bluuebunny/crossref_metadata_2025_split huggingface dataset:
FAILURE OF ASPIRIN TO MODIFY THE HYPOTENSIVE ACTION OF CAPTOPRIL IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: DiNicolantonio R. , Dusting G. J. , Hutchinson J. S. , Mendelsohn F. A. O. 
Published: June 2007

SUMMARY1. Oral administration of the angiotensin converting enzyme inhibitor, captopril (30 mg/kg per day) to spontaneously hypertensive rats of the Okamoto strain progressively reduced arterial blood pressure by 60 mmHg over 4–5 days.2. Oral treatment of spontaneously hypertensive rats with aspirin (200 mg/kg per day) for one week did not alter blood pressure, but it greatly reduced the vasodepressor effects of intravenous injections of arachidonic acid (3 mg/kg).3. The fall in blood pressure of spontaneously hypertensive rats treated concurrently with both aspirin (200 mg/kg per day) and captopril (30 mg/kg per day) was not different to the fall observed in rats treated with captopril alone.4. The hypotensive action of captopril in spontaneously hypertensive rats does not appear to be due to stimulation of vasodilator prostanoid biosynthesis.
ALCOHOL AND BLOOD PRESSURE IN A WORKING POPULATION
Authors: Arkwright P. D. , Beilin L. J. , Rouse I. , Armstrong B. , Vandongen R. 
Published: June 2007

SUMMARY1. The association between alcohol consumption and blood pressure was studied in 491 Government employees. The men, aged 21–45 years, volunteered to complete a health questionnaire and submitted to standardized measurements of blood pressure, heart rate and body size.2. Average weekly alcohol consumption correlated with systolic pressure (R = 0.18, P<0.001) but not with diastolic pressure. Systolic pressure increased progressively with increasing alcohol consumption with no obvious threshold effect. An effect of alcohol was seen independent of age, obesity (Quetelet's index) or cigarette smoking.3. Results indicate that alcohol ranks close to obesity as a preventable cause of essential hypertension in the community.
HYPERTENSION THROUGH ADRENALINE ACTIVATION OF PREJUNCTIONAL β‐ADRENOCEPTORS
Authors: Majewski H. , Tung L.‐H. , Rand M. J. 
Published: June 2007

SUMMARY1. Adrenaline can enhance the stimulation‐induced release of transmitter noradrenaline in sympathetically innervated tissues by activating prejunctional β‐adrenoceptors.2. Adrenaline incorporated into sympathetic transmitter stores by neuronal uptake can be subsequently released as a co‐transmitter and can then activate prejunctional β‐adrenoceptors, thus completing a facilitatory feedback loop.3. Rats chronically treated with adrenaline develop elevated blood pressures compared to control rats, β‐adrenoceptor blockade prevents the rise in blood pressure.4. Activation by adrenaline of facilitatory prejunctional β‐adrenoceptors of sympathetic nerves innervating cardiovascular effector tissues may explain adrenaline‐induced rises in blood pressure.
PSYCHOSOCIAL STRESS INDUCES TUBULOINTERSTITIAL NEPHRITIS UNRELATED TO HYPERTENSION IN CBA MICE
Authors: Henry James P. , Stephens Patricia M. 
Published: June 2007

SUMMARY1. Groups of mice interacting socially in complex population cages become hypertensive. Some also develop fatal chronic tubulointerstitial nephritis.2. Long‐term administration of the cardioselective β‐blocker metoprolol controls stress‐induced elevation of plasma renin and adrenal tyrosine hydroxylase. It also normalizes blood pressure. Despite the effectiveness of this sympathetic blockade, the incidence of nephritis was not diminished.3. The fact that stress‐induced increases of adrenal weight and plasma cortico‐sterone persist during metoprolol treatment points to the independence of the pituitary‐adrenal cortical system and its possible role in the aetiology of renal disease.
DUAL EFFECTS OF CLONIDINE ON RAT PREJUNCTIONAL α‐ADRENOCEPTORS
Authors: Medgett I. C. , Rand M. J. 
Published: June 2007

