bluuebunny/crossref_metadata_2025_split huggingface dataset:
TIME COURSE OF CHANGES IN BLOOD PRESSURE, ALDOSTERONE AND BODY FLUIDS DURING ENALAPRIL TREATMENT: A DOUBLE‐BLIND RANDOMIZED STUDY VS HYDROCHLOROTHIAZIDE PLUS PROPRANOLOL IN ESSENTIAL HYPERTENSION
Authors: Semplicini A. , Rossi G. P. , Bongiovì S. , Perissinotto F. , Samà B. , Mozzato M. G. , Pessina A. C. 
Published: June 2007

SUMMARY1. Aldosterone suppression is said to play a major role in the long term hypotensive efficacy of angiotensin converting enzyme inhibitors. However, in previous reports from other laboratories, plasma volume has been found mostly increased and sodium balance sometimes positive.2. The effects of the angiotensin converting enzyme inhibitor enalapril (10‐40 mg/day, p.o., for 6 weeks) on blood pressure, body fluid volumes, renal function and plasma aldosterone were compared to those of hydrochlorothiazide (50 mg/day, p.o.) alone for 2 weeks and in association with propranolol (80‐160 mg/day, p.o.) for 4 more weeks during a randomized double‐blind parallel study in 14 essential hypertensives.3. Hydrochlorothiazide alone and in combination with propranolol induced slight and not significant change in either blood pressure and body fluids.4. The maximum hypotensive response to enalapril was achieved only after 2 weeks of continuous treatment possibly because after 1 week the hypotensive efficacy was lessened by a significant (P < 0.05) fluid retention secondary to a transient and not significant fall in renal perfusion. At this time aldosterone was not significantly changed compared to pretreatment values.5. After 6 weeks on enalapril, blood pressure was significantly reduced, plasma aldosterone further but not significantly decreased and extracellular fluid volume was normal.6. These findings indicate that aldosterone suppression contributes to the blood pressure lowering effect of enalapril by offsetting the salt and water retention observed on starting treatment and due to direct vasodilation.
THE RELATIONSHIP BETWEEN TISSUE LEVELS OF CYCLIC GMP AND TRACHEAL SMOOTH MUSCLE RELAXATION IN THE GUINEA‐PIG
Authors: Suzuki Kiyoshi , Takagi Kenzo , Satake Tatsuo , Sugiyama Satoru , Ozawa Takayuki 
Published: June 2007

SUMMARY1. The effect of cyclic GMP was investigated using guinea‐pig tracheal smooth muscle.2. 8‐Bromo‐cyclic GMP showed a dose‐dependent relaxation of spontaneous tension of tracheal smooth muscle.3. Administration of sodium nitroprusside induced dose‐dependent relaxation of tracheal smooth muscle as well as an increase in tissue levels of cyclic GMP.4. Nicorandil, N‐(2‐hydroxyethyl) nicotinamide nitrate showed dose‐dependent relaxation of tracheal smooth muscle and an increase in cyclic GMP levels in the tissue.5. N‐(2‐aminoethyl) nicotinamide dihydrochloride, which is a nicorandil derivative and differs minimally in its molecular structure (‐NH2 vs ‐NO2), had neither a relaxant effect on tracheal smooth muscle nor did it increase the level of cyclic GMP in the tissue.6. The rise in cyclic GMP levels preceded the relaxation of tracheal smooth muscle induced by sodium nitroprusside.7. These results suggest that cyclic GMP is one of the relaxant factors and that nitro‐derivatives exhibit their relaxant effect on the smooth muscle mediated by an increase in cyclic GMP level.
AROMATIC l‐AMINO ACID DECARBOXYLASE: HISTOCHEMICAL LOCALIZATION IN RAT KIDNEY AND LACK OF EFFECT OF DIETARY POTASSIUM OR SODIUM LOADING ON ENZYME DISTRIBUTION
Authors: Adam William R. , Culvenor Anne J. , Hall John , Jarrott Bevyn , Wellard R. Mark 
Published: June 2007

