bluuebunny/crossref_metadata_2025_split huggingface dataset:
ACUTE CHANGES IN BLOOD PRESSURE AND VASOACTIVE HORMONES AFTER CAPTOPRIL IN HYPERTENSIVE PATIENTS
Authors: McGrath Barry P. , Matthews P. Geoffrey , Johnston Colin I. 
Published: June 2007

SUMMARY1. The acute effects of captopril on blood pressure, renin, angiotensin, bra‐dykinin and catecholamines were examined in patients with essential (n= 10, Group 1), accelerated (n=6, Group 2) and renal hypertension (n= 14, Group 3).2. Blood pressure showed little change in Group 1, fell significantly in Group 2, with a marked fall in Group 3. Heart rate did not change.3. The fall in blood pressure was positively correlated with pretreatment renin and angiotensin II.4. Angiotensin II fell, with reciprocal increases in renin and angiotensin I. No changes occurred in bradykinin or catecholamines.5. The rise in renin after captopril was greatest in renovascular hypertension which may prove useful as a screening test for such patients.
RENAL, ADRENAL AND VASCULAR CHANGES DURING INHIBITION OF CONVERTING ENZYME WITH CAPTOPRIL
Authors: Clappison B. H. , Millar J. A. , Casley D. J. , Anderson W. P. , Johnston C. I. 
Published: June 2007

SUMMARY1. In rats treated continuously with captopril (80 μg/h, i.p.), for 2 days, blood pressure decreased and adrenal angiotensin II receptor concentration was decreased from 160 fmol/mg protein (s.e.m.=9) in controls to 131 fmol/mg protein (s.e.m. = 7, P < 0.01, n= 10). However, after 5 days of continuous treatment, blood pressure had returned to normal and adrenal receptor concentrations in treated rats were not significantly different from controls (180 fmol/mg, s.e.m. = 11 and 203 fmol/mg protein s.e.m. = 14 respectively, 0.1>P>005).2. Vascular reactivity, defined as the pressor response to exogenous angiotensin II, increased concurrently by 166 and 33% respectively.3. In anaesthetized dogs (n= 8), captopril (1.5 mg/kg, i.v.) caused a fall in blood pressure, and urine bradykinin excretion increased from 1 08 (s.e.m.=0 14) to 1 64 μg/h (s.e.m.=0 33, P < 0 025) at 15 min. Renal blood flow increased significantly (P < 0 01) with no change in glomerular filtration rate, and there was no change in either renal venous or arterial blood bradykinin levels.4. Thus, converting enzyme inhibition produces transient secondary changes in angiotensin receptors and vascular reactivity. Increased urine bradykinin probably reflects decreased catabolism of intrarenal bradykinin. The hypotensive effect of captopril may be due in part to raised levels of bradykinin in the kidney.
COMPARISON OF INITIAL RESPONSES TO RENAL ARTERY STENOSIS IN PENTOBARBITONE–ANAESTHETIZED AND CONSCIOUS DOGS
Authors: Anderson W. P. 
Published: June 2007

SUMMARY1. Trained chronically‐instrumented dogs were subjected to renal artery stenosis twice. A 50 mmHg stenosis pressure gradient was established while the dogs were conscious or anaesthetized with pentobarbitone and prepared for renal surgery.2. Prior to stenosis, the anaesthetized dogs had significantly higher mean arterial pressure, renal vascular resistance and plasma renin activity than when they were conscious.3. Twenty‐four hours after stenosis, when all dogs were fully conscious, significant elevations in mean arterial pressure and plasma renin activity were seen only in the dogs anaesthetized for stenosis production. Creatinine clearance over this period was also markedly less than after renal artery stenosis of conscious animals.4. It seems likely that more severe renal artery stenosis is required to produce a given pressure gradient in anaesthetized dogs than in the conscious dogs.
THE PRESENT STATUS OF THE AUTOREGULATION THEORY OF THE PATHOGENESIS OF HYPERTENSION
Authors: Korner P. I. 
Published: June 2007

