bluuebunny/crossref_metadata_2025_split huggingface dataset:
CONVERSION OF ANGIOTENSIN I TO ANGIOTENSIN II IN SHEEP
Authors: Fernley R. T. , Coghlan J. P. , Cran E. J. , Fei T. W. , Scoggins B. A. , McGregor A. 
Published: June 2007

SUMMARY1. The methodology for measurement of angiotensin I in whole blood is described.2. Angiotensin I was measured in arterial and venous blood samples from sodium‐loaded, sodium‐replete and sodium‐depleted sheep. Venous blood concentrations were higher than arterial angiotensin I concentrations. Arterial angiotensin I concentrations increased with increasing sodium deficiency.3. Angiotensin II was infused into six sodium‐replete sheep, the blood concentrations of angiotensin II measured and the metabolic clearance rates calculated. The average value was 121 ± 21 1/h.4. Angiotensin I was then infused into these sheep and arterial and venous blood concentrations of angiotensins I and II determined. From this data and the metabolic clearance rate of angiotensin II, the degree of conversion of angiotensin I to II was calculated. The values varied in different sheep from 54 ± 2% to 105 ± 6% (n= 6).
EFFECT OF SOME PROSTAGLANDIN SYNTHESIS INHIBITORS ON THE ANTINOCICEPTIVE ACTION OF MORPHINE IN ALBINO RATS
Authors: Srivastava D. N. , Bhattacharya S. K. , Sanyal A. K. 
Published: June 2007

SUMMARY1. Five prostaglandin synthesis inhibitors, indomethacin, diclofenac, mefenamic acid, ibufen and paracetamol, were found to inhibit the antinociceptive action of morphine without affecting the antinociceptive response of an equi‐analgesic dose of prostaglandin E12. Diclofenac was found to be the most potent and longest acting, whereas paracetamol was the least potent and shortest acting. Indomethacin, mefenamic acid and ibufen occupied an intermediate position, both in potency and duration of action.3. The results suggest that prostaglandins may be involved in the antinociceptive action of morphine in albino rats.
THE EFFECT OF PRAZOSIN ON PRE‐ AND POSTSYNAPTIC α‐RECEPTORS IN THE PITHED RAT
Authors: Hua A. S. P. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. Prazosin had a marked inhibitory effect on post‐synaptic a‐receptors in the pithed rat, as measured by the blood pressure response to the cumulative administration of clonidine.2. Prazosin had no inhibitory effect, however, on the pre‐synaptic a‐receptor, as measured by the clonidine‐induced reduction in the tachycardia produced by stimulation of the cardiac nerves.3. These results suggest that prazosin has a selective antagonistic affinity for post‐synaptic a‐receptors.
LACK OF EFFECT OF BROMOCRIPTINE ON SERUM LEVELS OF CALCIUM IN THE RAT
Authors: Tan C. M. , Tan G. J. S. 
Published: June 2007

SUMMARY1. The effect of bromocriptine (a prolactin suppressant drug) on the serum levels of calcium was studied in the male rat. The drug was administered subcutaneously at a dosage of 100μg per 100 g body weight three times per day.2. Chronic treatment with bromocriptine had no significant effect on the serum calcium levels. It appears that neither bromocriptine per se nor normal circulating prolactin levels exert any significant influence on blood calcium homeostasis.
THE ANTAGONISM BY PROPRANOLOL AND α‐METHYLPROPRANOLOL (ICI 77602) OF VASCULAR AND CARDIAC RESPONSES TO ISOPRENALINE IN ANAESTHETIZED DOGS
Authors: Fitzgerald J. D. , O'Donnell Stella R. 
Published: June 2007