SUMMARY1. The effects of clonidine (1.0 μmol/l) and phentolamine (3.0 μmol/l) on the stimulation‐induced efflux of radioactivity were assessed in rat isolated atria and tail arteries in which transmitter stores had been labelled with (3H)‐noradrenaline.2. In atria, clonidine did not affect transmitter release when stimulation was for 10 s periods at frequencies of 1, 2 or 5 Hz, whereas at 10 Hz there was a significant 1.2‐fold enhancement of release. Phentolamine enhanced release with stimulation at 5 Hz and 10 Hz by 1.5‐ and 2.5‐fold respectively.3. In tail arteries, clonidine reduced release when stimulation was for 30 s periods at a frequency of 1 Hz, but did not affect release at 2 Hz or 5 Hz. Phentolamine in each case produced an approximately 1.5‐fold enhancement of release.4. In the pithed rat, spinal stimulation of cardioaccelerator fibres produced a tachycardia, the magnitude of which depended on the frequency and duration of stimulation. Clonidine (10jug/kg, i.v.) caused either a reduction or an enhancement of the response depending on the frequency and duration of stimulation; in the presence of phentolamine (2 mg/kg, i.v.), clonidine had no effect.5. The results are consistent with partial agonistic actions of clonidine at prejunctional a‐adrenoceptors in the rat cardiovascular system; such effects may be of relevance to the mechanism of the clonidine withdrawal syndrome.
REGULATION OF UTERINE SMOOTH MUSCLE BRADYKININ RECEPTORS BY BRADYKININ LEVELS AND ANGIOTENSIN CONVERTING ENZYME INHIBITOR IN THE RAT
Authors: Yasujima M. , Matthews P. G. , Johnston C. I. 
Published: June 2007

SUMMARY1. Bradykinin infusion (0.1 μg/min i.v.) decreased the number of uterine bradykinin receptors by 20% at Day 2. Bradykinin receptors returned to control levels at Day 7.2. Captopril infusion (1.7μg/min i.v.) induced prolonged decreases in the number of uterine bradykinin receptors of 15% at Day 2 and of 13% at Day 7, respectively.3. The number of uterine bradykinin receptors was increased in two‐kidney, one clip hypertensive rats by 19%.4. These results suggest that endogenous bradykinin participates in the regulation of uterine bradykinin receptors.5. Decreased uterine bradykinin receptors induced by captopril might reflect increased endogenous bradykinin.
IMPORTANCE OF ANTIDIURETIC PROPERTIES OF VASOPRESSIN IN EXPERIMENTAL RENAL HYPERTENSION
Authors: Woods R. L. , Johnston C. I. 
Published: June 2007

SUMMARY1. Homozygous Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI) developed one‐kidney, one‐clip (1K–1C) and two‐kidney, one‐clip (2K–1C) Goldblatt renal hypertension.2. However, the systolic blood pressure (SBP) in 1K–1C Brattleboro rats was significantly lower than in non‐DI hypertensive 1K–1C Long‐Evans (LE) rats.3. Treatment with the synthetic antidiuretic analogue of vasopressin, DDAVP (l‐desamino‐8‐D‐arginine vasopressin), increased the SBP in the DI rats to the same level as in 1K–1C Long‐Evans. This elevation of SBP was associated with increased extracellular fluid volume in the DI rats after DDAVP.4. The results suggest that vasopressin is not essential for the development of renal hypertension but the absolute levels of blood pressure achieved in 1K–1C hypertension are volume‐dependent and thus influenced by the water‐retaining properties of vasopressin.
OPIATES INHIBIT THE DOPAMINERGIC ENHANCEMENT OF THE RENAL RESPONSE TO ALDOSTERONE IN THE RAT
Authors: Adam William R. , Danks Janine A. , Goland Gary 
Published: June 2007

SUMMARY1. Both naloxone, an opiate antagonist, and levorphanol, an opiate agonist, inhibit the enhanced renal response to aldosterone produced by both ℓ‐dopa pretreatment and a high K+ diet.2. This supports the evidence for a common mechanism of action for the enhancement of the renal response to aldosterone produced by ℓ‐dopa and a high K+ diet. Whether this mechanism is dopaminergic or opiate is uncertain.3. The inhibition of the enhanced response, produced by ℓ‐dopa, by opiates is consistent with previous findings of displacement of 3H‐dopamine from renal homo‐genates by opiates and supports the hypothesis that the binding sites relate to the renal response to aldosterone.
HAEMODYNAMIC RESPONSE TO ACTH ADMINISTRATION IN ESSENTIAL HYPERTENSION
Authors: Whitworth Judith A. , Saines D. , Andrews J. , Sloman J. G. , Scoggins B. A. 
Published: June 2007