SUMMARY1. The autoregulation theory of hypertension has been attractive because it postulates a mechanism whereby an early rise in cardiac output becomes ‘transformed’ through normal autoregulatory processes into an elevated total peripheral resistance.2. ‘Normal’ autoregulation involved in control of blood flow of regional beds is a rapid process compared with the slow changes postulated by the autoregulation theory.3. Evidence is presented that under appropriate experimental conditions ‘volume’ factors (cardiac output) and ‘constrictor’ factors exert independent long‐term effects in developing and in established hypertension. There is little evidence to support the autoregulation theory of hypertension.
HYPOTENSIVE EFFECTS OF CAPTOPRIL ADMINISTERED CENTRALLY IN INTACT CONSCIOUS SPONTANEOUSLY HYPERTENSIVE RATS AND PERIPHERALLY IN ANEPHRIC ANAESTHETIZED SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Hutchinson J. S. , Mendelsohn F. A. O. 
Published: June 2007

SUMMARY1. The hypotensive response to captopril in anaesthetized spontaneously hypertensive rats (SHR) is not modified by bilateral nephrectomy performed 1 or 24 h previously.2. Intracerebroventricular injection (i.c.v.) of captopril (2 mg kg−1) significantly lowered blood pressure of conscious SHR over a 7‐h period of observation but there was no significant blood pressure response to i.c.v. vehicle, or to intravenous captopril (2 mg kg−1) in SHR.3. There was no significant blood pressure response to captopril (2 mg kg”') i.c.v. in the normotensive Wistar Kyoto controls (NT‐WK).4. These results indicate that captopril can lower the blood pressure of SHR by mechanisms independent of the kidneys or the circulating renin‐angiotensin system.5. The hypotensive effect of central captopril in SHR but not in the NT‐WK suggests biochemical differences between the brains of the two rat strains.
FACILITATION OF SYMPATHETIC TRANSMISSION BY PREJUNCTIONAL β‐ADRENOCEPTORS IN CARDIAC AND VASCULAR TISSUES
Authors: Medgett I. C. , McCulloch M. W. , Rand M. J. , Story D. F. 
Published: June 2007

SUMMARY1. In rat isolated tail arteries and atria in which transmitter stores are labelled with (3H)‐noradrenaline, isoprenaline in low concentrations facilitates the stimulation‐induced efflux of tritium.2. This effect is dependent on the frequency and duration of electrical stimulation, being observed only at low frequency (2 Hz) and short duration (10 s in atria and 30 s in arteries) or at high frequency (5 Hz) and long duration (1 min in atria and 4 min in arteries).3. In atria, phentolamine enhances tritium efflux with stimulation at 5 Hz for 1 min but not at 2 Hz for 10 s. Conversely, propranolol reduces tritium efflux with stimulation at 2 Hz for 10 s but not at 5 Hz for 1 min.4. The results can be interpreted in terms of the selective operation, depending on the frequency and duration of electrical stimulation, of inhibitory and facilitatory feedback loops for transmitter release involving prejunctional a‐and β‐adrenoceptors, respectively.
THE INFLUENCE OF DIETHYL MALEATE ON THE BILIARY EXCRETION OF INFUSED SULPHOBROMOPHTHALEIN SODIUM AND ITS GLUTATHIONE CONJUGATE IN GUINEA‐PIGS
Authors: Whelan Gregory 
Published: June 2007

SUMMARY1. Hepatic sulphobromophthalein (BSP) transport was studied in guinea‐pigs pretreated intraperitoneally with 0 7 ml of diethyl maleate to depress hepatic glutathione levels.2. Diethyl maleate depressed the hepatic transport of infused conjugated BSP from hepatocytes into bile without influencing hepatic uptake.3. Unconjugated BSP transport was also depressed markedly as a result of (a) a reduction in the intrahepatic conjugation of BSP with glutathione and (b) suppression of conjugated BSP excretion.
SYSTEMIC AND REGIONAL HAEMODYNAMICS IN EXPERIMENTAL RENAL HYPERTENSION IN CONSCIOUS RABBITS
Authors: van Boom Martin , Saxena Pramod R. 
Published: June 2007

