bluuebunny/crossref_metadata_2025_split huggingface dataset:
RENAL AUTOTRANSPLANTS IN SHEEP: INVESTIGATION OF RENAL FUNCTION AND RENOVASCULAR HYPERTENSION
Authors: McDougall John G. , Coghlan John P. , Denton Derek A. , Fei David T. W. , Hammond Timothy G. , Hardy Kenneth J. , Potocnik Simon J. , Scoggins Bruce A. , Wright R. Douglas 
Published: June 2007

SUMMARY1. A novel surgical preparation of sheep with a cervical renal autotransplant has been developed.2. Glomerular filtration rate and effective renal plasma flow were 25.1 ± 1.0 ml/min and 208 ± 10 ml/min respectively (n= 26).3. The responses to water load and deprivation, to AVP injection, to Na depletion and intravenous hypertonic saline load show the kidneys responded in an appropriate physiological manner.4. Constriction of the carotid‐renal artery to reduce mean renal arterial pressure to 23 ± 4 mmHg (n= 4) resulted in an increase in systemic mean arterial pressure from 70 ± 4 mmHg to 75 ± 4 mmHg within 5 min. Systemic blood pressure further increased to 110 ± 7 mmHg with 2 h of constriction, when renal arterial pressure had increased to 45 ± 2 mmHg.
ROLE OF THE KALLIKREIN‐KININ SYSTEM IN THE RENAL EFFECTS OF ANGIOTENSIN‐CONVERTING ENZYME INHIBITION IN ANAESTHETIZED DOGS
Authors: Clappison B. H. , Anderson W. P. , Johnston C. I. 
Published: June 2007

SUMMARY1. Administration of captopril (1.5mg/kg i.v.) to anaesthetized dogs was associated with an increase in renal blood flow of 56 ml min‐1 (s.e.m. = 13, n= 9) despite a significant fall of 17 mmHg (s.e.m. = 5, n= 9) in mean arterial pressure.2. Treatment of dogs with the angiotensin receptor antagonist, Sar'lle8‐angiotensin II (2.5 fxgjkg per min i.v.), or the cyclo‐oxygenase inhibitor indo‐methacin (10 mg/kg i.v.) did not prevent the renal vasodilation and hypotension following angiotensin‐converting enzyme inhibition. This suggests that these effects are neither solely due to inhibition of the renin‐angiotensin system nor mediated by prostaglandins.3. Increased urinary kinin excretion, possibly reflecting increased renal concentrations of kinins, accompanied the renal vasodilation after both captopril and renal artery occlusion.4. The kallikrein‐kinin system may play a role in the regulation of the renal vasculature in anaesthetized dogs.
DIFFERING NORADRENALINE KINETICS IN ESSENTIAL HYPERTENSION AND DEPRESSIVE ILLNESS, TWO DISEASES IN WHICH THE PLASMA CONCENTRATION OF NORADRENALINE IS SOMETIMES ELEVATED
Authors: Esler M. , Turbott J. , Schwarz R. , Leonard P. , Jackman G. , Skews H. , Bobik A. , Jennings G. , Korner P. 
Published: June 2007

SUMMARY1. The rate of spill‐over of noradrenaline to plasma, and neuronal noradrenaline uptake, which influences spill‐over, were studied in patients with essential hypertension and depressive illness.2. Noradrenaline spill‐over was increased in seven of thirty‐four patients with essential hypertension and five of eleven patients with primary depressive illness, compared with values in seventeen normal subjects (range 1.0–3.63 nmol/min perm2).3. Faulty neuronal reuptake of noradrenaline seemed to be the cause of higher noradrenaline spill‐over in patients with essential hypertension. Increased sympathetic nerve firing rates apparently were responsible in the primary depres‐sives, despite their normal blood pressure.4. These puzzling findings suggest that hypertension occurs when neurotransmitter excess is due to defective noradrenaline reuptake (in essential hypertension), but not chronically increased nerve firing (in depressive illness).
THE EFFECTS OF INDOMETHACIN IN TREATED HYPERTENSIVE PATIENTS
Authors: Wing L. M. H. , Bune A. J. C. , Chalmers J. P. , Graham J. R. , West M. J. 
Published: June 2007