SUMMARY1. In anaesthetized dogs, α‐methylpropranolol was less potent than propranolol in antagonizing both vascular (hind limb perfusion pressure) and cardiac heart rate) responses to isoprenaline.2. α‐Methylpropranolol was more potent in antagonizing vascular than cardiac responses to isoprenaline, but this selectivity was no greater than that seen also with propranolol.3. Isoprenaline sensitivity was greater in the hind limb than the heart and vascular‐selective antagonism was more pronounced in those dogs in which this differential sensitivity was the greatest.4. Introduction of an a‐methyl group into propranolol decreases its 0‐adrenoceptor antagonist potency but does not enhance vascular selectivity.
COMPARISON OF THE ANORECTIC AND MOTOR ACTIVITY EFFECTS OF SOME AMINOINDANES, 2‐AMINOTETRALIN AND AMPHETAMINE IN THE RAT
Authors: Mrongovius R. I. , Bolt A. G. , Hellyer R. O. 
Published: June 2007

SUMMARY1. The anorectic and motor activity effects of 1‐aminoindane, 2‐aminoindane, some N‐substituted 2‐aminoindanes,2‐aminotetralin, amphetamine and fenfluramine were determined in rats.2. The two compounds with structures most like the extended conformation of amphetamine, 2‐aminotetralin and 2‐aminoindane, were potent anorectics. At dosages which halved the intake of food over 1 h, amphetamine increased motor activity, 2‐aminotetralin had no effect, and 2‐aminoindane reduced motor activity.’3. Both the anorectic and central stimulant actions of 2‐aminoindane were absent in N‐ethyl‐ and N‐isopropyl‐2‐aminoindane.4. 1‐Aminoindane, whose structure is like the folded conformation of amphetamine, produced a small anorectic effect and depressed motor activity.
INTERACTIONS BETWEEN METHAQUALONE AND ETHANOL IN RATS AND MICE DURING ACUTE AND CHRONIC STATES
Authors: Ho C. C. , Ho A. K. S. 
Published: June 2007

SUMMARY1. The effects of acute and chronic treatment of methaqualone on ethanol preference, the rate of disappearance of ethanol and on toxicity were studied in mice and rats.2. Acute treatment with methaqualone showed a dose‐dependent suppression in the voluntary intake of ethanol in C57B1/6J mice and rats. No significant change in ethanol intake was observed during chronic methaqualone treatment and withdrawal.3. Methaqualone pretreatment significantly (P &lt 0.005) delayed the disappearance of ethanol in the blood and brain over a period of 50 to 200 min after a loading dose of 2.0 g/kg, i.p., of ethanol.4. Methaqualone pretreatment at doses of 140 and 200 mg/kg significantly increased ethanol toxicity by 11% and 28%, respectively. Co‐administration of ethanol using 6.0, 7.0 and 8.0 g/kg also reduced the LD50 of methaqualone by 19%, 24% and 40%, respectively.5. Chronic administration with ethanol decreased the toxicity due to methaqualone. Potentiation of ethanol toxicity by methaqualone may be of clinical importance in view of the narrow range of safety margin of ethanol.
BLOOD PRESSURE AND METABOLIC EFFECTS OF ACTH IN ANEPHRIC SHEEP
Authors: Fan J. S. K. , Coghlan J. P. , Denton D. A. , Scoggins B. A. , Whitworth Judith A. 
Published: June 2007

SUMMARY1. ACTH (80–100 iu/day) was administered to seven sheep for 3–5 days following bilateral nephrectomy.2. ACTH treatment produced rises in mean arterial pressure in anephric sheep similar to those observed in intact animals. Following withdrawal of ACTH, blood pressure declined over the following 72 h.3. ACTH produced a transient fall in plasma potassium in anephric sheep, suggesting an internal redistribution mechanism for this ion.4. These studies demonstrate that adrenal steroid hormones can modify blood pressure in the absence of the kidney.
HAEMODYNAMIC EFFECTS OF NICERGOLINE IN MAN AT REST AND DURING EXERCISE
Authors: Boismare F. , Lefrançois J. 
Published: June 2007