SUMMARY1. The radioactive microsphere method was used to measure the distribution of cardiac output, regional flows and resistances in conscious normotensive and hypertensive rabbits implanted with an electromagnetic flow probe on the ascending aorta or pulmonary artery. Hypertension was induced by wrapping one kidney with cellophane and removing the other, and studies were performed about 5 weeks later.2. Heart rate, stroke volume, cardiac output and total renal mass were reduced in the hypertensive animals, while the weight of, and the cardiac output distribution to left ventricle and the remaining kidney were increased.3. In renal hypertensive rabbits, the weight normalized regional blood flow was diminished in a number of tissues, including the kidney, and, except for some organs in the splanchnic area (stomach, small intestine, mesentery and pancreas) and the fat, there was a rather uniform increase in tissue vascular resistance.
THE HYPOTENSIVE RESPONSE TO COMPOUND 48/80 IN NORMOTENSIVE AND HYPERTENSIVE RATS
Authors: Kirkendol Paul L. , Cauvin Cynthia A. 
Published: June 2007

SUMMARY1. The administration of an initial dose of 50 μg/kg of 48/80 produced a sharp fall in the blood pressure of normotensive rats but produced little change in blood pressure in spontaneously hypertensive rats.2. The administration of an additional 50 μg/kg and 100 μg/kg of 48/80 in normotensive and spontaneously hypertensive rats resulted in equivalent decreases in pressure in both groups.3. Both groups had equivalent decreases in blood pressure in response to methylhistamine.4. Spontaneously hypertensive rats appear to have a reduced ability to release histamine in response to 48/80 due to either an increased threshold for 48/80 or a diminished histamine storage pool.
BOOK REVIEWS
Authors: Doyle A. E. , Bowman W. C. , Yeomans Neville D. 
Published: June 2007

Cardiovascular Drugs. Volume 4, Antihypertensive Drugs Today. Ed. by R.N. Brogden. Cross‐Bridge Mechanism in Muscle Contraction. Ed. by Haruo Sugi and Gerald H. Pollack. Glucagon in Gastroenterology. Edited by J. Picazo.
IN‐VIVO MODIFICATION OF ANGIOTENSIN 11 PRESSOR RESPONSIVENESS IN SHEEP BY INDOMETHACIN
Authors: Beilby David S. , Coghlan John P. , Denton Derek A. , Graham William F. , Humphery Timothy J. , Scoggins Bruce A. , Whit worth Judith A. 
Published: June 2007

SUMMARY1. Sodium (Na) depletion, due to uncompensated loss of parotid saliva, reduces the pressor responsiveness to angiotensin II (AII) in intact conscious sheep.2. Inhibition of prostaglandin synthesis by indomethacin restored All pressor responsiveness in Na‐deplete sheep.3. Indomethacin infusion also increased the pressor responsiveness to AII in the Na‐replete sheep.4. These findings suggest that in vivo prostaglandins may play a role in modulating the pressor responsiveness to angiotensin II in sheep.
ALTERED CARDIAC NORADRENALINE STORES IN DOCA‐SALT HYPERTENSIVE RATS
Authors: Howe P. R. C. , West M. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. The storage of noradrenaline (NA) in hearts of DOCA‐salt hypertensive rats was examined after in vivo administration of labelled NA.2. The cardiac N A concentration and the neuronal NA storage capacity were reduced in these rats compared with normotensive controls. The extent of reduction was dependent on the duration of hypertension.3. These findings are similar to observations on spontaneously hypertensive rats and support the hypothesis that storage of the cardiac sympathetic transmitter is impaired in DOCA‐salt hypertension.
A STUDY OF THE EFFECTS OF HYPOTHYROIDISM INDUCED BY PROPYLTHIOURACIL ON ADRENOCEPTORS AND NORADRENALINE LEVELS IN THE VAS DEFERENS OF THE RAT
Authors: Leedham J. A. , Handberg G. M. , Ishac E. J. , Pennefather J. N. 
Published: June 2007