SUMMARY1. Twelve treated hypertensive patients (ages 58–71 years) who had also been treated for joint disease participated in a randomized double‐blind crossover placebo‐controlled study to investigate the effects of indomethacin (25 mg three times daily) on blood pressure and biochemical parameters over a 6‐week period.2. Blood pressure was increased in all patients throughout the indomethacin treatment period (P<0.001) ‐ average mean blood pressure increases were 9 mmHg (casual), 8 mmHg (supine), 10 mmHg (standing).3. The blood pressure increase during indomethacin treatment was independent of the particular antihypertensive regimen in use.4. Plasma aldosterone concentration was reduced by 50% (P<0.01), plasma renin activity was reduced by 43% (P= 0.102) and plasma urea concentration was increased by 17% (P<0.001) during indomethacin treatment.5. The findings confirm that indomethacin impairs the blood pressure lowering effect of antihypertensive regimens.
EFFECTS OF MECLOFENAMATE AND CAPTOPRIL ON BLOOD FLOW TO THE KIDNEY AND SPLEEN IN CONSCIOUS RABBITS SUBJECTED TO MILD HAEMORRHAGE
Authors: Banks Richard A. , Beilin Lawrence J. , Soltys Jan , Davidson Lisa 
Published: June 2007

SUMMARY1. Regional haemodynamic responses to mild haemorrhage were studied in three groups each of seven conscious rabbits, in the presence of either buffer, the prostaglandin cyclo‐oxygenase inhibitor meclofenamate, or the kininase II inhibitor captopril.2. Renal and splenic vasoconstriction occurred with meclofenamate in haemorrhaged animals, and were accentuated by the subsequent administration of captopril.3. Captopril alone caused mild renal vasodilatation, but subsequent administration of meclofenamate again caused vasoconstriction.4. Flow to the adrenal coronary, cerebral and hepatic artery circulations was unaffected by meclofenamate or captopril after haemorrhage.5. The results indicated that the enhanced vasopressor activity occurring during haemorrhage greatly increased the dependence on vasodilator prostaglandins of flow to the renal and splenic vascular beds.6. The vasoconstrictor effect of meclofenamate does not appear to be due to unopposed action of angiotensin II when prostaglandin synthesis is suppressed.
CARDIOHAEMODYNAMIC EFFECTS OF LONG‐TERM INTRAVENOUS ADMINISTRATION OFW‐(2‐HYDROXYETHYL)NICOTINAMIDE NITRATE (SG‐75), A POTENT CORONARY VASODILATOR: COMPARISON WITH GLYCERYL TRINITRATE
Authors: Sakai K. , Shiraki Y. , Yamazaki T. , Akima M. , Nabata H. , Ohba Y. 
Published: June 2007

SUMMARY1. Cardiohaemodynamic changes have been studied in beagle dogs treated with intravenous injections of either 300 μg/kg of N‐(2‐hydroxyethyl) nicotinamide nitrate (SG‐75) or 30 μg/kg of glyceryl trinitrate three times a day for 1 ‐2 months. Throughout the experimental period, no significant changes in general behaviour, body weights and plasma levels of enzymes and substrates were observed in either the SG‐75‐ or glyceryl‐trinitrate‐treated groups.2. At 1 and 2 months after the start of chronic drug administrations, the dogs were anaesthetized and measurements were made of resting systemic blood pressure, pulse pressure, heart rate, right atrial pressure, coronary blood flow, aortic blood flow, left ventricular (LV) pressure and LVdP/dt: there were no significant differences between non‐treated dogs and dogs treated chronically with SG‐75 or glyceryl trinitrate.3. The effects of the acute intravenous administration of SG‐75 and glyceryl trinitrate were examined in dogs pretreated intravenously with SG‐75 (300 μg/kg) and glyceryl trinitrate (30 μg/kg), respectively, three times a day for 1‐2 months. The depressor and coronary vasodilator responses to the two drugs remained unchanged in comparison with those in non‐treated dogs.4. These results indicated that, with the doses used, neither SG‐75 nor glyceryl trinitrate produced changes in sensitivity or tolerance after long‐term intravenous administration.
THE EFFECT OF LONG‐TERM CHLORPROMAZINE AND DESIPRAMINE TREATMENT ON ADRENAL CORTICOSTERONE, CYCLIC AMP, AND CHOLESTEROL DISTRIBUTION IN RATS
Authors: Hung Francis , Chan Mo‐Yin 
Published: June 2007