SUMMARY1. The intravenous administration of nicergoline (5 mg) was followed by a rapid and sustained lowering of blood pressure; less rapid effects were bradycardia and an elevation of cardiac output. These delayed effects are consistent with an indirect action on the α‐adrenoreceptors of the central nervous system.2. Following the oral administration of nicergoline (30 mg), a partial reduction of exercise‐induced lactacidaemia was demonstrated, which is consistent with the haemodynamic changes shown at rest.
TRITIUM EXCRETION AFTER INTRAVENOUS ADMINISTRATION OF TRITIUM LABELLED ADRENALINE AND NORADRENALINE AND DIGITAL VASCULAR REACTIVITY TO ADRENALINE AND NORADRENALINE IN NORMOTENSIVE AND LABILE HYPERTENSIVE SUBJECTS
Authors: Guia Daisy De , Mendlowitz Milton , Vlachakis Nicolas D. , Gitlow Stanley E. , Nissenbaum Mark 
Published: June 2007

SUMMARY1. The 24‐h urinary excretion of tritium after tritiated adrenaline administration and digital vascular reactivity to exogenously administered adrenaline and noradrenaline were measured in ten normotensive and in twenty‐eight labile essential hypertensive subjects. Tritiated noradrenaline excretion and apparent noradrenaline secretion rate were also measured in ten and eleven of these subjects, respectively.2. Despite overlapping, the mean 24‐h tritium excretion after 3H‐adrenaline administration as well as reactivity to adrenaline were significantly greater in the hypertensive than in the normotensive subjects, whether or not they had increased responsiveness to noradrenaline. Significant correlation, however, was observed between tritium excretion of adrenaline and reactivity to adrenaline in both labile hypertensive and normotensive subjects. These measurements were also both significantly correlated with percentage variability in systolic and diastolic blood pressure in the labile hypertensive subjects.3. No significant correlation was observed between adrenaline as against noradrenaline measurements, whether physiological or biochemical, in either hypertensive or normotensive subjects.
ARE NEURONAL UPTAKE MECHANISMS RESPONSIBLE FOR THE DIFFERENCE IN SENSITIVITY TO NORADRENALINE BETWEEN HUMAN ARTERIES AND VEINS?
Authors: Stevens M. J. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. The sensitivity of human metacarpal veins and digital arteries obtained post‐mortem to noradrenaline and phenylephrine has been tested.2. pED50 values for noradrenaline were significantly higher in the veins (699, s.e.m. = 008) than in the arteries (6.56, s.e.m. = 009), whereas pED50 values for phenylephrine in the two tissues were not significantly different (arteries: 6.24, s.e.m. = 009; veins: 6.26, s.e.m. = 005).3. The addition of propranolol (4 × 10−6 mol/l) alone, or in combination with hydrocortisone (4 × 10−5 mol/l), did not affect the responses to either noradrenaline or phenylephrine. The further addition of cocaine (3 × 10−5 mol/l) slightly shifted the noradrenaline and phenylephrine concentration‐effect curves to the left in both arteries and veins, but veins were still found to be more sensitive than arteries to noradrenaline whilst there was still no difference in the sensitivity of veins and arteries to phenylephrine.4. Cocaine also slightly potentiated responses to barium chloride, potassium chloride and serotonin.5. It is concluded that the difference in sensitivity to noradrenaline between arteries and veins cannot be explained by differences in neuronal uptake and it is possible that there may be differences in the properties of the postsynaptic α‐adrenoreceptors of the two tissues. It is also concluded that the potentiation of the contractile effect of noradrenaline produced by cocaine is not solely due to inhibition of neuronal uptake of amines.
COMPARISON OF HAEMODYNAMIC RESPONSES TO POSITIVE‐END‐EXPIRATORY VENTILATION AND PERICARDIAL EFFUSION IN DOGS
Authors: Rabkin Simon W. , Morris Andrew L. , Sharma Gyan P. , Ayotte Brian 
Published: June 2007