SUMMARY1.The haemodynamic and volume response to ACTH administration was investigated in six patients with mild, untreated essential hypertension and two patients with Addison's disease on maintenance steroids. Blood pressure, heart rate and weight were recorded daily. Plasma volume (125I‐HSA) and cardiac output (thermo‐dilution) were measured during the control period and on the 5th day of ACTH treatment.2. In the hypertensive subjects, mean arterial pressure rose from 94.3 ± 2.2 to 105.7 ± 2.8 mmHg on the 5th day of ACTH administration (P<0.02). Plasma volume rose from 29.8 ± 2.2 to 34 ± 2.2 ml/kg. Cardiac index increased from 2.85 ± 0.21 to 3.32 ± 0.14 l/min per m2 (P<0.05). Cardiac output rose from 5.81 ± 0.69 to 6.72 ± 0.59 l/min. Calculated total peripheral resistance, heart rate and body weight were unchanged. No such changes were seen in patients with Addison's disease.3. The haemodynamic characteristics of ACTH in patients with mild untreated essential hypertension are similar to those in the experimental model of ACTH induced hypertension in sheep.
EFFECTS OF NEONATAL SYMPATHECTOMY BY 6‐HYDROXYDOPAMINE ON BLOOD PRESSURE AND INTRAVASCULAR VOLUME IN YOUNG STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Rascher Wolfgang , Dietz Rainer , Schömig Albert , Voss Ute , Gross Franz 
Published: June 2007

SUMMARY1. Stroke‐prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY) were ‘chemically sympathectomized’ immediately after birth with 6‐hydroxydopamine (6‐OHDA, 100 mg/kg s.c. daily) for the first 10 days of life.2. Body weight gain was diminished in both groups as compared with sham‐treated controls. Blood pressure was reduced in ‘sympathectomized’ SHRSP, and also WKY rats had a slightly lower blood pressure than control rats.3. Plasma concentration of angotensin II and renin content of the kidney were not influenced by 6‐OHDA.4. ‘Sympathectomized’ SHRSP retained similar amounts of sodium than sham‐treated SHRSP when sodium retention is expressed per body weight gained. Plasma and blood volumes were increased in both SHRSP and WKY rats, whereas packed cell volume was significantly decreased.5. These results demonstrate the significance of an intact sympathetic nervous system for the development of hypertension in SHRSP. The expanded plasma and blood volume in ‘sympathectomized’ rats indicate an important role of the sympathetic nervous system and/or the arterial blood pressure for the regulation of intravascular volume.
A COMPARISON OF THE ACTIVITY OF THE ANGIOTENSIN CONVERTING ENZYME INHIBITORS SQ 14 225, SA 446, AND MK 421
Authors: Takata Y. , Nicolantonio R. Di , Mendelsohn F. A. O. , Hutchinson J. S. , Doyle A. E. 
Published: June 2007

