bluuebunny/crossref_metadata_2025_split huggingface dataset:
IN VIVO GENERATION AND ELIMINATION OF ANGIOTENSIN IN THE RAT
Authors: Jacobsen Jørgen , Poulsen Knud 
Published: June 2007

ABSTRACT1. Combined high performance liquid chromatography (HPLC) and radioimmunoassays were used to study the in vivo kinetics of the renin‐angiotensin system in the rat. The HPLC‐verified plasma concentrations of angiotensin I (AI) were 1.0 nmol/L (0.52–1.6) in anaesthetized normal and 4.2 nmol/L (2.5–7.0) in salt‐depleted rats. The plasma concentrations of angiotensin II (AII) were 0.07 nmol/L (0.04–0.13) in anaesthetized normal and 1.0 (0.60–1.6) nmol/L in saltdepleted rats.2. The fate of injected AI and AII passing through the vascular bed of the lungs was determined. Two‐thirds of the injected AI was converted to AII and one‐third was unchanged after a single passage through the lungs. Only trace amounts of angiotensin III (AIII), the only other metabolite, were demonstrated.3. This verifies that the majority of AI is metabolized through AII. Injected AII disappeared from the circulation with formation of only trace amounts of AIII, the half‐life being about 10 s. This corresponds to a calculated in vivo generation rate of AII of about 12 nmol/L per h in normal rats. It is in agreement with the AI generation rate (plasma renin activity) measured as 9.5 nmol/L per h in vitro.
EFFECTS OF BLOOD GAS/pH ABNORMALITIES ON THE CARDIOVASCULAR ACTIONS OF VERAPAMIL IN RATS
Authors: Achike Francis I. , Dai Soter 
Published: June 2007

SUMMARY1. The effects of hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis or hypercarbia with acidosis on the blood pressure and pulse rate responses to verapamil were studied in chloralose‐anaesthetized rats.2. At a fixed stroke volume (10 mL/kg) and rate (80 strokes/min; except for the hypocarbic group at 160 strokes/min), hypoxaemia, hyperoxaemia, hypercarbia with acidosis, or hypocarbia with alkalosis was induced by artificial ventilation with gas mixtures containing 17% O2, 28% O2, 23% O2, with 5% CO2, or 17% O2, without CO2 respectively. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3 respectively, in animals artificially ventilated with room air.3. Changes in individual blood gas/pH parameters had no significant effect on blood pressure except for acidosis which caused a significant decrease. Effects on pulse rate were significant increases in the alkalosis and hypercarbia groups, decrease in the acidosis group, while in other conditions no significant changes were recorded.4. In the controls, intravenous injections of verapamil 20–320 μg/kg caused dose‐dependent increases in mean blood pressure, while effects on pulse rate were not marked.5. The hypotensive responses to verapamil were significantly alleviated or enhanced in the presence of alkalosis or acidosis respectively. Verapamil also caused greater falls in pulse rate during acidosis. Effects of P02 changes were not statistically significant. The influence of PCO2 changes remained unclear.6. The present findings suggest that changes in blood pH may play a more important role than P02, alterations in affecting the cardiovascular responses to verapamil in the presence of blood gas abnormalities.
PATHWAYS LINKING RENAL EXCRETION AND ARTERIAL PRESSURE WITH VASCULAR STRUCTURE AND FUNCTION
Authors: Cowley Allen W. , Roman R. J. , Krieger J. E. 
Published: June 2007

SUMMARY1. A brief review is presented which summarizes the role of the kidney in the long‐term regulation of arterial pressure and the mechanism whereby changes in body fluid volume can influence the function and structure of the systemic vasculature.2. Studies indicate that the kidney detects changes of arterial pressure via changes of medullary blood flow which in the volume expanded state is poorly autoregulated. Elevations of renal arterial pressure raise vasa recta capillary pressure and renal interstitial fluid pressure, which in turn reduces tubular reabsorption of sodium and water.3. The sensitivity of the pressure–diuresis relationship is controlled by renal sympathetic nerve activity and a variety of hormone and autocrine systems.4. Evidence is also reviewed which shows that small changes of blood volume (5%) resulting from reduced renal excretion can acutely and chronically result in 25% increases of total peripheral resistance and arterial pressure.5. Short‐term increases of vascular resistance are predicted by regional autoregulatory responses while long‐term elevations of vascular resistance appear to result from the structural changes of large vessel hypertrophy and microvascular rarefaction within skeletal muscle.
THE ACETYLCHOLINE PARADOX: A CONSTRICTOR OF HUMAN SMALL CORONARY ARTERIES EVEN IN THE PRESENCE OF ENDOTHELIUM
Authors: Angus James A. , Cocks Thomas M. , McPherson Grant A. , Broughton Arch 
Published: June 2007