SUMMARY1. The haemodynamic responses to progressive increments in positive end‐expiratory pressure ventilation (PEEP) were assessed in dogs in the presence and absence of pericardial effusion (2‐2 ml saline/kg).2. Increasing levels of PEEP (0, 4, 8, 16 cm H2O) were associated with increases in right atrial, left atrial, pericardial and pulmonary artery diastolic pressure; increases in pulmonary vascular resistance; decreases in aortic blood pressure; and decreases in cardiac index or stroke index.3. Pericardial effusion that was associated with an increase in pericardial pressure of 3 mmHg was not associated with significant changes in aortic blood pressure or stroke index. In contrast 8 cm PEEP was associated with significant decreases in both these haemodynamic variables yet pericardial pressure increased only 2‐2 mmHg.4. For these levels of PEEP and pericardial effusion, the same haemodynamic response to PEEP was observed regardless of the presence or the absence of pericardial effusion.5. Similar changes in aortic blood pressure and stroke index despite different pericardial pressures is reflected by significantly different intercepts in the linear model relating these haemodynamic variables to pericardial pressure in the presence and absence of pericardial effusion.6. The results suggest that these haemodynamic consequences of PEEP are primarily a function of pulmonary hyperinflation and are less dependent on increases in extracardiac pressure per se.
FAILURE OF SUPPRESSION OF INTRARENAL ANGIOTENSIN II IN THE CONTRALATERAL KIDNEY OF ONE‐CLIP TWO‐KIDNEY HYPERTENSIVE RATS
Authors: Mendelsohn F. A. O. 
Published: June 2007

SUMMARY1. Two‐kidney one‐clip hypertension was produced in rats by application of a 0‐20 mm clip to the left renal artery.2. After three weeks, the animals had mildly elevated PRA, kidney renin was elevated in the clipped kidney and markedly suppressed in the contralateral kidney when compared to values in sham‐operated rats.3. Intrarenal All was elevated in the clipped kidney either when compared to the contralateral kidney or to values in the controls. However, in the contralateral kidney, All was not different from controls.4. Changes in intrarenal AH do not, therefore, always parallel those of renal renin. Failure of suppression of All in the contralateral kidney is likely to be of pathogenetic importance in development of hypertension in this experimental model.
THE EFFECT OF METOPROLOL AND ATENOLOL ON PLASMA HIGH DENSITY LIPOPROTEIN LEVELS IN MAN
Authors: England John D. F. , Simons Leon A. , Gibson Joyce C. , Carlton Michael 
Published: June 2007

SUMMARY1. The effects of two β‐adrenoreceptor blocking drugs, metoprolol and atenolol, on plasma lipoproteins were studied in thirty‐four patients using a single‐blind cross‐over design, with a 10‐day placebo washout period between drugs.2. Compared with placebo values, neither metoprolol nor atenolol influenced total plasma cholesterol levels, while total plasma triglycerides increased slightly.3. Low density lipoprotein protein level remained unaltered, while high density lipoprotein (HDL) cholesterol and protein were significantly reduced by both β‐adrenoreceptor blockers.4. The ratio of total cholesterol to HDL cholesterol was increased by both drugs.5. The data suggest that patients taking these drugs over many years may be exposing themselves to increased vascular risk, despite other anticipated benefits from such therapy.
A METHOD OF DETERMINING INTRINSIC HEPATIC CLEARANCE FROM THE FIRST‐PASS EFFECT
Authors: Bass L. , Winkler K. 
Published: June 2007

SUMMARY1. The relation between systemic hepatic clearance, intrinsic hepatic clearance and hepatic blood flow is considered from the point of view of the sinusoidal perfusion (parallel tube) model of the liver.2. It is shown how intrinsic hepatic clearance may be calculated, for substrates eliminated in the liver and the kidney only, from data obtained by introducing successively an oral and an intravenous dose (i.e., by using the first‐pass effect) without the clinically cumbersome catheterization of the liver vein.3. The rate of hepatic blood flow is shown to follow from the same data.
THE ACTION OF ASPIRIN ON PLASMA KININOGEN AND OTHER PLASMA PROTEINS IN RHEUMATOID PATIENTS: RELATIONSHIP TO DISEASE ACTIVITY
Authors: Sharma J. N. , Zeitlin I. J. , Brooks P. M. , Buchanan W. W. , Dick W. C. 
Published: June 2007