SUMMARYThis study was designed to compare the activity of three structurally different drugs (SQ 14 225, SA 446, and MK 421) as inhibitors of angiotensin converting enzyme in vivo and to compare their effects in two experimental models of hypertension.2 MK 421 was less effective than SA 446 or SQ 14 225 in suppressing the pressor responses to intravenous angiotensin I 3 min after the administration of low doses of the converting enzyme inhibitors (CEIs) but more effective than SA 446 or SQ 14 225 30 min or longer after doses of CEIs ranging from 25 to 2500 nmol/kg i.v.3 The CEIs administered at 8 μmol/kg intravenously blocked the pressor response to angiotensin I (AI) to a similar maximal effect but the time for recovery was much slower for MK 421 than for SQ 14 225 or SA 446. After oral administration (15 mg/kg) prolonged blockade was observed with each of the three drugs although some recovery occurred with SA 446 after 5 h. The effect of a small dose of MK 421 intravenously (0.4 μmol/kg) was more prolonged in anaesthetized than in conscious spontaneously hypertensive rats (SHR).4 Anaesthetized adult SHR showed slow progressive falls of blood pressure after 8 /unol/kg of each drug intravenously although the effect of SA 446 was less than for SQ 14 225 or MK 421 which were equipotent. After acute oral administration of each CEI at 80 μmol/kg, conscious SHR showed significant falls in blood pressure but the effect of SA 446 was less than the other two inhibitors which appeared equipotent.6 After chronic oral administration of the drugs to conscious SHR, SA 446 (80 μmol/kg per day) did not alter blood pressure although SQ 14 225 was effective at this dose. At a higher dose of 160 /μmol/kg per day SA 446 significantly lowered blood pressure of SHR in a manner similar to the same dose of SQ 14 225 or MK 421.7. We conclude that the three drugs are potent, orally effective converting enzyme inhibitors. The duration of action was in the order MK 421 >SQ 14 225 >SA 446. MK 421 appears the most potent due to both a higher affinity for converting enzyme in vitro and a longer persistence of action in vivo. In renal hypertension, the drugs appeared equipotent but in the SHR at low doses, SA 446 was ineffective.
EFFECT OF INDOMETHACIN ON RESPONSES OF SHEEP ISOLATED CORONARY ARTERY TO ARACHIDONIC ACID
Authors: Cornish E. J. , Goldie R. G. , Krstew E. V. , Miller R. C. 
Published: June 2007

SUMMARYIndomethacin (2.8 μmol/1) did not consistently affect basal tone of sheep coronary artery strips, while a ten‐fold higher concentration increased tension in 50% of the preparations tested. When acetylcholine was used as a spasmogen, oscillations in induced tone and relaxations produced by arachidonic acid (6.6 μmol/1) were abolished by indomethacin, 2.8 μmol/1 and 7 μmol/1, respectively.Prostacyclin (PGI2) and prostaglandin E1 decreased and PGE2 increased arterial tension while PGF2α was inactive. Responses to PGI2 were reduced by indomethacin (28 μmol/1) but not by indomethacin (2.8 μmol/1).It is suggested that sheep isolated coronary arteries synthesize and release prostacyclin in the presence of acetylcholine and arachidonic acid and that such synthesis can be inhibited by indomethacin.
REVERSAL OF RENOVASCULAR HYPERTENSION
Authors: Swales J. D. , Bing R. F. , Russell G. I. , Thurston H. 
Published: June 2007

SUMMARY1. The fall in blood pressure observed in both early and chronic phase Goldblatt 2‐kidney 1‐clip hypertension produced by removing or unclipping the ischaemic kidney is due to a profound fall in peripheral resistance.2. The two procedures have an equal effect upon peripheral resistance and the lesser efficacy of nephrectomy in lowering blood pressure is due to a greater rise in stroke volume perhaps associated with a greater degree of sodium retention.3. Neither changes in sodium balance, in the renin‐angiotensin system nor in vascular reactivity explain the fall in blood pressure.4. A reduction in renal sympathetic afferent activity and a medullary based vasoactive humoral system may play a role although the nature and extent of that role remain to be defined.
INHIBITION OF GUINEA‐PIG RENAL [Na + K]‐ATPase BY NORMOTENSIVE HUMAN PLASMA: EFFECTS OF A HIGH SODIUM DIET
Authors: Wellard R. M. , Myers J. B. , Danks J. A. , Morgan T. O. , Adam W. R. 
Published: June 2007

SUMMARY1. The effect of plasma taken from normotensive humans, while on a low and high sodium diet, on [Na + K]‐ATPase and 3H‐ouabain binding was measured in tubules from guinea‐pig kidneys.2. Plasma from the high sodium, compared to the low sodium, diet period: (a) inhibited [Na + K]‐ATPase activity; (b) decreased 3H‐ouabain affinity for binding sites; (c) increased the number of available 3H‐ouabain binding sites; (d) decreased [Na + K]‐ATPase turnover (activity/3H‐ouabain binding sites).3. The inhibition of [Na plus; K]‐ATPase suggests an increase in a (possible) natriuretic factor. The decreased affinity of 3H‐ouabain binding suggests an endogenous ouabainoid, which may be the natriuretic factor.
ELEVATION OF BLOOD PRESSURE IN HYPERTENSIVE RATS AFTER LESIONING SEROTONIN NERVES IN THE DORSOMEDIAL MEDULLA OBLONGATA
Authors: Howe P. R. C. , Rogers P. F. , King R. A. , Smith R. M. 
Published: June 2007