SUMMARY1.Male rats were injected intraperitoneally with chlorpromazine (10 mg/kg) and desipramine (10 mg/kg), respectively, twice daily for 2 weeks.2. The adrenal corticosterone concentrations were significantly lowered in chlorpromazine‐ and desipramine‐treated rats.3. Large dose of corticotrophin would increase the adrenal corticosterone level in chlorpromazine‐treated rats but the adrenal response was significantly less than in the untreated controls.4. The adrenal cyclic AMP level was similar in treated and control rats and the adrenal response to corticotrophin was not decreased at the cyclic AMP level.5. The cholesteryl ester concentrations in the adrenals were significantly increased by drug treatment, although the free cholesterol concentrations were unchanged in the cytosol and mitochondrial cell fractions.6. The possible site of action of chlorpromazine in suppressing corticosterone production is discussed.
EFFECTS OF 2‐NICOTINAMIDOETHYL NITRATE (SG‐75) ON PANCREATIC SECRETION IN THE ISOLATED, BLOOD‐PERFUSED PANCREAS OF THE DOG
Authors: Iwatsuki K. , Ikeda K. , Chiba S. 
Published: June 2007

SUMMARY1. The effects of 2‐nicotinamidoethyl nitrate (SG‐75) on the secretion of pancreatic juice were compared with those of acetylcholine, secretin and pancreozymin in the isolated, blood‐perfused dog pancreas.2. Intra‐arterial administration of SG‐75 (0.3‐3 mg) elicited a dose‐dependent increase in pancreatic secretion. Acetylcholine (10‐100 μg), secretin (0.03‐0.3 units) and pancreozymin (0.1‐1.0 units) also elicited increased secretion.3. Secretory responses to acetylcholine were inhibited by treatment with atropine, while SG‐75‐, secretin‐, and pancreozymin‐induced secretions were not modified.4. Bicarbonate concentrations in pancreatic juice induced by SG‐75 and secretin were increased in a dose‐dependent manner. However, there were slight changes with acetylcholine or pancreozymin.5. Amylase activity in pancreatic juice was increased by SG‐75, acetylcholine and pancreozymin, but was decreased by secretin.6. These results suggest that SG‐75 stimulates pancreatic secretion by acting both on the acinar and ductular cells of the dog pancreas.
POTENTIATION OF THE NEGATIVE CHRONOTROPIC AND INOTROPIC EFFECTS OF ADENOSINE BY 2‐PHENYLAMINOADENOSINE
Authors: Chiba Shigetoshi , Watanabe Hidehiko 
Published: June 2007

SUMMARYEffects of 2‐phenylaminoadenosine on SA nodal pacemaker activity and atrial contractility were studied, using eleven isolated, blood‐perfused dog atrial preparations. The compounds were administered via the cannulated sinus node artery of the isolated atrium.2‐Phenylaminoadenosine induced negative chronotropic and inotropic effects and was 100 times less potent than adenosine in this action.The interaction between adenosine and 2‐phenylaminoadenosine was studied. 2‐Phenylaminoadenosine potentiated the effect of adenosine on atrial muscle, but not that of acetylcholine.
THE EFFECT OF PHENTOLAMINE ON ACTIVE AND INACTIVE RENIN RELEASE IN HUMAN RENOVASCULAR HYPERTENSION
Authors: Pedrinelli R. , Arzilli F. , Sassano P. , Salvetti A. 
Published: June 2007