SUMMARY1. When six female seropositive rheumatoid patients were given placebo therapy for 48 h, their mean plasma kininogen level, 9.2 ± 0.7 μg bradykinin equivalents (bk eq) per ml, was found to be 59% greater than that of a group of eight healthy female volunteers (5.8 ± 0.5 μg/ml).2. When the rheumatoid patients received aspirin therapy for 1 week, their mean plasma kininogen concentration fell by 31% to 6.3 ± 0.8 μg Bk eq/ml. This was accompanied by a 20.4% fall in mean plasma α2‐globuKn level. Haematocrit and total plasma protein were not significantly altered (P > 0.05).3. The fall in kininogen was very rapid, the main reduction occurring within the first hour.4. Aspirin therapy greatly reduced the pain assessments but had no effect on plasma concentrations of IgG, IgA, IgM, complement component C3, nor on ESR, haemoglobin, leucocyte count, nor ring size. Left hand grip strength was increased while right hand grip strength was unchanged.5. The action of aspirin on plasma kininogen and α2‐globulin was similar to that of indomethacin. Plasma kininogen has been considered to be an acute phase reactant. The possible diagnostic value of plasma kininogen estimation is discussed.
CHANGES IN PLASMA NORADRENALINE AND ADRENALINE DURING ISOMETRIC EXERCISE
Authors: Watson R. D. S. , Littler W. A. , Eriksson B‐M 
Published: June 2007

SUMMARY1. Plasma noradrenaline and adrenaline were measured radioenzymatically in twelve hypertensive and four normotensive subjects before and during handgrip. In the resting arm (n= 11), plasma noradrenaline increased by 17% (P<0 01) and plasma adrenaline by 27% (P<0 01). In the exercising arm, plasma adrenaline increased by 97% (P< 0 005) but the mean increase of noradrenaline of 10% was not significant (P>0 1).2. The noradrenaline response suggests a small and variable sympathetic adrenergic response; the significant difference (P<0 05) in adrenaline responses between resting and exercising arms may reflect local variation in tissue clearance.
ROUTE AND RATE OF HYDRALLAZINE ADMINISTRATION AS DETERMINANTS TO ITS HYPOTENSIVE EFFECT IN RABBITS
Authors: Talseth T. , McNay J. L. , Clementi W. A. 
Published: June 2007

SUMMARY1. The cardiovascular responses to varying doses of hydralazine were studied in renal hypertensive rabbits.2. The depressor effect of hydralazine was independent of the rate of its i.v. administration (bolus v. a 15 min constant infusion).3. Intraperitoneally administered hydralazine was significantly less active than equimolar i.v. doses, and the relative potency (i.p. v. i.v.) did not increase with increasing doses.4. In spite of inferential evidence to the contrary, we did not find any pharmacodynamic support for non‐linear processes being involved in metabolism of hydralazine.
DOES THE BARORECEPTOR‐HEART RATE REFLEX INDICATE THE CAPACITY OF THE ARTERIAL BARORECEPTORS TO CONTROL BLOOD PRESSURE?
Authors: Ludbrook J. , Mancia G. , Zanchetti A. 
Published: June 2007

SUMMARY1. We have examined the question asked in the title by studying: the carotid baroreceptor reflex in man with a variable‐pressure neck chamber; the carotid baroreceptor reflex in conscious rabbits with a variable‐pressure capsule around the carotid bifurcation; and the baroreceptor‐heart rate reflex.2. At rest, the association between the sensitivities of the carotid barorecep‐tor‐blood pressure and ‐heart rate reflexes, and of these with the baroreceptor‐heart rate reflex, is weak. Exercise causes dissociation between control of blood pressure and heart rate. In hypertension, depression of the baroreceptor‐heart rate reflex does not reflect the altered characteristics of the carotid sinus‐blood pressure reflex.
REDUCED RESPONSES TO NORADRENALINE OF ISOLATED DIGITAL ARTERIES FROM HYPERTENSIVES
Authors: Moulds Robert F. W. 
Published: June 2007