SUMMARY1. The anti‐thyroid drug, propylthiouracil (0.05% w/v in drinking water) was administered to rats for 3–4 weeks. This treatment decreased the rate at which rats gained body weight but did not affect the weight of the vasa deferentia. Circulating levels of thyroxine and triiodothyronine were markedly decreased.2. The potencies of postjunctional α‐adrenoceptor agonists, 1‐noradrenaline and 1‐phenylephrine, in eliciting contraction of the epididymal end of the vas deferens were unaffected by propylthiouracil treatment. In contrast, the potency of the β‐adrenoceptor agonist, 1‐isoprenaline, in inhibiting field stimulation‐induced twitches of the prostatic end of the vas deferens was decreased in tissues from propylthiouracil‐treated rats. Thus hypothyroidism induced by propylthiouracil produced an apparent change in the properties of postjunctional β‐adrenoceptors without a concomitant reciprocal change in the properties of postjunctional α‐adrenoceptors.3. Treatment of rats with propylthiouracil led to a small increase in the concentration of noradrenaline in the vas deferens, and a concomitant small increase in the rate of accumulation of 3 H‐noradrenaline in in vitro experiments. Extra‐neuronal uptake of 3H‐isoprenaline was unaffected by propylthiouracil treatment.4. The potencies of the prejunctional α‐adrenoceptor agonists, xylazine and 1‐noradrenaline, in producing inhibition of twitches evoked by field stimulation of preparations of the prostatic end of the vas deferens, were similar in preparations from propylthiouracil‐treated and control rats, although the slope of the log dose‐response curve to xylazine was decreased in the former group. Thus unequivocal changes in the properties of prejunctional α‐adrenoceptors did not accompany the other prejunctional effects of propylthiouracil upon endogenous noradrenaline levels and neuronal uptake of 3H‐noradrenaline in this organ.
INOTROPIC RESPONSES OF ISOLATED ATRIAL AND VENTRICULAR MUSCLE FROM THE DOG HEART TO INOSINE, GUANOSINE AND ADENOSINE
Authors: Chiba Shigetoshi , Watanabe Hidehiko , Furukawa Yasuyuki 
Published: June 2007

SUMMARY1. The inotropic effects of inosine, adenosine and guanosine were compared in isolated and blood‐perfused canine atrial and ventricular muscle preparations paced at 1.5 2.5 Hz.2. In isolated atria, guanosine and inosine usually had positive inotropic effects, but adenosine consistently had a marked negative inotropic effect.3. In ventricular muscles, the three purine compounds examined produced dose‐related positive inotropic responses, but adenosine also produced a slight negative inotropic response which preceded the positive inotropic response.
EFFECTS OF THYROID HORMONES, ANTITHYROID DRUGS AND IODIDE ON IN VITRO CONVERSION OF THYROXINE TO TRIIODOTHYRONINE
Authors: Aizawa Toru , Yamada Takashi 
Published: June 2007

SUMMARYIn an attempt to study the effects of thyroid hormones, antithyroid drugs and iodide on the conversion of thyroxine (T4) to triiodothyronine (T3), the liver was obtained from normal, hypothyroid and hyperthyroid rats treated with T4 or T3. T4 was incubated with liver homogenates and generated T3 was measured.1. The conversion of T4 to T3 was less in the liver homogenates from thyroidectomized, methylmercaptoimidazole (MMI)‐treated and propylthiouracil (PTLT)‐treated rats. The magnitude of decrease was the same in thyroidectomized and MMI‐treated rats, but was greater in PTU‐treated rats.2. Administration of T4 and T3 to thyroidectomized and MMI‐treated rats restored the converting activity. When excess T4 was administered, the converting activity was above normal. In contrast, administration of graded doses of T4 failed to restore the converting activity of the liver from PTU‐treated rats.3. In vitro addition of MMI failed to affect converting activity of the liver, but addition of excess iodide and PTU significantly depressed it.
EFFECT OF SUSTAINED HYPERNATRAEMIA ON THE RENIN‐ALDOSTERONE SYSTEM IN THE DOG
Authors: Young David B. , McCaa Robert E. 
Published: June 2007