SUMMARY1. Utilizing a mono‐specific antiserum produced in rabbits to hog kidney aromatic l‐amino acid decarboxylase (AADC), the enzyme was localized in rat kidney by immunoperoxidase staining.2. AADC was located predominantly in the proximal convoluted tubules; there was also weak staining in the distal convoluted tubules and collecting ducts.3. An increase in dietary potassium or sodium intake produced no change in density or distribution of AADC staining in kidney.4. An assay of AADC enzyme activity showed no difference in cortex or medulla with chronic potassium loading.5. A change in distribution or activity of renal AADC does not explain the postulated dopaminergic modulation of renal function that occurs with potassium or sodium loading.
SAR1‐LEU8‐ANGIOTENSIN II REVERSES THE EFFECTS OF CAPTOPRIL ON RENAL FUNCTION IN RATS
Authors: Harris P. J. , Mitchell K. D. , Munro J. O. 
Published: June 2007

SUMMARY1. In Inactin‐anaesthetized rats inhibition of angiotensin converting enzyme by captopril resulted in a small decrease in mean arterial blood pressure accompanied by increases in the rates of glomerular filtration, water and electrolyte excretion.2. Infusion (100 pmol/min) of sar1‐leu8‐angiotensin II (sar1‐leu8‐AII) during continuing converting enzyme blockade reversed these changes in renal function but had no effect on arterial blood pressure.3. The data indicate that sar1‐leu8‐AII has partial agonist activity in the kidney although it acts as an antagonist of AII in the systemic circulation. This supports the proposai that angiotensin receptors within the kidney differ from those in the peripheral circulation.
DISTRIBUTION AND KINETICS OF INJECTED NICKEL IN THE PREGNANT RAT
Authors: Mas A. , Peligero M. J. , Arola LI. , Alemany M. 
Published: June 2007

SUMMARY1. Radioactive nickel (Ni) was injected intraperitoneally both carrier‐free and in 4 mg/kg body weight of Ni as NiCl2 doses in control and pregnant rats on days 12 and 19 after impregnation.2. The time‐course of disappearance of radioactivity from the tissues and blood of the rat was determined, as well as the degree of incorporation of radioactivity from the injected doses.3. The maximal uptake of the metal 15 min after injection corresponded to kidney uptake, followed by pancreas, blood plasma and then all other target organs studied. The presence of cold nickel resulted in higher uptake of the metal without much change in the proportion of distribution between tissues. The kinetics of disappearance was similar in all tissues and was little affected by pregnancy, with mean half‐lives of about 3‐5 h irrespective of doses.
NATRIURETIC AND HYPOTENSIVE EFFECTS OF α‐HUMAN ATRIAL NATRIURETIC POLYPEPTIDE IN ANAESTHETIZED DOCA‐SALT HYPERTENSIVE RATS
Authors: Kondo K. , Kida O. , Kangawa K. , Matsuo H. , Tanaka K. 
Published: June 2007

SUMMARY1. Both natriuretic and hyportensive effects of α‐human atrial natriuretic polypeptide (α‐hANP) were investigated in anaesthetized DOCA‐salt hypertensive rats and control rats.2. An intravenous injection of two doses (0.3 and 3.0 μg/kg body weight) of α‐hANP produced a rapid and marked increase in natriuresis and fall in blood pressure in DOCA‐salt rats.3. Natriuretic and hypotensive effects of α‐hANP in DOCA‐salt rats were significantly greater than those in the control rats.4. It is suggested that DOCA‐salt rats may have an enhanced natriuretic and hypotensive responsiveness to α‐hANP.
DICLOFENAC SODIUM IN THE TREATMENT OF PRIMARY NOCTURNAL ENURESIS: DOUBLE‐BLIND CROSSOVER STUDY
Authors: AL‐Waili Noori S. 
Published: June 2007

SUMMARY1. The prostaglandin synthesis inhibitor diclofenac sodium has been compared with a placebo in the treatment of primary nocturnal enuresis in a double‐blind crossover trial.2. Twenty patients were entered: 14 female, six male; age range 6–17 years.3. The results showed that diclofenac sodium was significantly more effective than placebo in the treatment of nocturnal enuresis.
NO EFFECT OF ATRIAL NATRIURETIC FACTOR ON CARDIAC RATE, FORCE AND TRANSMITTER RELEASE
Authors: Hiwatari Masao , Satoh Keisuke , Angus James A. , Johnstond̊ Colin I. 
Published: June 2007