SUMMARY1. In animal experiments, acetylcholine is generally a vasodilator acting indirectly by releasing endothelium‐derived relaxing factor (EDRF); for example, in dog and rabbit small coronaries mounted in a myograph, acetylcholine caused concentration‐dependent relaxation.2. In human small coronary arteries taken from the atrial appendage, however, acetylcholine caused concentration‐dependent contraction with a funcionally intact endothelium as shown by the relaxation in response to substance P, another stimulant of EDRF release.3. We propose that coronary microvessels from various species have variable populations of acetylcholine receptors on the medial smooth muscle that cause contraction and on the endothelium that cause the release of EDRF. In humans, the medial smooth muscle receptors appear to predominate, and may thus play a role in coronary vasoconstriction.
NORADRENALINE RELEASE FROM THE RAT HEART DURING ANOXIA: EFFECTS OF CHANGES IN EXTRACELLULAR SODIUM CONCENTRATION AND INHIBITION OF SODIUM UPTAKE MECHANISMS
Authors: Dart A. M. , Riemersma R. A. 
Published: June 2007

SUMMARY1. Anoxic perfusion of the isolated rat heart releases noradrenaline in the absence of sympathetic nerve fibre stimulation.2. Anoxic noradrenaline release is enhanced by reducing the extracellular Na+ concentration, consistent with the proposal that such release occurs by carrier‐mediated efflux.3. Release is also enhanced by lignocaine but inhibited by amiloride and ethylisopropylamiloride, suggesting that sodium entry into adrenergic nerve terminals during anoxia occurs by Na+/H+ (and possibly Na+/Ca2+) exchange.
VOLUNTARY BLOOD PRESSURE CONTROL BY BIOFEEDBACK: RELATIONSHIP TO PSYCHOLOGICAL CHARACTERISTICS
Authors: Hunyor S. N. , Bartrop R. , Craig A. , Cejnar M. , Liggins G. , Henderson R. , Jones M. 
Published: June 2007

SUMMARY1. Psychological characteristics were studied in 25 hypertensives (mean and standard deviation of blood pressure 150/95 ± 12/5 mmHg), who received blood pressure (BP) biofeedback (BFB). Personality factors and success in BFB–BP modifying ability were correlated and the predictive value of psychological factors was estimated.2. Questionnaires consisted of a Locus of Control of Behaviour (LCB) scale, the Spielberger state trait anxiety inventory and the Framingham Type A personality inventory.3. BP was monitored continuously from the finger by volume clamp plethysmography during eight BFB sessions, each with three trials of raising, ignoring and lowering systolic blood pressure (SP).4. SP was raised/lowered by 12 ± 11/6 ± 9 mmHg and heart rate (HR) increased by 10 ± 3.9/+ 1 ± 6.1. Ten subjects were able to lower SP by ≥5 mmHg (15 ± 7.5) and raise it by 17 ± 11. The others achieved no decrease in SP and were also less successful at raising (8 mmHg, P= 0.04).5. Changes in LCB and trait anxiety correlated with DP rise, whereas type A and pre‐study state anxiety correlated with rising HR. Lowering of SP correlated weakly with change in LCB (r= 0.47, P= 0.06).6. Combinations of psychological factors had independent predictive value for BP and HR change: trait anxiety (P= 0.03) and change in LCB (P= 0.009) with rise in diastolic blood pressure (DP); type A (P= 0.009), pre‐study LCB (P= 0.02) and pre‐study state anxiety (P= 0.01) with HR rise.7. These findings suggest that psychological factors correlate with BP and HR changes during attempted BFB control of SP. The best predictor for a rise in DP was change in LCB.
A COMPARISON OF THE ANTICONVULSANT EFFECTS OF PROPOFOL AND THIOPENTONE AGAINST PENTYLENETETRAZOL‐INDUCED CONVULSIONS IN THE RAT
Authors: Hasan Zuheir , Hasan Mazen , Al‐Hader AbdelFattah , Takrouri Mohammad 
Published: June 2007