SUMMARY1. To determine if increases in plasma sodium concentration P[Na] have any sustained effects of the renin‐aldosterone system, P[Na] was increased in a group of six dogs over a period of 6 days by increasing sodium intake from 10 to 200 mmol per day while a fixed 700 ml per day water intake was maintained along with a continuous i.v. infusion of antidiuretic hormone (ADH) at a rate of 2.4 units per day.2. P[Na] rose from 137.3 ± 2.0 to 153.6 ± 6.5 mmol/1 during the high intake period. Plasma potassium concentration, 22Na space, and mean arterial pressure all remained near control levels in response to Na loading.3. Plasma renin activity (PRA) averaged 1.0 ± 0.1 ngAI/ml per hour on the final low Na day and fell transiently to 0.6 ± 0.2 ngAI/ml per hour on the first day of sodium loading. For the duration of the study it remained at the control level. Plasma aldosterone concentration fell from the low Na level of 15.4 ± 2.4 ng/100 ml to 10.5 ± 1.5 ng/100 ml on the final day of high Na intake.4. We conclude that increases in P[Na] in the absence of concomitant changes in P[K], 22Na space and MAP do not have a sustained effect on control of renin release but may exert a negative effect on aldosterone secretion.
SERUM CONCENTRATIONS OF DIGOXIN ENTRAPPED IN LIPOSOMES AFTER INTRAVENOUS ADMINISTRATION IN DOGS
Authors: Fountain M. W. , Pedersoli W. D. , Ravis W. R. , Ganjam V. K. 
Published: June 2007

SUMMARY1. Digoxin was associated into phosphotidylcholine liposomes at concentrations of 28–33 mol% in Hank's Buffer, pH 7.4 at 28°C.2. Digoxin‐liposomes (digoxin concentration 0.022 mg/kg per dog per day) administered intravenously in five adult male dogs attained therapeutic serum concentrations (0.7–3.0 ng/ml) beginning with day 1 of administration.3. Digoxin serum concentrations obtained by intravenous digoxin‐liposomes compared favorably with normal oral digoxin administration (0.022 mg/kg per dog per day) in all 5 dogs monitoring serum digoxin levels for 7 days showed no significant (P<0.05) differences in mean serum digoxin concentrations ± s.e.m. on 6 of 7 days of treatments.
PIRETANIDE AND URINARY EXCRETION OF IONS IN RAT. EFFECT OF INDOMETHACIN
Authors: Nguyen‐Simonnet H. , Gauthier C. , Pellet M. 
Published: June 2007

SUMMARY1. Piretanide is a new loop diuretic resembling furosemide. The effects of this diuretic on various parameters of renal function and on the excretion of the major ions were studied on anaesthetized, hydrated rats.2. Piretanide induced a marked diuresis and increased sodium, potassium, chloride and calcium excretion. Calcium excretion increased more than that of sodium. Urinary osmolality and water reabsorption decreased.3. Inulin clearance and phosphate excretion were significantly altered by piretanide.4. Pretreatment of rats with indomethacin did not suppress the effects of piretanide on diuresis nor its effects on urinary excretion of sodium, chloride and potassium, since these parameters increased in the same proportion in the presence or in the absence of indomethacin.5. Pretreatment with indomethacin abolished piretanide‐induced dissociation of sodium and calcium excretions.
RESIDUAL CATECHOLAMINES IN EXTRINSICALLY DENERVATED GUINEA‐PIG ILEUM
Authors: Howe P. R. C. , Provis J. C. , Furness J. B. , Costa M. , Chalmers J. P. 
Published: June 2007

SUMMARY1. Concentrations of noradrenaline, adrenaline and dopamine were measured in the submucosa and myenteric plexus of innervated and extrinsically denervated guinea‐pig ileum using a sensitive radioisotope enzymatic assay for catecholamines.2. Subcellular fractionation studies indicated that the microsomal fraction obtained from both layers of the normal ileum was greatly enriched with noradrenaline compared to the total homogenate. Low levels of adrenaline and dopamine were also detected in both layers of the ileum.3. After extrinsic denervation or pretreatment with reserpine, noradrenaline was reduced to less than 3% and could no longer be visualized histochemically. Small proportions of the adrenaline and dopamine also disappeared after extrinsic denervation.4. The residual amounts of noradrenaline, adrenaline and dopamine present after extrinsic denervation were not sensitive to reserpine and were not concentrated in microsomal fractions suggesting that these amines are not stored as neurotransmitters in intrinsic neurons of the intestine.
BIOSYNTHESIS OF PREPRORENIN AND INTRACELLULAR CONVERSION OF PRORENIN TO RENIN
Authors: Morris Brian J. , Catanzaro Daniel F. 
Published: June 2007

