibrating the perfusate with O2/N2 mixtures.2. In two experiments, in which the rate of oxygen delivery was increased or decreased within the hypoxic range (< 4–5 μmol/min per g liver) every 5 min for 120 min, propranolol clearance responded very rapidly in the same direction as the change in oxygen delivery.3. In five experiments, propranolol clearance, measured at steady state during an initial 30 min normoxia phase and three subsequent 30 min hypoxia phases (oxygen delivery in the range 1.35–5.89 μmol/min per g liver), was linearly related to hepatic oxygen delivery and consumption (r= 0.92 ± 0.07).4. These data, combined with those from six further experiments that used one normoxia phase followed by one hypoxia phase, showed that there was a threshold for oxygen delivery of about 6 μmol/min per g liver, below which propranolol clearance decreased with decreasing oxygenation.5. This study shows that in the intact liver propranolol elimination is very sensitive to hepatic oxygen supply, with impairment in clearance occurring at the lower limit of what is considered normal hepatic oxygenation in the rat.
RENIN AND PRORENIN IN REPRODUCTIVE TISSUES DURING GESTATION IN PIGS AND CATTLE
Authors: Hagemann Arne , Dantzer Vibeke , Nielsen Arne H. , Poulsen Knud 
Published: June 2007

SUMMARY1. High concentrations of prorenin and active renin were previously found in ovarian follicular fluid from cattle but not from pigs. In the present study female reproductive tissues and fluids from cattle and pigs during gestation were investigated to clarify a possible species difference in active renin and prorenin concentrations.2. Very high concentrations of active renin but no prorenin were found in corpus luteum from both species.3. Relatively low concentrations of active renin, in the same order as in maternal blood plasma, were found in myometrium, endometrium, placenta and fetal membranes from both species. Prorenin was undetectable in these tissues except for bovine myometrium and porcine endometrium in some animals.4. The concentrations of active renin and prorenin in amnionic fluid from both species were below the maternal plasma values. In allantoic fluid the concentrations were higher than in amnionic fluid.5. The plasma concentrations of active renin and prorenin did not change during gestation in pigs. This finding is in contrast to the observations in humans and does not support a systemic effect of prorenin during gestation.6. The presence of renin in the reproductive tissues, especially the very high concentrations in the corpus luteum, indicates a local function of the renin‐angiotensin system during gestation.
ANALGESIC ACTIVITY OF CERTAIN FLAVONE DERIVATIVES: A STRUCTURE‐ACTIVITY STUDY
Authors: Thirugnanasambantham P. , Viswanathan S. , Ramaswamy S. , Krishnamurty V. , Mythirayee C. , Kameswaran L. 
Published: June 2007

SUMMARY1. Flavone, its methoxy derivatives and flavanone were synthesized by standard methods and were tested for analgesic activity in mice by employing acetic acid writhing and tail flick methods.2. All the tested compounds except flavanone exhibited significant dose‐dependent analgesic activity in both the assay models. Some of the compounds were found to involve opioid mechanisms in their analgesic effect.3. A definite structure‐activity relationship was observed in the analgesic activity of flavone derivatives as well as in their mechanism of action.
A1‐and A2‐PURINOCEPTORS IN THE GUINEA‐PIG UTERUS
Authors: Haynes John M. , Pennefather Jocelyn N. 
Published: June 2007

SUMMARY1. Radioligand binding and functional studies were undertaken to investigate the P1‐purinoceptors present in the separated myometrial layers and the endometrium of the guinea‐pig uterus.2. In preparations of endometrium‐denuded circular myometrium, the A2‐selective agonists (2‐p‐(2‐carboxyethyl)phenethylamino‐5'‐N‐ethylcarboxamido‐adenosine (CGS 21680, 100 μmol/L) and N‐ethylcarboxamido adenosine (NECA, 1–10 μmol/L) inhibited contractile responses to phenylephrine. In preparations of endometrium‐intact circular myometrium, NECA (10 μmol/L) enhanced responses to phenylephrine. NECA did not modulate the spontaneous contractions of longitudinal myometrium.3. Homogenate binding studies with circular myometrium, longitudinal myometrium and endometrium revealed saturable high affinity [3H]‐NECA binding sites. The mean maximal densities of binding sites (Bmax) were 2.08, 14.7 and 15.5 fmol/mg protein, and pKD (neg. log dissociation constant) values were 9.82, 9.19 and 7.44, respectively.4. (R‐) and (S‐) ‐N6‐(2‐phenylisopropyl)adenosine (R‐ and S‐PIA) both competed for two [3H]‐NECA binding sites in preparations of circular myometrium. CGS 21680 competed for two [3H]‐NECA binding sites in preparations of endometrium and longitudinal myometrium. All other agonist competition was for one site only. The rank orders of potency of high affinity binding were S‐PIA ≥ R‐PIA ≥ CGS 21680 (circular myometrium), R‐PIA ≥ CGS 21680 ≥ S‐PIA (longitudinal myometrium) and CGS 21680 > > S‐PIA ≥ R‐PIA (endometrium).5. In preparations of circular myometrium, longitudinal myometrium and endometrium the selective A1‐purinoceptor antagonist, 1,3‐dipropyl‐8‐(2‐amino‐4‐chloro)‐phenylxanthine (PACPX), competed for two [3H]‐NECA binding sites, the non‐selective antagonist 3,7‐dimethyl‐1‐propargylxanthine (DMPX), competed for one site only.6. NECA increased cyclic adenosine monophosphate (CAMP) levels in preparations of both circular myometrium and endometrium.7. These results indicate that P1‐purinoceptors of the A2‐subtype mediate the inhibitory effects of adenosine analogues on the phenylephrine‐induced contractions of the circular myometrium of the guinea‐pig, this effect is modified by the presence of the endometrium. There is no evidence that the [3H]‐NECA binding sites of the longitudinal myometrium correlate with functional P1‐purinoceptors in this tissue.
EFFECT OF BREATHING PATTERN ON BLOOD PRESSURE AND HEART RATE OSCILLATIONS IN HUMANS
Authors: Laude Dominique , Goldman Michael , Escourrou Pierre , Elghozi Jean‐Luc 
Published: June 2007

SUMMARY1. The relationships of respiratory sinus arrhythmia (RS A) and respiratory changes in systolic blood pressure (SBP) to tidal volume (VT) and breathing frequency (BF), were quantified during voluntary control of VT and BF in healthy subjects.2. Respiration was measured non‐invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non‐invasively by the Finapres.3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most VT and BF approximating 0.9 s. The magnitude of RS A increased with increases in VT and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160°. The magnitude of the inspiratory fall in SBP increased with increases in VT. Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory‐related influences and those due to ‘slow waves’ of vasomotor tone.4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR.