bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF REGULAR ALCOHOL USE ON BLOOD PRESSURE CONTROL IN TREATED HYPERTENSIVE SUBJECTS: A CONTROLLED STUDY
Authors: Puddey I. B. , Beilin L. J. , Vandongen R. 
Published: June 2007

SUMMARY1. Forty‐four males with treated essential hypertension and a moderate‐to‐heavy alcohol intake participated in a randomized controlled crossover trial of the effects of varying alcohol intake on blood pressure control. Usual antihypertensive therapy was maintained unchanged throughout.2. Self‐reported alcohol consumption fell from 452 ml ethanol/week (s.e.m. = 29) during normal drinking habits to 64 ml/week (s.e.m. = 8) while drinking low alcohol content beer.3. Mean systolic and diastolic blood pressures were significantly lower during the last 2 weeks of reduced alcohol (supine 5.0 mmHg, s.e.m. = 1.4, and 3.0 mmHg, s.e.m. = 0.9, respectively; erect 5.9 mmHg, s.e.m. = 1.6, and 2.9 mmHg, s.e.m. = 1.0, respectively).4. Body weight was also lower (0.94 kg, s.e.m. = 0.25) at the conclusion of the low alcohol intake period.5. Regression analysis suggested that reduction in alcohol intake contributed independently to the fall in both systolic and diastolic blood pressure, while weight change contributed independently to the fall in systolic blood pressure alone.6. It was concluded that curtailing moderate to heavy alcohol intake leads to improved blood pressure control in treated essential hypertensive males.
INFLUENCE OF AGE, SEX AND WEIGHT ON MEASUREMENTS OF INTRACELLULAR Na+ AND K+ IN ESSENTIAL HYPERTENSION
Authors: Bramley P. M. , Paulin J. M. , Millar J. A. 
Published: June 2007

SUMMARY1. Na+ and K+ concentrations were measured in red cells from 22 patients with untreated essential hypertension and 22 normotensive control subjects who were individually and prospectively matched for age, sex and weight and in a separate population of 31 hypertensive patients and 41 normotensive subjects who were not so matched.2. Intracellular Na+ and K+ concentrations were similar in the matched subjects. Significant positive correlations were found between intracellular Na+ and body weight (r=0.27, P < 0.041), and between intracellular K+ and age (r= 0.29, P < 0.028).3. In the unmatched population, intracellular Na+ was significantly increased in patients with hypertension and was correlated significantly with age (r=0.25, P < 0.017). After correction for age, intracellular Na+ was similar in both hypertensive and normotensive subjects. Age‐corrected intracellular K+ was similar in both hypertensive and normotensive groups but was significantly lower in male subjects.4. These results highlight the importance of matching study groups for age, sex and weight when studying possible abnormalities in cell ionic composition in hypertension. False positive results may arise if study groups are not matched for these characteristics. Red cell Na+ and K+ are not altered in essential hypertension.
SYMPATHETIC DENERVATION OF THE RAT VAS DEFERENS FOLLOWING UNILATERAL VASECTOMY
Authors: DeGaris Richard M. , Pennefather Jocelyn N. 
Published: June 2007

SUMMARY1. This paper describes an investigation of the time course of changes in noradrenaline levels in epididymal and prostatic segments of rat vasa deferentia, for up to 91 days following unilateral vasectomy by medial transection, together with an investigation of the responses of isolated preparations of these segments to field stimulation of sympathetic terminals.2. No atrophy of testes or seminal vesicles, or of the prostatic and epididymal segments of operated vasa deferentia, was evident at 2, 4, 7, 28 and 91 days after unilateral vasectomy.3. Spectrophotofluorometric assay revealed that noradrenaline levels in epididymal segments of operated vasa deferentia declined rapidly (within 2 days) after unilateral vasectomy and remained below 10% of those in unoperated epididymal segments at days 4, 7, 28 and 91 post‐vasectomy. Noradrenaline levels in prostatic segments of operated vasa deferentia were unaffected by vasectomy.4. Histochemical studies revealed that catecholamine fluorescence in epididymal segments of operated vasa deferentia declined in parallel with the decline in tissue noradrenaline levels; no comparable changes occurred in prostatic segments.5. Field stimulation (10 pulses, 60 V, 1 ms, applied at 0.1–50 Hz) evoked frequency‐dependent contractions of unoperated epididymal segments and of operated and unoperated prostatic segments at 2, 4, 7, 28 and 91 days post‐vasectomy. At day 2 and 4 responses of prostatic segments of operated tissues, to frequencies below 5 Hz, exceeded those of corresponding unoperated segments, however, by day 91, there was a small but significant decline in responses. Responses of epididymal segments of operated vasa deferentia to all frequencies of stimulation declined by day 2 post‐vasectomy and were absent thereafter except in three of the 18 preparations studied at day 91.6. These results, taken together, confirm that there is a rapid decline in catecholamine levels in the epididymal segment of medially transected vasa deferentia following unilateral vasectomy. Minimal, if any, reinnervation of this segment occurs during the 3 month period following unilateral vasectomy.
EFFECT OF SODIUM NITROPRUSSIDE ON THE BIOPHASE CONCENTRATION OF D‐TUBOCURARINE AT THE NEUROMUSCULAR JUNCTION
Authors: Chang P. , Geh S. L. 
Published: June 2007

SUMMARY1. d‐Tubocurarine (dTC) at an intravenous dose of 250 μg/kg, or at an intra‐arterial dose of 25 μg/kg, produced about a 50% block on the twitch tension of the indirectly stimulated tibialis anterior muscle of anaesthetized cats.2. The dTC‐induced neuromuscular block was abolished if it was given intravenously but not intra‐arterially, 30 min after the commencement of sodium nitroprusside (SNP) infusion (5 μg/kg per min) when there was a maximum decrease in blood pressure.3. The results indicate that the biophase concentration of dTC at the neuromuscular junction may be decreased as a consequence of the vasodilation induced by SNP leading to a reduced transport of the blocker to the site of action.
PREVENTION OF DOCA‐INDUCED HYPERTENSION IN RATS BY CHRONIC TREATMENT WITH TRYPTOPHAN
Authors: Fregly Melvin J. , Fater Dennis C. 
Published: June 2007

SUMMARY1. Hypertension developed within 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA, 30 mg/kg, s.c., weekly) and given isotonic saline to drink. Chronic dietary administration of tryptophan (50 g/kg food) reduced intake of saline solution and prevented the elevation of systolic blood pressure induced by treatment with DOCA alone.2. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24 h dehydration that is characteristic of DOCA‐treated rats.3. Other tests were carried out to assess the responsiveness to the β‐adrenergic agonist, isoproterenol. The tests included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking response of DOCA‐treated rats to acute administration of isoproterenol was returned to that of untreated controls by chronic treatment with tryptophan. However, the reduced chronotropic response of the heart of DOCA‐treated rats to administration of isoproterenol was unaffected.4. The cardiac hypertrophy characteristic of DOCA‐treatment was attenuated significantly by chronic treatment with tryptophan.5. These results suggest that tryptophan provides significant protection against the development of DOCA‐induced hypertension, polydipsia, and cardiac hypertrophy in rats. The mechanism by which tryptophan protects is unknown and requires additional study.
CAPTOPRIL DOES NOT POTENTIATE HYPOTENSION AND ALGESIA BY SUBSTANCE P
Authors: Hui S‐C. G. , Ogle C. W. 
Published: June 2007

SUMMARY1. Captopril (1–5 mg/kg, i.v.) did not affect the vasodepressor responses to substance P (1–30 μg/kg, i.v.) in anaesthetized rats.2. Substance P (100 μg/kg, s.c.) produced significant algesia in mice; this was not potentiated by the smaller doses of captopril (1–2 mg/kg, i.p.), but was instead antagonized by the high dose (5 mg/kg, i.p.).3. It is concluded that captopril does not have any influence on substance P degradation in vivo since the pharmacological actions of the undecapeptide are not enhanced after captopril treatment.
ATTENUATION OF PRESSOR RESPONSES TO SYMPATHETIC STIMULI IN THE RAT BY ENALAPRIL
Authors: Rechtman M. P. , Ishac E. J. N. , Boura A. L. A. , King R. G. , Walters W. A. W. 
Published: June 2007

SUMMARY1. Intravenous administration to pithed Wistar rats of the angiotensin converting enzyme inhibitor enalapril (0.1–1.0 mg/kg) lowered the diastolic blood pressure and reduced pressor responses occurring during electrical stimulation (1–30 Hz) of the spinal sympathetic outflow.2. These doses of enalapril given intravenously also attenuated pressor responses to intravenous injection of the muscarinic ganglion stimulant McNeil‐A‐343 (50, 100, 150 μg/kg) and noradrenaline (0.1–5.0 μg/kg). Enalapril (1.0 mg/kg, i. v.) reduced pressor responses to the nicotinic ganglion stimulant 1,1‐dimethyl‐4‐phenylpiperazinium (300 μg/kg, i.v.).3. These results confirmed that the actions of enalapril resemble those of captopril in the pithed rat, by causing reductions in both blood pressure and pressor responses to sympathetic stimuli.
EFFECT OF SODIUM DEPLETION ON PRESSOR RESPONSIVENESS IN ACTH‐INDUCED HYPERTENSION IN MAN
Authors: Connell John M. C. , Fisher B. Miles , Davidson Gillian , Fraser Robert , Whitworth Judith A. 
Published: June 2007

SUMMARY1. Pressor responsiveness to angiotensin II (AII) and phenylephrine (PHE) was measured before and after 5 days of ACTH (1 mg i.m. daily) in six normal men maintained on low sodium diet (15 mmol daily).2. ACTH caused a significant increase in systolic blood pressure of 9 mmHg.3. There was no change in pressor responsiveness to AII with ACTH.4. ACTH increased pressor responsiveness to PHE for both systolic and diastolic blood pressure, with a fall in the threshold for response from 0.9 to 0.6 μg/kg per min.5. Increased pressor sensitivity to catecholamines during ACTH administration in man is not sodium‐dependent.
THE EFFECTS OF SIMULTANEOUS ATROPINE AND LABETALOL ADMINISTRATION ON CARDIOVASCULAR PARAMETERS DURING ANTICHOLINESTERASE POISONING IN ANAESTHETIZED CAT
Authors: Merican Zainuddin , Mahmud Zahari , Morat Paden , Idid Syed Zahir , Bi Khatiza 
Published: June 2007

SUMMARY1. The effects of atropine administration during anticholinesterase poisoning on heart rate, blood pressure and electrocardiographic changes (ECG) were studied in the cat.2. Administration of atropine intravenously during anticholinesterase poisoning caused a significant increase in heart rate and blood pressure; ECG changes were also seen.3. The simultaneous intravenous administration of atropine and labetalol during anticholinesterase poisoning abolished the increase in blood pressure and heart rate; ECG readings remained normal.4. It is suggested that labetalol may be a useful adjuvant in the treatment of anticholinesterase poisoning especially in patients with compromised heart function.
HYPOTENSIVE RESPONSE TO ATRIAL NATRIURETIC FACTOR IN CONSCIOUS RENAL HYPERTENSIVE BEAGLES
Authors: Lee K. C. , Rodzinski J. A. , Bex F. J. , Lappe R. W. , Wendt R. L. 
Published: June 2007

SUMMARY1. The hemodynamic responses to i.v. infusion of 0.3 and 0.6 μg/kg per min of human atrial natriuretic factor (hANF [102–126]) in intact, conscious, one‐kidney, perinephritic, hypertensive beagles were examined and compared with the responses in ganglionic‐blocked dogs.2. Blood pressure and heart rate were not affected but plasma ANF‐like immunoreactivity was increased by as much as 627%.3. After hexamethonium (20 mg/kg, i.v.) blockade, a dose‐dependent hypotensive response of up to 29 mmHg with no change in heart rate was observed.4. It is concluded that the compensatory mechanisms of the neurally mediated baroreflex system masked the depressor actions of hANF.
CARDIOVASCULAR RESPONSIVENESS TO ARGININE VASOPRESSIN IN WATER‐LOADED AND SODIUM‐DEPLETED PREGNANT AND NON‐PREGNANT SHEEP
Authors: Wintour E. Marelyn , Coghlan John P. , Congiu Mario , Grim Clarence E. , Laurence Brenda M. , Meehan Peter J. , McDougall John G. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. In conscious ewes pregnancy was associated with a significantly increased heart rate and cardiac output, while mean arterial pressure (MAP) and stroke volume were unchanged.2. The present study examines the effect of arginine vasopressin (AVP) infused at 0.3, 1, 3.0, and 10 μg/h, into water‐loaded and sodium‐depleted ewes, either non‐pregnant or during the last third of gestation.3. In the water‐loaded state, MAP rose significantly at the lowest rate of infusion in both pregnant and non‐pregnant ewes. Bradycardia occurred first at 0.3 μg/h in the pregnant ewes but not until 3.0 μg/h in the non‐pregnant animals.4. In sodium deficiency there was no increase in MAP at any rate of infusion in either group. Bradycardia occurred in both groups at 1 μg/h.5. This study shows that the pressor effects of AVP are unchanged by pregnancy. However, pregnant ewes are more sensitive to AVP‐induced bradycardia when the ewes are water‐loaded.
MODIFICATION BY DILTIAZEM, A CALCIUM ANTAGONIST, OF THE PULMONARY VAGAL AND CARDIAC SYMPATHETIC CHEMOREFLEXES IN THE DOG
Authors: Staszewska‐Woolley Janina 
Published: June 2007

SUMMARY1. Experiments were performed on anaesthetized, open‐chest dogs to determine the effects of diltiazem on: the pulmonary vagal chemoreflex evoked by intravenous (i.v.) injection of capsaicin; cardiac sympathetic chemoreflexes activated by epicardial application of bradykinin or capsaicin; and baroreflex‐mediated changes in heart rate resulting from both pressor and depressor effects produced by i.v. injections of noradrenaline and bradykinin, respectively.2. Diltiazem infused i.v. at a rate of 10–30 μg/kg per min (mean cumulative dose 0.53 ± 0.05 mg/kg, n= 9), did not affect basal heart rate, despite significant (P<0.001) reduction of resting blood pressure.3. Diltiazem treatment did not affect the pressor responses to i.v. noradrenaline (0.3 μg/kg) or the hypotensive effects of i.v. bradykinin (0.3 μg/kg), but reduced significantly both the baroreflex‐mediated bradycardia (P<0.01) and tachycardia (P<0.05) occurring with noradrenaline and bradykinin, respectively.4. In contrast, diltiazem greatly enhanced reflex bradycardia (P<0.001) and systemic hypotension (P<0.01) resulting from activation of the afferent vagal pulmonary receptors by i.v. capsaicin (3–5 μg/kg).5. Reflex pressor responses evoked by activation of the afferent cardiac sympathetic neurons by epicardial application of bradykinin (1 μg) or capsaicin (10–20 μg) were not affected by diltiazem, but the corresponding reflex increases in heart rate evoked by both substances were significantly (P<0.01) reduced.6. The results indicate that diltiazem, while reducing the influence of sinoaortic baroreceptors on heart rate, facilitates the reflex vagal control of the cardiac pacemaker by the afferent cardiopulmonary vagal receptors. These nervous reflex mechanisms, which include attenuation of positive chronotrophic effects that may result from ischaemia‐induced activation of the afferent cardiac sympathetic neurons, may play an important role in the protective action of diltiazem in ischaemic heart disease.
THE EFFECTS OF HIGH Na AND Cl CONCENTRATIONS ON RAT PROXIMAL VOLUME AND Na FLUXES AT ZERO TUBULAR FLOW
Authors: Gyory A. Z. , Ng J. , McNeil D. 
Published: June 2007

SUMMARY1. In vivo micropuncture techniques, with and without peritubular capillary perfusion, were used to study the effects of high extracellular Na and Cl concentrations on transepithelial volume (Jv) and sodium (JNa) fluxes in rat proximal tubules.2. In a double blind manner, the shrinking drop technique of Gertz was used to measure Jv; JNa was calculated from this and the tubular fluid Na concentration.3. At both 184 and 279 mmol/l pericellular Na concentrations (both inside and outside the tubular epithelium), net Jv decreased significantly by 15 and 64%, respectively. Net JNa remained constant at 184 but decreased by 29% at 279 mmol/l Na concentration.4. Thus, at both Na concentrations, when translated to free flow conditions, fractional Na reabsorption must have decreased. These findings, also supported by previous results at these Na concentrations, indicate that active Na transport was inhibited by high pericellular Na concentrations.5. When intratubular Cl concentration was varied between 108 and 138 mmol/l while peritubular Cl was maintained constant (blood perfusing the capillaries), neither Jv nor JNa changed. Thus, at zero tubular flow, differential Cl/HCO3 concentrations do not provide significant driving forces for net Jv or JNa.6. When only intratubular but not peritubular Na was elevated to 279 mmol/l, Jv and JNa increased markedly by 50 and 187%, providing evidence that a true solvent drag (solute drag) effect does exist in rat proximal tubules.7. These findings offer a mechanism to explain why Na reabsorption is not increased when the filtered load of Na is increased with an elevation of plasma Na. That is, the high Na, which surrounds the tubular epithelium, inhibits Na and volume flux at the cellular level by mechanisms as yet unknown. The results also showed that differential Cl/HCO3 concentrations made no difference to Na or volume fluxes at zero tubular flow.
FACILITATION OF DRUG ENTRY INTO BRAIN BY OSMOTIC OPENING OF THE BLOOD‐BRAIN BARRIER
Authors: Robinson Peter J. 
Published: June 2007

SUMMARY1. After osmotic opening, the blood‐brain barrier (BBB) has been shown to reclose more rapidly to large than to small neutral, water‐soluble molecules. Quantitative analysis of these data supports the creation of interendothelial pores with radii of about 200 Å through which such molecules pass by both restricted diffusion and bulk flow (with solute drag) from blood to brain.2. The major reduction in BBB permeability from 6 to 35 min following osmotic opening seems to be due to a reduction in bulk flow by a factor of about 10, rather than marked decreases in pore densities or effective pore size. On this basis, quantitative predictions of brain uptake of neutral, water soluble substances are made for various times after osmotic opening of the BBB, as a function of molecular size.3. Implications of these results are discussed for enhancement of uptake of drugs, including enzymes and certain anti‐cancer agents, by the brain.4. The idea of a ‘therapeutic window’ as the period of time, following reversible osmotic opening, during which the permeability of the BBB is enhanced significantly for a particular compound, is introduced. Since the BBB is normally highly impermeable to plasma proteins, the effect of BBB opening on the uptake of highly protein‐bound drugs is discussed briefly.5. The effect of molecular charge on the passage of molecules through interendothelial pores into the brain is also discussed.
THE EFFECT OF CAPTOPRIL OR ENALAPRILIC ACID ON THE Na APPETITE OF Na‐DEPLETE RATS
Authors: Weisinger R. S. , Denton D. A. , Nicolantonio R. Di , McKinley M. J. 
Published: June 2007

SUMMARY1. The converting enzyme inhibitors, captopril (SQ14 225, Squibb) or enalaprilic acid (MK 422, Merck Sharp and Dohme), were used to evaluate the role of angiotensin II in sodium (Na) appetite of Na‐deplete rats given a choice of water and 0.5 mol/1 NaCl to drink. Also, the effect of these drugs on taste was evaluated in water‐deprived Na‐replete rats and in Na‐deplete rats given a choice of NaCl, sucrose and water.2. Intraperitoneal (i.p.) injection of furosemide (20 mg/kg) increased urinary Na loss by 1.3–1.4 mmol and subsequent Na intake by 1.5–1.8 mmol. This increase in Na intake was abolished by a high dose of captopril (50 mg/kg, i.p.) or enalaprilic acid (80 mg/kg, i.p.), but was enhanced by a low dose of captopril (50 μg/kg, i.p.).3. There was no clear evidence that either captopril or enalapril affected taste for NaCl, sucrose or water in water‐deprived Na‐replete rats. However, the high dose of captopril or enalapril decreased the intake of NaCl and sucrose in Na‐deplete rats.4. Thus, while the results are consistent with the possibility that angiotensin II is involved in Na appetite induced by Na depletion and that the difference between the high and low doses of converting enzyme inhibitors on Na appetite may be related to their relative effectiveness in blocking angiotensin I conversion at central sites, the observation that sucrose intake is decreased by high dose converting enzyme inhibitor in Na‐deplete rats suggests that other actions of the converting enzyme inhibitors may be involved.
STUDIES ON THE SPECIFICITY OF THE INHIBITORY ACTION OF N,N‐DIISOPROPYL‐N'‐ISOAMYL‐N'‐DIETHYLAMINOETHYLUREA (P‐286) ON ADRENAL CATECHOLAMINE RELEASE IN THE ANAESTHETIZED RAT
Authors: Malta Errol , Angus James A. 
Published: June 2007