SUMMARY1. Phentolamine was infused at low increasing doses (0.2, 0.3, 0.4 and 0.5 mg/min) in five patients with unilateral renal artery stenosis measuring active and inactive (cryoactivable) renin in the renal veins from the stenosed and nonstenosed kidney and in a peripheral vein.2. PRA values from the stenosed kidney (11.59, s.e.m. = 5.79 pmol ang I/ml per h) were higher than those in the peripheral vein (5.19, s.e.m. =2.64) while these latter were similar to those from the contralateral kidney (5.09, s.e.m. =2.93). Phentolamine significantly increased PRA from the stenosed kidney and in the peripheral vein in a dose‐related manner. PRA changes were unrelated both to blood pressure decrements and to heart rate increments induced by the drug.3. Before phentolamine, inactive renin from the stenosed kidney (5.19, s.e.m. = 2.84 pmol ang I/ml per h) did not differ significantly from that on the contralateral side (3.15, s.e.m. = 1.96) and in the peripheral vein (4.40, s.e.m. = 1.96). Phentolamine induced significant (P < 0.005) increments of inactive renin only from the stenosed kidney at the doses of 0.3, 0.4 and 0.5 mg/min. Inactive renin from the contralateral kidney was unchanged and it tended to increase, but not to a significant extent, in the peripheral vein. A highly significant relationship was found between active and inactive renin from the stenosed kidney (r = 0.79, P < 0.001, n= 25) and in peripheral blood (r = 0.71, P < 0.001, n= 25) but not from the stenosed kidney (r = 0.29, n= 25).4. These results suggest that phentolamine, infused at low increasing doses causes an increase of PRA only in the stenosed kidney, an action which does not seem to be wholly explained by either sympathetic nervous system activation or decrease of renal perfusion pressure, and which suggests an action on intrarenal a‐adrenoreceptors. Furthermore, phentolamine stimulated inactive renin release only from the stenosed kidney without evidence of intrarenal conversion of the inactive into the active form.
THE EFFECT OF LONG TERM TREATMENT WITH A β‐ADRENOCEPTOR BLOCKER, l‐PROPRANOLOL, ON THE DISTRIBUTION OF CARDIAC OUTPUT OF THE LATE GESTATIONAL GUINEA‐PIG
Authors: Bjellin Leif , Mårtensson Lena 
Published: June 2007

SUMMARYThe effects of daily administration of propranolol on the distribution of cardiac output were studied in the late pregnant guinea‐pig.The animals were given either saline, 5 or 50 mg/kg per day ofl‐propranolol for 15 days during the last trimester of gestation.Blood flow responses were assessed by injecting 15 μm microspheres into the conscious animal one to two days prior to parturition.The fraction of cardiac output reaching the placentas was significantly reduced in both groups (P<0.5 andP< 0.001, respectively), while flow to all other organs studied remained unaltered.It is suggested that propranolol exerts a selective effect on the placental vascular bed in the guinea‐pig.
BLOOD PRESSURE AND ITS RELATIONSHIP TO LOW LEVELS OF ALCOHOL CONSUMPTION
Authors: Cooke Kenneth M. , Frost Gavin W. , Stokes Gordon S. 
Published: June 2007

SUMMARY1. The association between average weekly alcohol consumption and blood pressure was studied in relation to age, adiposity and smoking in 13 535 men and 7385 women.2. There was a progressive increase in blood pressure with increasing alcohol consumption, even at low levels of consumption.
VASCULAR SMOOTH MUSCLE SEROTONIN AND α‐ADRENOCEPTORS
Authors: Marwood John F. , Stokes Gordon S. 
Published: June 2007

SUMMARY1. Rat isolated perfused tail arteries were used to investigate interactions between serotonin receptors and α‐adrenoceptors.2. Ketanserin was shown to be a potent serotonin antagonist (pA2=9.17, s.e.m. =0.06, n= 6) which also antagonized phenylephrine {pA2= 7.47, s.e.m. =0.10, n= 4) and noradrenaline (pA2= 7.55, s.e.m. =0.14, n = 6).3. Ketanserin reduced the maximal response to serotonin but not to phenylephrine or noradrenaline.4. Prazosin antagonized phenylephrine (pA2= 9.60, s.e.m. =0.12, n= 5) and noradrenaline (pA2= 9.14, s.e.m.=0.11, n= 6) and had no effect on maximal responses. Prazosin reduced the maximal response to serotonin but did not displace the dose‐response curve.5. These results are interpreted to indicate the existence of separate, but overlapping, serotonin and a‐adrenoceptors.
ERYTHROCYTE CATION FLUXES IN NORMAL AND HYPERTENSIVE HUMAN SUBJECTS
Authors: Stokes G. S. , Monaghan J. C. , Middleton A. T. 
Published: June 2007