SUMMARY1. The effects of atrial natriuretic factor (ANF, 1‐300 nmol/l) on cardiac rate, force and neurotransmitter release were examined in guinea‐pig isolated heart preparations.2. Synthetic ANF had little effect on the contractile force of electrically driven papillary muscle regardless of the presence or absence of isoprenaline.3. The pulse period of spontaneously beating right atria was not affected by ANF. Neither the positive nor negative chronotropic effect of isoprenaline or bethanechol respectively were changed in the presence of ANF.4. ANF did not affect the release of neurotransmitter from the nerve endings in the isolated atrium.5. ANF was confirmed to relax isolated aortic rings precontracted with either noradrenaline (ANF, IC50= 3 nmol/l, s.e.m. = 0.2, n= 5) or potassium (ANF, IC50= 24 nmol/l, s.e.m. = 0.2, n= 5).6. These results demonstrate that ANF within doses effective for vasorelaxation has no appreciable effect on myocardial function or neutrotransmitter release in the heart.
PROSTAGLANDIN SYNTHETASE INHIBITION WITH INDOMETHACIN RECTAL SUPPOSITORIES IN THE TREATMENT OF ACUTE AND CHRONIC URINARY CALCULUS OBSTRUCTION
Authors: AL‐Waili Noori S. 
Published: June 2007

SUMMARY1. The effect of indomethacin suppositories on both acute urinary colic and urinary calculus, resistant or refractory to conventional therapy with analgesics and spasmolytics was investigated.2. Fifty‐five patients with acute urinary colic refractory to treatment with repeated injections of antispasmodics and analgesics had dramatic or complete pain relief after receiving indomethacin suppositories (100 mg) (P<0.01). Fifteen of the 55 patients passed urinary stones within 30 days of treatment with indomethacin. Three out of 30 other patients with renal or ureteric stones were treated with indomethacin suppositories (100 mg) twice daily. Twenty‐one of the 30 patients passed their stones within 30 days of treatment.4. It is concluded that indomethacin suppositories can relieve acute urinary colic resistant to treatment with analgesic/antispasmodic drugs, and facilitate expulsion of urinary calculi.5. The mechanism of action of indomethacin is discussed in terms of its analgesic and anti‐inflammatory effects and its prostaglandin synthesis inhibition.
ADRENOCORTICOID‐DEPENDENT α‐LACTALBUMIN SYNTHESIS IN RAT MAMMARY GLAND EXPLANTS: ANTAGONIST STUDIES
Authors: Quirk Susan J. , Gannell Jennifer E. , Funder John W. 
Published: June 2007

SUMMARY1. Though adrenal steroids are required for the production of α‐lactalbumin by mammary gland explants, the physiological class of steroid activity (mineralocorticoid, glucocorticoid) remains to be established.2. α‐Lactalbumin production by mammary gland explants from mid‐pregnant rats has been shown in previous studies to be increased by high doses of aldosterone, but not by deoxycorticosterone; in six of 11 experiments corticosterone, the physiological glucocorticoid in the rat, elevated α‐lactalbumin; in five other studies corticosterone had no effect.3. In the present studies the mineralocorticoid antagonist, spirolactone, at very high doses (3‐10 μmol/1) blocked the stimulatory effect on α‐lactalbumin levels of both 30 nmol/1 corticosterone and 3 nmol/1 RU 26988, a pure synthetic glucocorticoid (Type II) receptor agonist.4. Receptor studies, however, indicated that this antagonism is consistent with Type II, glucocorticoid receptor occupancy by spirolactone.5. Since deoxycorticosterone is without agonist effect, and only very high doses of spirolactone affect α‐lactalbumin synthesis, we conclude that the effect of adrenal steroids on α‐lactalbumin production is a manifestation of glucocorticoid and not mineralocorticoid activity.
EFFECTS OF ENDOTHELIUM‐DERIVED RELAXING FACTOR ON THE SMOOTH MUSCLE OF THE RAT TAIL ARTERY
Authors: Kotecha N. , Neild T. O. 
Published: June 2007

