bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE STUDY OF TACHYKININ RECEPTORS
Authors: Burcher Elizabeth 
Published: June 2007

SUMMARY1. Three high affinity receptors (NK1, NK2 and NK3) recognizing the C‐terminal end of tachykinins have been described, with probable endogenous ligands substance P (SP‐), neurokinin A and neurokinin B, respectively.2. Other receptors recognizing the N‐terminal regions of SP exist in adrenal medulla and central nervous system (CNS) with a low affinity receptor on mast cells.3. NK1 receptors are associated with blood vessels, all types of smooth muscle, enteric ganglia and glands. NK2 receptors are found on gastrointestinal and urinary smooth muscle, but few peripheral NK3 receptors have been described. In contrast, NK1, NK3 but not NK2 receptors are widely distributed in the CNS.4. Problems associated with the study of tachykinin receptors include low selectivity of endogenous tachykinins, poor antagonists and susceptibility of peptides to enzymatic degradation.
RECEPTOR ALKYLATING AGENTS: NOVEL TOOLS FOR THE STUDY OF RECEPTOR FUNCTION IN THE CENTRAL NERVOUS SYSTEM OF THE RAT
Authors: Crocker Ann D. , Cameron Donald L. 
Published: June 2007

SUMMARY1. The use of alkylating agents to investigate receptor function in the central nervous system is discussed.2. Examples of strategies which can be used are illustrated by studies with the irreversible dopamine receptor blocker, N‐ethoxycarbonyl‐2‐ethoxy‐1,2‐dihydro‐quinoline (EEDQ).3. Recent work, in which EEDQ was injected into selected sites of the striatum and receptor loss assessed by quantitative autoradiography, is described to show how this approach can be used to elucidate dopamine receptor function in the striatum.
NEW TOOLS FOR THE LOCALIZATION OF SECOND MESSENGER SYSTEMS
Authors: Summers Roger J. , McMartin Lynne R. 
Published: June 2007

SUMMARY1. Probes available for the localization of components of second messenger systems include G‐protein oligonucleotides which have been used to produce cDNA probes to label G‐protein mRNA by in situ hybridization histochemistry.2. Enzymes involved in second messenger responses have been labelled with [3H]‐forskolin (Gs‐linked adenylate cyclase), [3H]‐cAMP (cAMP‐dependent protein kinase) and [3H]‐PDBu2 (protein kinase C).3. [3H]‐Inositol 1,4,5 trisphosphate labels a site on sarcoplasmic reticulum believed to trigger Ca2+ release.4. These probes allow the comparison of location of receptors and second messengers and the examination of changes in second messenger systems with drug treatment and disease.
PROGESTERONE ANTAGONIZES DEVELOPMENT BUT NOT MAINTENANCE OF ACTH‐INDUCED HYPERTENSION IN SHEEP
Authors: Spence Campbell D. , Reid Amanda F. , Coghlan John P. , Mills Eric H. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. This study investigated the effect of progesterone, which, under certain circumstances, can antagonize both the mineralocorticoid and glucocorticoid activities of steroid hormones, on the development and maintenance of adrenocorticotrophic hormone (ACTH)‐induced hypertension in conscious sheep.2. Progesterone (500 mg/day) alone, for 5 days, had no effect on blood pressure, but increased urinary Na excretion by 38 ± 10 mmol/day (P < 0.05) during the first 24 h.3. Infusion of ACTH (5 μg/kg per day), alone, for 3 days, increased mean arterial pressure by 21 ± 2 mmHg (P < 0.001) associated with hypernatraemia, hypokalaemia, urinary Na retention, and increased fasting plasma glucose concentration.4. Progesterone (500 mg/day) concurrently with ACTH blocked the rise in mean arterial pressure and the mineralocorticoid (urinary Na retention) but not the glucocorticoid (increase in plasma glucose concentration) effects associated with ACTH administration.5. Progesterone (500 and 1000 mg/day) failed to reverse the hypertension and hypokalaemia in sheep pretreated for 3 days with ACTH.6. Thus, progesterone blocked the onset but did not affect established ACTH hypertension. The mechanism by which progesterone blocked the development of ACTH hypertension appears to be related to the ability of progesterone to block the essential mineralocorticoid component of the adrenocortical steroids involved in the development of ACTH hypertension.
EFFECTS OF SODIUM RESTRICTION ON CARDIAC 3,4‐DIHYDROXYPHENYLETHYLENE GLYCOL AND CATECHOLAMINE LEVELS IN RATS
Authors: Howes L. G. , Hodsman G. P. 
Published: June 2007