SUMMARY1. The existence of a biosynthetic precursor of renin (prorenin) has been inferred, but never established experimentally. The aim of the present study was to provide this evidence.2. In a continuous labelling experiment using submandibular glands of male Quackenbush mice (an extraordinarily rich source of renin) a molecule of Mr 44 500 was immunoprecipitated with antiserum to renin.3. The Mr 44 500 protein was converted to Mr 40 000 renin in a time‐dependent fashion during incubation of tissue at 37Â°C: 15min after addition of [35S] methionine only 16% of immunoprecipitable radioactivity was renin, whereas by 4 h this had increased to 86%. The Mr 44 500 protein would therefore appear to be a ‘pro’ form of renin.4. Submandibular gland mRNA was translated in a cell‐free system derived from rabbit reticulocyte lysate and a molecule of Mr 46 000 was immunoprecipitated with antirenin. This was preprorenin and the Mr of the ‘pre’ region would thus be 1500, which is consistent with the size generally found for the ‘pre’ region of secretory proteins.5. The present study has therefore demonstrated for the first time the biosynthesis of a ‘pro’ form of renin (prorenin) and its conversion to renin intra‐cellularly.
EFFECT OF CONVERTING ENZYME INHIBITION WITH CAPTOPRIL ON IN VITRO ANGIOTENSIN PRODUCTION IN SHEEP
Authors: Fei David T. W. , Coghlan John P. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. The effect of captopril on in vitro production of angiotensin I (ANG I), [Val5] ‐angiotensin II ([Vals]‐ANG II) and [Val4]‐angiotensin III ([Val5]‐ANG‐(2–8)) in central venous blood taken from sodium‐deficient sheep was studied.2. Captopril enhances in vitro production of ANG I but blocks the in vitro production of [Val5] ‐ANG II and [Val5] ‐ANG‐(2–8).3. The production of ANG I in blood is faster than that of [Val5]‐ANG II and [Val5] ‐ANG‐(2–8).4. The half‐life of [Val5]‐ANG II and [Val5]‐ANG‐(2–8) in vitro in blood in the presence of captopril was 10 and 14 min, respectively.5. This in vitro study suggests that the production of [Val5]‐ANG II and [Val5] ‐ANG‐(2–8) in blood forms a small part of the total body production of each peptide.
ADRENALINE SYNTHESIZING NERVE CELLS IN THE MEDULLA OF NORMOTENSIVE AND HYPERTENSIVE RATS
Authors: Chalmers J. P. , Howe P. R. C. , Costa M. , Furness J. , Lovenberg W. , Wallman Y. 
Published: June 2007

SUMMARY1. We have studied the number and distribution of adrenaline synthesizing nerve cells in the medulla oblongata of the rat, using a combination of immunofluorescence to visualize the enzyme phenylethanolamine‐N‐methyltransferase (PNMT) and catecholamine fluorescence to detect central catecholamines.2. The distribution of adrenaline synthesizing nerve cells was similar in normo‐tensive (Wistar Kyoto) rats, spontaneous hypertensive rats, and stroke‐prone rats. Few of the cells visualized by PNMT immunofluorescence were detected by the Faglu fluorescence method for catecholamines. The CI (ventrolateral) and C2 (dorsomedial) groups of PNMT cells were anatomically distinct from the Al and A2 groups of catecholamine fluorescent cells and lay rostral to these cells within the medulla. There was a third group of adrenaline synthesizing cells close to the midline in the rostral medulla, and we have called this the C3 group.3. There was a 32% increase in the number of PNMT cells in the medulla of 4‐week‐old stroke‐prone rats.4. PNMT enzyme activity in a cross‐segment of the medulla containing the adrenaline synthesizing cells was also increased by 30% in both spontaneous hypertensive rats and stroke‐prone rats.