SUMMARY1. Simultaneous measurements of smooth muscle membrane potential and tension were made from isolated pieces of rat tail artery.2. A single electrical stimulus to the perivascular nerves produced a transient contraction of the smooth muscle. The amplitude of the contraction was increased after removal of the endothelium.3. The excitatory junction potentials and action potentials in the smooth muscle had the same amplitudes before and after removal of the endothelium.4. Tension obtained by direct stimulation of the arterial muscle in guanethidine‐treated arteries was also increased by removal of the endothelium.5. When the artery was constricted by noradrenaline or 5‐hydroxytryptamine, electrical stimulation caused a relaxation that was reduced by removing the endothelium.6. It was concluded that the electrical stimulus released the endothelium‐derived relaxing factor (EDRF) which reduced the amount of contractile force that could be produced by an action potential in the smooth muscle.
EFFECT OF SODIUM INTAKE AND SODIUM DELIVERY TO THE MACULA DENSA ON RENAL RENIN CONTENT AND JUXTAGLOMERULAR APPARATUS MORPHOLOGY
Authors: Wong T. , Morgan T. O. , Alcorn D. , Ryan G. B. 
Published: June 2007

SUMMARY1. Active and inactive renin were measured in individual juxtaglomerular apparatus (JGA) and in whole kidney homogenates.2. The morphology of the JGA was examined in microbiopsy glomerular specimens and in kidneys fixed by arterial perfusion.3. In rats on high and normal salt intake the total renin content of a single JGA was 14 (s.e.m. = 3) and 29 (s.e.m. = 4) ng AI/h, respectively. The amount of cystoplasm occupied by renin granules was 20% and 27%. Crystalline cores were seen in 1.5% and 7% of the granules, respectively.4. Increased delivery of NaCl to the macula densa did not alter total renin, but decreased inactive renin from 30% to 0, crystalline core‐containing cells from 33% to 14% and decreased the percentage of granules with crystalline cores from 12% to 2.2%.5. Increased sodium in the diet and increased delivery of NaCl to the macula densa decreased the proportion of renin present in the inactive form and decreased the proportion of crystalline cores.6. These coincidental alterations suggest that crystalline cores contain inactive renin and suggest that the delivery of sodium to the macula densa activates renin.
EFFECTS OF TETRADECAPEPTIDE RENIN SUBSTRATE ON ISOLATED PREPARATIONS OF RAT CAUDAL ARTERY, GUINEA‐PIG ATRIA AND ON PITHED RAT BLOOD PRESSURE
Authors: Ziogas J. , Story D. F. , Rand M. J. 
Published: June 2007

SUMMARY1. In rat isolated caudal artery preparations, tetradecapeptide renin substrate enhanced the responses to sympathetic nerve stimulation (0.5 Hz, 10 s).2. In guinea‐pig isolated atria, previously incubated in 3H‐noradrenaline, tetradecapeptide renin substrate enhanced the stimulation‐induced efflux of radioactivity.3. The facilitation of noradrenergic transmission in rat caudal arteries and guinea‐pig atria was blocked by the angiotensin II receptor antagonist saralasin, but was not altered by converting enzyme inhibitors.4. In the pithed rat tetradecapeptide renin substrate increased blood pressure and this effect was reduced by the converting enzyme inhibitor, captopril.
MODULATION OF PROXIMAL TUBULAR REABSORPTION BY ANGIOTENSIN II
Authors: Zhuo J. , Harris P. J. , Skinner S. L. 
Published: June 2007

SUMMARY1. In shrinking‐drop micropuncture studies in anaesthetized rats proximal tubular fluid reabsorption (Jva) decreased by 36% following intravenous infusion of enalapril. In a separate group of rats enalapril reduced fractional lithium clearance indicating decreased proximal fluid reabsorption.2. Following enalapril, GFR rose by 46% but absolute proximal reabsorption rose by 22% indicating 48% effectiveness of proximal glomerulo‐tubular balance (GTB). Since renal blood flow and glomerular filtration rate (GFR) increased in parallel and arterial pressure fell, fluid uptake and proximal GTB were unlikely to have been decreased by peritubular physical forces.3. In anaesthetized rats proximal fluid reabsorption and proximal GTB are modulated by endogenous All through direct stimulation of proximal tubular transport.
EFFECTS OF SHORT‐TERM MODIFICATION OF DIETARY SODIUM INTAKE ON PLASMA CATECHOLAMINES AND BLOOD PRESSURE IN PREHYPERTENSIVE CHILDREN
Authors: Howe P. R. C. , Rogers P. F. , Smith R. M. , Jureidini K. F. 
Published: June 2007