SUMMARY1. The possibility that serotonin (5HT) nerve endings in the dorsomedial medulla oblongata participate in the control of blood pressure was investigated in stroke‐prone hypertensive rats and in normotensive rats.2. 5HT nerves were destroyed by injecting 5,7‐dihydroxytryptamine bilaterally into the solitary tract nucleus. Immunohistochemical and biochemical examination revealed a selective loss of 5HT nerves throughout the dorsomedial medulla with little damage in adjacent regions.3. Arterial blood pressure and heart rate, measured at daily intervals, were similar in lesioned and sham‐operated normotensive rats. However, in the hypertensive rats, blood pressure was substantially elevated at 6‐9 days after the lesions compared with sham operations. There were no accompanying changes in heart rate.
THE DISTRIBUTION OF ARTERIOLOSCLEROSIS ALONG THE ARTERIOLES IN DOCA HYPERTENSIVE RATS
Authors: Walker M. B. , Boyd G. W. 
Published: June 2007

SUMMARY1. The development of structural changes along the length of small arterioles (mean internal diameter 20‐30 &#x006d;̈m) was studied in uninephrectomized DOCA/salt hypertensive rats over a period of 10 weeks, by casting the arteriolar branchings in the ileum with Microfil (coloured silicone rubber).2. Along with a reduction in mean arteriolar diameter, irregular structural changes, manifested as focal narrowings along the arteriolar lengths, developed in the hypertensive animals, becoming most marked after 8‐10 weeks.3. The severity of the changes appeared to be related to both the level and duration of the hypertension.4. The irregular nature of the changes is difficult to account for on the basis of any direct local pressure effect.
THE EFFECT OF KETANSERIN IN ESSENTIAL HYPERTENSION
Authors: Anderson A. , Morgan T. , Dumpys R. 
Published: June 2007

SUMMARY1. Ketanserin, a 5HT2‐receptor blocking drug was given to 17 patients with essential hypertension.2. Satisfactory control was achieved in 13 patients.3. Control was not as satisfactory when given once daily.4. There was no rebound effect when the drug was ceased.5. Side‐effects were few.6. Ketanserin was a satisfactory drug to reduce blood pressure in patients with moderate hypertension.
PREVENTION OF STRUCTURAL ARTERIOLAR CHANGES IN DOCA HYPERTENSION WITH HYDRALLAZINE
Authors: Vial J. H. , Yong A. C. , Boyd G. W. 
Published: June 2007

SUMMARY1. Structural changes in resistance vessels were studied by (a) hindquarter perfusion; and (b) planimetry of cross‐sections of renal arterioles in uninephrectomized rats treated for 10 weeks with saline and either DOCA (deoxycorticosterone acetate), DOCA plus hydralazine, vehicle plus hydralazine or vehicle only.2. DOCA‐treated rats developed hypertension and structural change. Addition of hydralazine prevented both hypertension and the development of structural change.3. Structural arteriolar change in DOCA/salt hypertension is related to the high blood pressure or a closely associated factor rather than some other effect of DOCA.
CAPILLARY PERMEABILITY IN NORMAL AND HYPERTENSIVE HUMAN PREGNANCY
Authors: Hunyor S. N. , McEniery P. T. , Roberts K. A. , Bellamy G. R. , Roffe D. J. , Gallery E. D. M. , Gyory A. Z. , Boyce E. S. 
Published: June 2007