SUMMARY1. Strips of digital arteries obtained post‐mortem from thirteen hypertensives have been compared with those from thirteen normotensives.2. The strips from hypertensives and from males had a significantly greater response to 80 mmol/1 KCl, but this was due to the increased cross‐sectional areas of the strips from hypertensives and from males.3. The maximum responses to noradrenaline and serotonin, but not the pED50 values, were significantly smaller in the strips from the hypertensives than in those from the normotensives, but there were no differences between the strips from hypertensives and normotensives in either the maximum response or pED50 values to angiotensin or barium chloride.4. It is concluded that these results suggest a decreased number of α‐receptors are present in human hypertensive vascular smooth muscle and this is a sequel either of the increased pressure itself, or of increased exposure in vivo of the blood vessels from hypertensives to noradrenaline.
INCREASED SODIUM PERMEABILITY OF ERYTHROCYTES IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Wiley J. S. , Hutchinson J. S. , Mendelsohn F. A. O. , Doyle A. E. 
Published: June 2007

SUMMARY1. The Na permeability of red cells from spontaneously hypertensive rats (SHR) has been studied. In the Japanese Wistar‐Kyoto strain, a significant increase of 30% in 22Na influx for male SHR was found compared with normotensive male controls. In contrast the Na influx for genetically hypertensive and normotensive New Zealand rats did not differ. Normotensive Wistar‐Kyoto rats rendered hypertensive by unilateral renal artery clipping, did not show any difference in Na influx from control animals.2. These results suggest that the Japanese strain of SHR has a genetically determined increase in erythrocyte Na permeability.
THE EFFECTS OF MECLOFENAMATE ON RENAL AND PERIPHERAL VASCULAR BEDS IN CONSCIOUS RABBITS
Authors: Banks R. A. , Beilin L. H. , Soltys J. S. 
Published: June 2007

SUMMARY1. Meclofenamate caused a dose‐dependent increase in renovascular resistance in conscious rabbits.2. This effect was greatest in inner cortical zones at the highest dose (6 mg/kg) but at the lowest dose (0‐75 mg/kg) vascular resistance in the outer cortex was preferentially increased.3. In contrast, meclofenamate increased cerebral perfusion and the proportion of cardiac output received by the testis. No effect was demonstrated on other organs studied.4. The results suggest a local vasodilator influence of renal prostaglandins in normal conscious rabbits.
ASSESSMENT OF NEURONAL UPTAKE OF NORADRENALINE IN HUMANS: DEFECTIVE UPTAKE IN SOME PATIENTS WITH ESSENTIAL HYPERTENSION
Authors: Esler Murray , Leonard Paul , Kelleher Dianne , Jackman Graham , Bobik Alex , Skews Helen , Jennings Garry , Korner Paul 
Published: June 2007

SUMMARY1. Disappearance of tritiated noradrenaline from plasma, after infusion to steady‐state, was studied to assess neuronal uptake of noradrenaline in essential hypertension.2. Plasma tritiated noradrenaline disappearance was biexponential. Rapid removal was dependent on neuronal uptake, being slowed both in normal subjects after desipramine, and in patients with sympathetic nerve dysfunction (autonomic insufficiency).3. In nine of thirty‐eight hypertensive patients the t1½ similarly was prolonged. Endogenous noradrenaline escaping uptake after release, and spilling over into plasma, was increased in these patients.4. Defective neuronal uptake of noradrenaline, by exposing adrenergic receptors to high local transmitter concentration, may be important in the pathogenesis of essential hypertension in some patients.
THE PATHO‐PHYSIOLOGY OF CHRONIC ARTERIAL HYPERTENSION: A HYPOTHESIS
Authors: Boyd G. W. 
Published: June 2007

SUMMARYAn important unresolved problem in hypertension is how an elevated blood pressure from any cause may eventually become self‐sustaining and apparently independent of the initiating event. Folkow has suggested that this results from arteriolar narrowing due to a physiological response or ‘structural adaptation’ to the higher pressure, but it is suggested here that the histological appearances within the arterioles in chronic hypertension are much more in keeping with a pathological process, and not vastly different from those observed after intimal damage to larger arteries in experimental atherosclerosis. From this, it is proposed that the arteriolar narrowing is secondary to the endothelial damage which arises when a maintained cardiac output is forced through a constricted arteriolar bed, so increasing substantially the shearing stress on their walls.