SUMMARY1. The influence of dietary sodium intake on plasma catecholamines was examined as part of a dietary intervention study in 21 prehypertensive school children.2. Diastolic blood pressure was significantly elevated in girls after 3 weeks on a high sodium diet compared with a low sodium diet. Plasma adrenaline levels were raised slightly by the high sodium intake but plasma noradrenaline was significantly reduced.3. Increases of plasma catecholamines in response to standing or cold stress were unaffected by changes in sodium intake.4. The results indicate that the pressor effect of dietary sodium in children is not attributable to increased sympathetic nerve activity.
PRESERVATION OF RENAL FUNCTION IN THE RAT REMNANT KIDNEY MODEL OF CHRONIC RENAL FAILURE BY BLOOD PRESSURE REDUCTION
Authors: Jackson B. , Debrevi L. , Cubela R. , Whitty M. , Johnston C. I. 
Published: June 2007

SUMMARY1. The remnant kidney model of chronic renal failure was established in female Sprague‐Dawley rats subjected to surgical removal of the right kidney and segmentai infarction of seven‐eighths of the left kidney. Plasma creatinine (μmol/1) rose from 65 (s.e.m. = 16, n= 18) to 153 (s.e.m. = 27, t‐test, P < 0.001, d.f. = 17) over 6 weeks. Histological glomerulosclerotic lesions were present from 2 weeks and prominent by 6 weeks post‐surgery.2. Rats were treated with enalapril (5 mg/kg per day, n= 11) or felodipine (30 mg/kg per day, n= 13) from 1 week post‐surgery, and their course compared to untreated rats (n= 18).3. Blood pressure (mmHg) was lowered by both treatments. Six weeks post‐nephrectomy, systolic blood pressure in the untreated group was 176 (s.e.m. = 7, n= 18), enalapril group 122 (s.e.m. = 5, t‐test, P < 0.001, d.f. = 27), and felodipine group 128 (s.e.m. = 3, t‐test, P < 0.001, d.f. = 29).4. Plasma creatinine (μmol/1) was lower in the enalapril group (110, s.e.m. = 8, t‐test, P &lt 0.05, d.f. = 27) but not the felodipine group (173, s.e.m. = 19, t‐test, n.s.) 6 weeks after subtotal nephrectomy compared to the untreated group (153, s.e.m. = 27).5. Glomerulosclerosis (blinded histological score) was reduced with enalapril treatment (1.93, s.e.m. = 0.03, t‐test, P < 0.05, d.f. = 27) but not felodipine treatment (2.15, s.e.m. = 0.04, c.f. untreated 2.36, s.e.m. = 0.12, t‐test, n.s.). Urinary protein excretion (mg/24 h) was 84 (s.e.m. = 22, n= 13) in untreated rats, 15 (s.e.m. = 3, t‐test, t‐test, P < 0.001, d.f. = 22) in enalapril‐treated rats and 221 (s.e.m. = 35, n= 10) with felodipine treatment.6. Functional and structural damage in the rat remnant kidney model of chronic renal failure was ameliorated by treatment with enalapril but not by treatment with felodipine.
THE SYNDROME OF HYPERTENSION AND HYPERKALAEMIA WITH NORMAL GFR. A UNIQUE PATHOPHYSIOLOGICAL MECHANISM FOR HYPERTENSION?
Authors: Gordon Richard D. 
Published: June 2007

SUMMARY1. Based on 28 reported patients, constant features of the syndrome of hypertension and hyperkalaemia are hyperkalaemia, hyperchloraemia, normal renal glomerular function and, in all adult patients, hypertension.2. Inconstant features include short stature, intellectual impairment and muscle weakness.3. Levels of renin and aldosterone are low, but respond to dietary salt restriction and diuretic therapy, both of which reverse the hypertension and hyperkalaemia.4. The basic abnormality is excessive renal sodium retention, leading to chronic suppression of renin and aldosterone; the latter is then hyporesponsive to the hyperkalaemic stimulus.5. Dietary salt loading or impaired production of any natriuretic or chloriuretic factor (for example atrial natriuretic peptide or renal natriuretic prostaglandins) would predispose to development of the syndrome. With normal GFR, this appears to be a unique mechanism for hypertension and hyperkalaemia.
STIMULATION OF PHOSPHATIDYLINOSITOL METABOLISM IN THE HEART
Authors: Leung E. , Johnston C. I. , Woodcock E. A. 
Published: June 2007