SUMMARY1. Capillary permeability (CP) is elevated in late normal pregnancy, when compared to postpartum values.2. In women with pregnancy associated hypertension (PAH), pregnancy CP levels are not different from postpartum and are less than in normal pregnancy.3. These changes in capillary permeability are not explained by alterations in serum albumin.
VASOACTIVITY GENERATED FROM PLATELETS BY IMMUNE COMPLEXES IN PRE‐ECLAMPSIA
Authors: Medcalf R. L. , Kuhn R. J. P. , Iwanov V. , Mathews J. D. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. Circulating immune complexes in excess of the equivalent of 20 &#x006d;̈g/ml heat‐aggregated IgG were found in fourteen out of twenty patients diagnosed as having preeclampsia.2. Only six of the nineteen controls tested had similar levels of immune complexes. Recent studies have established that concentrations of heat aggregated IgG in excess of 20 &#x006d;̈g/ml activate human platelets to release sufficient concentrations of vasoactive agents to constrict a human blood vessel in vitro.3. It is therefore suggested that in vivo platelet activation by circulating immune complexes may release sufficient concentrations of vasoactive agents to contribute to the hypertension in pre‐eclampsia.
RESPONSES OF HUMAN ARTERIAL MUSCLE TO STABLE VASOACTIVE SUBSTANCES RELEASED FROM HUMAN PLATELETS BY COLLAGEN AND HEAT AGGREGATED IgG
Authors: Medcalf R. L. , Iwanov V. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. The supernatant solutions obtained after aggregation or sonication of washed human platelets were superfused over preparations of human isolated digital arteries using a small volume bioassay method. The agents released from the platelets caused strong contractions of the artery strips.2. Platelet aggregation induced by 10 μg/ml collagen or by 100 μg/ml heat aggregated IgG, released 31.5% and 38.5% respectively, of the contractile activity produced by sonication of the platelets.3. The quantitative contractile effect of supernatants from platelets aggregated by 50 μg/ml IgG was significantly less than that for 100 μg/ml HA IgG. Similarly, the maximum contractile effect of supernatants from platelets aggregated by 300 ng/ml collagen was significantly less than that for 1 μg/ml collagen. This suggests that the concentration of contractile agents released from platelets depends on the concentration of aggregating stimulus.4. Comparison with concentration‐effect curves for exogenous serotonin suggests that if the contractility of the platelet supernatant occurring after sonication of platelets is solely due to serotonin, then it is present in a concentration of approximately 3.3 times 10‐6 mol/1 (6.6 nmol per 109 platelets).5. It is suggested from this study that in certain clinical situations characterized by hypertension, and in which circulating immune complexes have been found, in vivo platelet activation by immune complexes may be releasing sufficient concentrations of serotonin to constrict peripheral blood vessels and contribute to the hypertension.
ADRENERGIC FACTORS INVOLVED IN THE CONTROL OF CRYPT CELL PROLIFERATION IN JEJUNUM AND DESCENDING COLON OF MOUSE
Authors: Kennedy M. F. G. , Tutton P. J. M. , Barkla D. H. 
Published: June 2007

SUMMARY1. The mitotic rates in the crypts of Lieberkühn of the proximal jejunum and descending colon of mouse, following different treatments, were measured using a stathmokinetic technique. Regression coefficients, representing mitotic rates, were then calculated by the method of least squares.2. Treatment with adrenaline, isoprenaline, phenylephrine, phentolamine, and yohimbine all resulted in decreased mitotic rate of jejunal and colonic crypt cells. Chemical sympathectomy and cryosympathectomy had a similar effect, and chemical sympathectomy was followed by a supersensitivity to clonidine.3. Intraperitoneal injection of metaraminol, clonidine, propranolol, prazosin, labetolol and simultaneous injection of propranolol and adrenaline all resulted in an increased rate of crypt cell proliferation in both jejunum and colon.4. A significant increase in mitotic rate was observed in both tissues at night. The amplitude of this diurnal variation was decreased in both jejunum and colon following chemical sympathectomy. In addition, the amplitude of this variation in jejunum was decreased after treatment with yohimbine or phentolamine.5. The results of the study suggest that the sympathetic nervous system stimulates epithelial cell proliferation in both the small and large intestine and that this effect is mediated by an α2‐adrenoceptor. By contrast, stimulation of α1‐ and β‐adrenoceptors is inhibitory to cell proliferation in these tissues.