b1. The ability of P‐286 (N,N‐diisopropyl‐N'‐isoamyl‐N'‐diethylaminoethylurea) to reduce selectively the release of catecholamines from the adrenal medulla has been studied in urethane‐anaesthetized rats.2. Pressor responses to acetylcholine (Ach) and the nicotinic receptor‐agonist 1,4‐dimethylphenylpiperazine (DMPP) in rats treated with atropine, (±)‐propranolol and guanethidine were used as the index of adrenal catecholamine release.3. The injection of P‐286 (1–10 mg/kg, i.v.) elicited a dose‐dependent bradycardia which was associated with hypotension. P‐286 reduced pressor responses to Ach and DMPP in a dose‐dependent manner with an IC50 of 2.5 mg/kg and, following near complete blockade, pressor responses to DMPP returned to 50% of control after 90 min.4. In non‐atropinized rats, P‐286 (30 mg/kg, i.v.) was without effect on the bradycardic responses elicited by stimulation of the right vagus nerve at frequencies of 5–40 Hz while pressor responses to DMPP in bilaterally adrenalectomized, non‐guanethidine treated rats were reduced by approximately 50% after P‐286 (10 mg/kg, i.v.).5. The latter effect of P‐286 on responses to DMPP in adrenalectomized rats cannot be attributed to ganglionic blockade since in rats with intact adrenals P‐286 (10 mg/kg, i.v.) also reduced pressor responses to i.v. adrenaline and i.v. angiotensin II by approximately 50%. Thus the reduction in response to DMPP in adrenalectomized rats and to the non‐nicotinic agonists may be a reflection of an action on the mechanism of contraction of vascular smooth muscle; that is, at a post‐receptor event.6. The results of the study show that P‐286 selectively reduces adrenal catecholamine release at doses which do not affect autonomic ganglia. Its usefulness as a tool in cardiovascular research, however, may be limited by an action of vascular smooth muscle.
RESISTANCE OF SYMPATHETIC CARDIAC NERVE FUNCTION IN THE PITHED RAT TO PREJUNCTIONAL EFFECTS OF ANGIOTENSIN II
Authors: Rechtman M. P. , King R. G. , Boura A. L. A. 
Published: June 2007

SUMMARY1. The spinal sympathetic outflow (C7‐T2) of pithed male Wistar rats was electrically stimulated (30–50 V, 0.5 ms, 0.1–1.0 Hz) and heart rate and arterial blood pressure were recorded. d‐Tubocurarine (1 mg/kg) and atropine (1 mg/kg) were administered intravenously (i.v.) to reduce voluntary and parasympathetic nerve activity.2. Angiotensin II (0.39–3.4 μg/kg per min) was infused at a rate which caused a sustained rise in diastolic blood pressure of at least 25 mmHg but which did not alter basal heart rate.3. Chronotropic responses to sympathetic nerve stimulation were not affected by infusion of angiotensin II, and were also unaltered by pretreatment of rats with indomethacin (5 mg/kg, i.v.) 10 min prior to commencement of stimulation.4. These results suggest that positive chronotropic responses to cardiac sympathetic nerve stimulation in pithed rats are not affected by increased angiotensin II levels. Indomethacin had no effect, which indicates that cyclo‐oxygenase products were not involved in modulation of chronotropic responses to cardiac sympathetic nerve stimulation.