SUMMARY1. Receptor‐stimulated hydrolysis of inositol phospholipids was studied in atrial and ventricular myocytes isolated from guinea‐pigs.2. Acetylcholine and carbachol stimulated inositol phosphate accumulation with a maximum of more than 12 times the unstimulated values in atrial myocytes and 7 times in ventricular myocytes.3. The vasoactive peptides angiotensin II and vasopressin also stimulated inositol phosphate accumulation, but the maximum effect was lower than that mediated through muscarinic receptors.4. However, the adenosine analogues, l‐N6‐phenylisopropyladenosine and 5'N‐ethylcarboxamidoadenosine which, like muscarinic agonists depress cardiac contractility, did not affect inositol phosphate accumulation at concentrations up to 10−4 mol/1.5. Stimulation of phosphatidylinositol turnover in heart bears no obvious relationship to either contractility or release of atrial natriuretic factor.
EVOLUTION OF RENIN
Authors: Morris B. J. , Catanzaro D. F. 
Published: June 2007

SUMMARY1. New gene data for three aspartyl proteases (human renin, mouse renin and human pepsin) permitted closer analysis of the gene duplication and fusion hypothesis for the evolution of this family of enzymes.2. Alignment of sequences in the hemilobes of human pepsin revealed only weak homology in amino acid sequences. Nucleotides were, however, more homologous.3. Splice junctions between putative duplicated exons did not match.4. Repeated sequences in the human renin gene were detected by hybridization with total human DNA labelled with 32P. These were not, however, consistent with unequal crossing‐over between repeated sequences of an ancestral gene having occurred.5. The data thus provide no immediate support for the gene duplication and fusion hypothesis. The symmetry in structure of an aspartyl protease may arise from the tendency of hydrophilic amino acids to be encoded at splice junctions. This would divide a molecule comprised mainly of β‐sheets into roughly superimposable domains.
FACTORS INFLUENCING THE EFFECTS OF INTRAVENOUS NALOXONE ON ARTERIAL PRESSURE AND HEART RATE AFTER HAEMORRHAGE IN CONSCIOUS RABBITS
Authors: Rutter Peter C. , Potocnik Simon J. , Ludbrook John 
Published: June 2007

SUMMARY1. The circulatory responses to different intravenous doses of naloxone were studied in conscious rabbits before and after haemorrhage, under different conditions including prior ganglion blockade.2. Unless there had been blood loss, naloxone elicited no pressor response, even in high dose. After bleeding so that arterial pressure fell to 40 mmHg, the dose‐response relationship for naloxone had two components. Over a low‐dose range (threshold 0.3 mg/kg) naloxone had a modest pressor effect but did not affect heart rate. Over a much higher dose range (threshold 0.6 mg/kg) naloxone caused a marked rise in arterial pressure and a profound bradycardia. The highest dose of naloxone examined (25 mg/kg) caused a rise in arterial pressure of 70 mmHg and a reduction in heart rate of 160 beats/min.3. The pressor and bradycardic effects of naloxone were the same whether post‐haemorrhagic hypotension lasted 5, 10, 20 or 30 min.4. The responses to naloxone in low or high dose depended much more closely on the volume of blood removed than on the level to which arterial pressure fell. Even after non‐hypotensive haemorrhage a high dose of naloxone had marked pressor and bradycardic effects.5. Ganglion blockade prior to haemorrhage abolished the pressor response to a low, but not to a high, dose of naloxone.6. It was concluded that prolonged and severe hypotension are not necessary to ‘prime’ the cardiovascular system to respond to naloxone after haemorrhage. In a high dose its pressor effects appear to be mediated post‐ganglionically, but in a low dose it may act within the central nervous system.