SUMMARY1. Intracellular cation concentrations ([Na]i, [K]i and influxes of 22Na and 86Rb were determined in the erythrocytes of hypertensive and control groups of subjects.2. In both groups [Na]i showed a positive correlation with frusemide‐resistant Na influx and was inversely correlated with ouabain‐sensitive Rb influx, whereas [K]i was inversely correlated with frusemide‐sensitive Na influx (FSNal).3. No significant differences between groups were found in [Na]i, [K]i or frusemide‐resistant Na influx.4. FSNal was greater in males than females.5. FSNal was slightly greater (P0.06) in the hypertensive group, but the significance of the difference diminished with sex‐matching.6. Ouabain‐sensitive Rb influx was increased in the hypertensive group.
SYNTHESIS OF MOUSE RENIN AS A 2‐5‐33‐5 KILODALTON PRE‐PRO‐ TWO‐CHAIN MOLECULE AND USE OF ITS cDNA TO IDENTIFY THE HUMAN GENE
Authors: Morris Brian J. , Catanzaro Daniel F. , Mullins John J. , Hardman Judy , Shine John 
Published: June 2007

SUMMARY1. A DNA coding for mouse submandibular gland (MSG) renin was used in studies of the biosynthesis and processing of MSG renin and precursors and as a probe for identification of the human renin gene.2. A 2 kilodalton signal peptide was demonstrated by cleavage of preprorenin (45 kilodaltons) in the presence of microsomal membranes from dog pancreas. Prior selection of renin mRNA by hybridization with its cDNA obviated the possibility that a protease translated from total MSG mRNA could be activated by the microsomal membranes and then act on the primary translation product.3. In vitro labelling experiments with female MSG demonstrated that prorenin (43 kilodaltons) is rapidly converted to renin (38 kilodaltons) and that testosterone stimulated synthesis by increasing transcription of renin mRNA.4. Electrophoresis under non‐reducing conditions demonstrated 38 kilodalton renin which when reduced ran as two bands of 33 and 5 kilodaltons. Thus, native MSG renin has two chains linked by disulphide bonding. Hydrolysis of the 38 kilodalton single chain occurred only slowly during in vitro labelling.5. Prorenin bound only weakly to a pepstatin affinity column and could be activated by adding trypsin to column fractions. Both 38 kilodalton single and two chain renin bound strongly however, suggesting that both are active.6. Base sequencing of MSG renin cDNA indicated an Arg‐Arg residue additional to the published amino acid sequence of the heavy chain. This may account for the two forms seen on isolectric focusing.7. Mouse renin cDNA was used as a hybridization probe in screening a human genomic library in order to identify the human renin gene. The DNA in positive colonies had overlapping restriction maps and the coding region was found.
DEMONSTRATION OF SPECIFIC RECEPTORS FOR ADENOSINE IN GUINEA‐PIG MYOCARDIUM
Authors: Leung E. , Johnston C. I. , Woodcock E. A. 
Published: June 2007

SUMMARY1 Adenosine analogues N6‐phenylisopropyladenosine and 5′‐N‐ethylcarbox‐amidoadenosine inhibit cardiac adenylate cyclase in a concentration dependent manner.2 Inhibition of adenylate cyclase required the presence of guanosine‐triphosphate and Mg2+ ion. The concentration of Na+ ion was critically important: maximal inhibition was observed at 50 mmol/1 Na+.3 8‐Phenyltheophylline and isobutylmethylxanthine antagonized the inhibition of adenylate cyclase mediated by adenosine analogues.4. Adenosine receptors of the inhibitory type (R1 or A1) are present in guinea‐pig myocardium and may mediate some actions of adenosine.
DIFFERENTIAL BLOOD PRESSURE AND METABOLIC EFFECTS OF 9α‐FLUOROCORTISOL IN MAN
Authors: Whitworth Judith A. , Saines Dianne , Thatcher Robin 
Published: June 2007