SUMMARY1. The anticonvulsant effects of subanaesthetic doses of propofol and thiopentone against PTZ‐induced seizures and mortality were examined in the rat.2. Administration of propofol (50 mg/kg, i.p.) 5 min prior to PTZ treatment increased the 2 h CD50 and the 24 h LD50 of PTZ by 3.4‐fold, whereas thiopentone pretreatment (20 mg/kg, i.p.) increased these values by more than five‐fold.3. Both propofol and thiopentone prolonged the latency to the onset of clonic seizure but the effects of the former were more marked.4. The data demonstrate that propofol was more effective than thiopentone in providing complete protection against PTZ‐induced seizures for the first 30–40 min of observation and that thiopentone, because of its sustained effects, was more effective in reducing the cumulative incidence of seizures and mortality over 2 and 24 h, respectively.5. We conclude that propofol is a very effective anticonvulsant and provides complete protection of short duration against PTZ‐induced seizures in the rat.
VASOPRESSIN RESPONSE TO HAEMORRHAGE IN RATS: EFFECT OF HYPOXIA AND WATER RESTRICTION
Authors: Raff Hershel , Rossing Mark H. , Doepker Sandra K. , Griffen Steven C. , Jankowski Barbara M. 
Published: June 2007

SUMMARY1. The aim of the present study was to determine the effect of water restriction and/or hypoxia on the vasopressin response to haemorrhage in conscious rats.2. Male, Long‐Evans rats (n= 39) were prepared with chronically indwelling femoral artery and vein catheters and exposed to 24 h of one of the following: normoxia with ad lib drinking water (N + W); normoxia with water restriction (N – W); hypoxia with ad lib drinking water (H + W); and hypoxia with water restriction (H – W). At the end of 24 h, a 15 mL/kg arterial haemorrhage was performed.3. Water restricted rats had elevated pre‐haemorrhage vasopressin levels. Haemorrhage induced an increase in vasopressin in all groups. Water restriction (N – W) or hypoxia (H + W) each augmented the vasopressin response to haemorrhage. However, the combination of hypoxia and water restriction (H – W) failed to augment the vasopressin response to haemorrhage as compared to normoxic, water replete (N + W) rats.4. Hypoxia or water restriction per se augment the vasopressin response to haemorrhage. This augmented vasopressin response to haemorrhage is not maintained when hypoxia and water restriction are combined.
ACTH HYPERTENSION IN THE RAT: ROLE OF KIDNEY AND GONADS
Authors: Whitworth J. A. , Hewitson T. D. 
Published: June 2007

SUMMARY1. Adrenocorticotrophin (ACTH) administration produces an adrenally dependent rise in blood pressure in rats.2. The haemodynamic and metabolic effects of ACTH were examined in nephrectomized, 5/6 nephrectomized and orchidectomized male Sprague‐Dawley rats and sham operated controls.3. Reduction in renal mass did not increase the blood pressure rise produced by ACTH.4. Gonadectomy did not reduce the blood pressure rise produced by ACTH, which was slightly higher in castrated animals.
INFLUENCE OF BETA‐BLOCKADE ON CIRCULATING PLASMA LEVELS OF 3‐METHOXY‐4‐HYDROXY PHENYLETHYLENE GLYCOL (MHPG) DURING EXERCISE IN MODERATE HYPERTENSION
Authors: Drici Milou D. , Roux Michel , Candito Mirande , Rimailho Alain , Morand Philippe , Lapalus P. 
Published: June 2007