SUMMARY1. The blood pressure and metabolic effects of 9α‐fluorocortisol at 0.15 mg/day and 1.5 mg/day were examined in man.2. At high dose, systolic pressure and body weight rose, and plasma [K+], urinary sodium excretion and renin concentration fell. At low dose similar metabolic effects were seen but blood pressure was unchanged.3. 9α‐Fluorocortisol has ‘mineralocorticoid’ effects in man at a dose which does not alter blood pressure. These studies do not provide evidence of a ‘hyperten‐sinogenic’ class of steroid hormone action in man.
VERAPAMIL‐INDUCED CONTRACTURE IN AN EXCISED, BLOOD‐PERFUSED SKELETAL MUSCLE PREPARATION FROM THE DOG
Authors: Sato T. , Suzuki K. , Aoyama T. , Ono H. 
Published: June 2007

SUMMARY1. The ability of verapamil to induce a contractile response in skeletal muscle was investigated using the canine isolated, blood‐perfused diaphragm preparation.2. Verapamil‐induced contracture was characterized by a biphasic increase in muscle tension consisting of an initial phasic and subsequent tonic contracture.3. The second tonic component of the verapamil‐induced contracture was inhibited by procaine, but procaine had no effect on the initial phasic contracture.4. Verapamil potentiated both KCl‐ and caffeine‐induced contractures during the second tonic stage. This action might be explained by enhancement by the drug of availability, or by an increased sensitivity of the contractile machinery to calcium liberated by membrane depolarization or by the calcium‐induced calcium release mechanism.5. The second tonic component of verapamil‐induced contracture was much less than the initial phasic component. It seems, therefore, that the calcium release induced by the procaine‐resistant process is the principal action of verapamil in inducing contracture in skeletal muscle.
CEREBRAL MECHANISMS INFLUENCING RENAL SODIUM EXCRETION IN DEHYDRATED SHEEP
Authors: McKinley M. J. , Denton D. A. , Fryday H. W. , Weisinger R. S. 
Published: June 2007

SUMMARY1. Reducing the cerebrospinal fluid concentration of NaCl by infusion into a lateral cerebral ventricle of isotonic solutions of 0.3 mol/1 mannitol or sucrose at 1 ml/h for 2 h caused a large reduction in renal Na excretion in conscious sheep deprived of water for 24 or 48 h.2. Infusion of 0.3 mol/1 mannitol into the lateral ventricle of water‐replete sheep did not alter renal Na excretion but induced a water diuresis.3. These data indicate that during dehydration, renal Na excretion may be under the control of the brain. The pathway(s) from brain to kidney mediating this antinatriuretic effect are not known.
INHIBITION OF AMINO ACID TRANSMITTER RELEASE FROM RAT BRAIN SLICES BY PHENYTOIN AND RELATED ANTICONVULSANTS
Authors: Skerritt John H. , Johnston Graham A. R. 
Published: June 2007

SUMMARY1. The in vitro effects of the major non‐benzodiazepine anticonvulsants were studied upon potassium‐stimulated release of radiolabelled GABA and D‐aspartate from minislices of rat cerebral cortex.2. At 100 μmol/1, some anticonvulsants effective in grand mal seizures (phenytoin, phenobarbitone, mephobarbitone and beclamide) selectively inhibited K+‐evoked release of the excitant amino acid D‐aspartate, consistent with an anticonvulsant action.3. In contrast, several other anticonvulsants, namely ethosuximide, methsuximide, carbamazepine, sulthiame and dipropylacetate failed to alter potassium‐evoked release of either amino acid.4. The ionic basis of phenytoin action on release was further studied; interactions with both neuronal calcium and sodium ion channels appear necessary for the drug's inhibitory action.