SUMMARY1. The effect of exercise testing and β‐blockade on plasma norepinephrine (PNE), and secretion of its metabolite 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG), was assessed in 28 mild‐to‐moderate hypertensives before and after the administration of dilevalol, a new β‐blocker with β2‐agonism.2. This double blind, placebo‐controlled study consisted of two successive submaximal exercise tests before and after the administration of a single oral dose of dilevalol (200 mg, 400 mg or 600 mg). Plasma norepinephrine levels were determined at rest, at 100 watts step of exercise and at maximal effort (Emax).3. During the control test, mean PNE levels increased from 1.73±0.52 nmol/L (resting value) to 8.01 ± 4.01 nmol/L at Emax (P<0.01) as MHPG levels increased from 11.18 ± 1.33 nmol/L (rest) to 17.50 ± 1.15 nmol/ L (Emax, P<0.01). After dilevalol, PNE increased significantly as compared to controls (P<0.05), from 2.32 ± 0.99 to 12.42 ± 5.97 nmol/L (P<0.01). PNE and MHPG levels were correlated, both at rest and during exercise. PNE levels after β‐blockade were linearly related to the dose of β‐blocker administered. MHPG levels were unaltered by the administration of dilevalol, both before and after exercise.4. The increase in MHPG that occurs during bicycle exercise is largely generated from an increase in central nervous system noradrenergic activity. While dilevalol increases the peripheral sympathetic nervous system, both at rest and during exercise (which is reflected by increases in PNE levels) the drug does not alter resting central nervous system noradrenergic activity nor amplify the increase in central noradrenergic activity that occurs during exercise.
TONIC CONTROL OF SUBRETROFACIAL VASOMOTOR NEURONS IN THE ROSTRAL VENTROLATERAL MEDULLA
Authors: Dampney R. A. L. , Sasaki S. 
Published: June 2007

SUMMARY1. Vasomotor pressor neurons in the subretrofacial nucleus of the rostral ventrolateral medulla receive afferent inputs from different sources that utilize different neurotransmitters. This paper briefly reviews recent studies on the role of inputs releasing: (i) GABA, and (ii) angiotensin II (AII) in the subretrofacial nucleus.2. There are two types of tonic GABAergic inhibitory inputs: one arises from peripheral baroreceptors, while the second is independent of peripheral baroreceptors.3. Blockade of receptors for AII elicits a decrease in blood pressure and sympathetic vasomotor activity, indicating that subretrofacial neurons are also tonically excited by AII. It is likely that the AII is released from nerve terminals in the subretrofacial nucleus, but the origin of the pathway is unknown.
EFFECTS OF ADRENALINE AND NORADRENALINE ON CLEARANCE OF TRIACYLGLYCEROL‐RICH LIPOPROTEINS FROM PLASMA: STUDIES WITH CHYLOMICRON‐LIKE LIPID EMULSIONS IN RATS
Authors: Mackintosh Veronica , Redgrave Trevor G. 
Published: June 2007

SUMMARY1. Adrenaline was infused intravenously in rats during the clearance from plasma of an injected lipid emulsion designed to model chylomicrons and the triacylglycerol‐rich plasma lipoproteins. The clearance rates of emulsion radiolabelled triolein (TO) and cholesteryl oleate (CO) were both increased, suggesting that hydrolysis of lipoprotein triglycerides and clearance of remnants from plasma were increased. The distribution of radiolabels in tissues showed more TO in skeletal and cardiac muscle after adrenaline, while more CO was found in liver compared with controls. Lesser amounts of both labels were found in the spleens of treated rats.2. In a similar experiment with noradrenaline, the clearance rate of emulsion CO was decreased. The removal of CO was retarded more than that of emulsion TO, which was not significantly affected, and CO label recovered in liver was significantly decreased, suggesting that the removal of remnants from plasma was slowed after noradrenaline. In experiments in which noradrenaline was infused continuously for 1 week the clearances of emulsion CO and TO were both reduced.3. Our findings suggest possible connections between plasma catecholamines and the development of arteriosclerosis, in view of the atherogenicity of remnants of the triacylglycerol‐rich plasma lipoproteins. Yet to be established is whether the linkage we have found between lipoprotein clearance, adrenaline and noradrenaline contributes to the atherogenic effects of chronic stress and for the protective effects of exercise.
NATRIURETIC EFFECT OF TMB‐8 IN ANAESTHETIZED DOGS
Authors: Takahara Akira , Ogasawara Aichi , Suzuki‐Kusaba Mizue , Hisa Hiroaki , Satoh Susumu 
Published: June 2007

SUMMARY1. Effects of 8‐(N,N‐diethylamino)octyl‐3,4,5‐trimethoxybenzoate hydrochloride (TMB‐8), an inhibitor of intracellular calcium release, on renal function were examined in anaesthetized dogs.2. Intrarenal arterial infusion of TMB‐8 (0.03 and 0.1 mg/kg per min) increased urine flow rate, urinary sodium excretion and fractional excretion of sodium without affecting blood pressure, renal blood flow or glomerular filtration rate.3. The results suggest that TMB‐8 inhibits tubular sodium reabsorption to induce natriuresis.
A CONTROLLED STUDY OF THE EFFECTS OF AEROBIC EXERCISE ON ANTIHYPERTENSIVE DRUG REQUIREMENTS OF ESSENTIAL HYPERTENSIVE PATIENTS IN THE GENERAL PRACTICE SETTING
Authors: Allen D. H. G. , Puddey I. B. , Morton A. R. , Beilin L. J. 
Published: June 2007

SUMMARY1. To investigate the effect of an exercise training programme on antihypertensive drug requirements, 19 sedentary subjects (14 men and five women) with mild essential hypertension (systolic blood pressure greater than 140 mmHg but less than 180 mmHg), aged 29–55 years, were randomly assigned to 16 weeks of moderate intensity exercise or light intensity exercise (control), and titrated on antihypertensive drug therapy (captopril and hydrochlorothiazide) until resting systolic blood pressure (sitting) of less than 140 mmHg was achieved.2. The moderate exercise group (n= 11) followed a graded walk‐jog programme to >60% age‐predicted maximum heart rate (HRmax), attending 45 min sessions, three times each week. The light exercise group (n= 8) followed a programme of flexibility (stretching exercises) and walking to <60% age‐predicted HRmax, attending 45 min sessions, three times each week.3. There was no difference between treatment groups for the level of reduction in both resting systolic and diastolic blood pressure over the 16 weeks (15.64 ± 10.6/12.81 ± 9.97 mmHg in the moderate intensity group and 15.31 ± 10.9/7.7 ± 7.1 mmHg in the light intensity group). The change in 24 h ambulatory blood pressure profile was also similar in both treatment groups. The final antihypertensive drug requirements to achieve these changes in blood pressure was not significantly different between the two treatment groups. This was despite a significant improvement in submaximal exercise performance in the moderate intensity exercise group (P < 0.001).4. We conclude that in these mildly hypertensive subjects, a 16 week aerobic exercise programme did not decrease antihypertensive drug requirements. Captopril therapy did not influence submaximal exercise performance or prevent a training effect from regular aerobic exercise.
HISTAMINE‐INDUCED CALCIUM OSCILLATIONS IN HUMAN VASCULAR SMOOTH MUSCLE: TEMPORAL SEQUENCE AND SPATIAL ORGANIZATION IN SINGLE CELLS
Authors: Neylon Craig B. , Mason William T. , Irvine Robin F. 
Published: June 2007

SUMMARY1. Video imaging of single, fura2‐loaded vascular smooth muscle cells was used to examine the spatial and temporal alterations in calcium, Ca2+, in response to low levels of vasoconstrictor stimuli.2. Histamine (0.5 μmol/L) produced repetitive oscillations in Ca2+, which appeared to show some variation in amplitude and frequency between cells.3. Individual oscillations consisted of an initial increase in Ca2+ in a localized region followed by a wave‐like propagation of this region of elevated Ca2+ throughout the rest of the cell cytoplasm.4. It is suggested that the subcellular spatial organization of Ca2+ that was observed during a Ca2+ oscillation allows a population of cells to operate in unison. Thus, oscillatory fluctuations in Ca2+ may contribute to myogenic tone.
L‐TYPE CALCIUM CHANNELS AND CRH‐MEDIATED ACTH AND CORTISOL RELEASE IN HUMANS
Authors: Hockings Gregory I. , Grice Jeffrey E. , Walters Margaret M. , Jackson Richard V. 
Published: June 2007

SUMMARY1. The effect of pretreatment with nifedipine on naloxone‐stimulated corticotrophin‐releasing hormone (CRH)‐induced adrenocorticotrophin (ACTH) release in humans was investigated. The mean peak plasma ACTH and cortisol levels and the mean peak change in cortisol levels from basal were significantly lower in the nifedipine/naloxone test than in the naloxone alone test. The integrated areas under the ACTH‐time and cortisol‐time curves were reduced by 33 and 49%, respectively, in the nifedipine/naloxone test compared with the naloxone alone test. These results correlate well with published in vitro studies.2. Acute administration of oral nifedipine partially inhibited naloxone‐stimulated ACTH and cortisol release, probably by blockade of plasma membrane voltage‐dependent L‐type calcium channels normally activated following binding of CRH to pituitary corticotroph receptors.3. Naloxone‐induced CRH release may replace insulin hypoglycaemia testing of pituitary ACTH reserve in humans.
MULTIPLE GROWTH ABNORMALITIES IN VASCULAR SMOOTH MUSCLE FROM SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Saltis John , Little Peter , Bobik Alex 
Published: June 2007

SUMMARY1. In tissue culture the growth characteristics of aortic smooth muscle cells isolated from spontaneously hypertensive rats (SHR) were compared with those of normotensive Wistar‐Kyoto (WKY) rats.2. Aortic smooth muscle cells from SHR exhibit enhanced proliferation when grown in the presence of low (1%) and moderate (5%) concentrations of fetal calf serum.3. Cell quiescence in cultures of smooth muscle from SHR becomes apparent at cell densities approximately 20% higher than in cultures from WKY rats.4. These different growth characteristics of smooth muscle between the two strains of rats may contribute to the early pre‐hypertensive development of vascular hypertrophy in the SHR.
CULTURING RAT NEONATAL MYOCYTES CAUSES CHANGES IN THE PHOSPHATIDYLINOSITOL TURNOVER PATHWAY
Authors: Woodcock Elizabeth A. , Fullerton Meryl , Land Sarah , Kuraja Ivana J. 
Published: June 2007

SUMMARY1. Cultured neonatal myocytes are commonly used as a model system for the study of cardiac phosphatidylinositol (PI) turnover.2. In neonatal myocytes stimulation with noradrenaline causes the release of the Ca2+‐releasing compound inositol‐1,4,5‐trisphosphate and the generation of the Ca2+‐regulatory compound inositol‐1,3,4,5‐tetrakisphosphate.3. Addition of noradrenaline to intact, neonatal rat hearts stimulates the release of inositol‐1,4,5‐trisphosphate, but not inositol‐1,3,4,5‐tetrakisphosphate.4. These findings show that the isolation and culture of the neonatal myocyte causes changes in the PI turnover pathway so that it becomes similar to that described in other cell types and different from that in intact myocardial tissue.5. The neonatal myocyte is not a useful model for the study of cardiac PI turnover.
A LOCUS ON THE LONG ARM OF CHROMOSOME 1 AS A POSSIBLE CAUSE OF ESSENTIAL HYPERTENSION
Authors: Griffiths Lyn R. , Zee Robert Y. L. , Ying Li‐Hua , Morris Brian J. 
Published: June 2007

SUMMARY1. None of the genes responsible for essential hypertension has been identified. Recent work in genetically hypertensive rats has shown linkage of blood pressure with alleles of the renin gene. Since the renin gene is a member of a conserved synteny group that in humans spans chromosome 1q21.3–32.3 and includes the gene for antithrombin III (AT3), we used linkage studies to examine the relationship between alleles of AT3 and hypertension in a family having 10 affected members.2. From the lod score obtained at a recombination fraction of zero the odds for linkage of AT3 and hypertension in this family were calculated as 6:1 in favour of linkage. This result provides grounds for further examination of the possible role of the 1q23 locus in the aetiology of essential hypertension.