SUMMARY1. The effects of low or high sodium intake for 4 weeks on cardiac catecholamines and 3,4‐dihydroxyphenylethylene glycol (DHPG) levels were studied in adult female Wistar rats.2. Rats receiving the low sodium diet had significantly higher plasma renin activity than rats receiving the high sodium diet.3. Dopamine concentrations in both the right and left ventricle were significantly higher in the low salt compared with the high salt rats, but noradrenaline, adrenaline and DHPG levels did not differ significantly between the two groups.4. These data do not support previous reports that sodium restriction reduces cardiac noradrenaline release, but suggest that alterations in sodium intake may influence cardiac noradrenaline metabolism.
EFFECT OF MAGNESIUM DEPLETION AND POTASSIUM DEPLETION AND CHLOROTHIAZIDE ON INTRACELLULAR pH IN THE RAT, STUDIED BY 31P NMR
Authors: Adam W. R. , Craik D. J. , Kneen M. , Wellard R. M. 
Published: June 2007

SUMMARY1. Both dietary magnesium depletion and potassium depletion (confirmed by tissue analysis) were induced in rats which were then compared with rats treated with chlorothiazide (250 mg/kg diet) and rats on a control synthetic diet.2. Brain and muscle intracellular pH was measured by using a surface coil and [31P]‐NMR to measure the chemical shift of inorganic phosphate. pH was also measured in isolated perfused hearts from control and magnesium‐deficient rats. Intracellular magnesium status was assessed by measuring the chemical shift of β‐ATP in brain.3. There was no evidence for magnesium deficiency in the chlorothiazide‐treated rats on tissue analysis or on chemical shift of β‐ATP in brain. Both magnesium and potassium deficiency, but not chlorothiazide treatment, were associated with an extracellular alkalosis.4. Magnesium deficiency led to an intracellular alkalosis in brain, muscle and heart. Chlorothiazide treatment led to an alkalosis in brain. Potassium deficiency was associated with a normal intracellular pH in brain and muscle.5. Magnesium depletion and chlorothiazide treatment produce intracellular alkalosis by unknown mechanism(s).
EFFECT OF NISOLDIPINE ON STRESS‐INDUCED MYOCARDIAL DAMAGE IN THE CONSCIOUS PIG
Authors: Herbaczyńska‐Cedro K. , Lewicki Z. , Barcikowski B. , Famulski K. , Gordon‐Majszak W. , Kloś J. , Wutzen J. , Ceremużyński L. 
Published: June 2007

SUMMARY1. The effect of the calcium channel blocker nisoldipine on the myocardial content of lipid peroxidation products (malondialdehyde (MDA), conjugated double bonds (CDB), fluorescent end‐products (RF) and mitochondrial adenine nucleotides) was investigated in conscious pigs (n= 14) subjected to 24 h of immobilization stress. Histoenzymatic and electron microscopic studies of the myocardium were also performed. Nisoldipine was given orally in a twice daily dose of 20 mg for 2 days before and on the day of the experiment. Results were compared with those obtained in immobilized untreated pigs (n= 10) and in non‐stressed treated controls (n= 8).2. Pretreatment with nisoldipine significantly attenuated stress‐induced increase in myocardial contents of CDB and RF and prevented decline of mitochondrial adenine nucleotides. Stress‐induced myocardial histoenzymatic changes (decrease of succinic dehydrogenase, ATPase, acid phosphatase activity) and ultrastructural alterations (mitochondrial damage, lysis of myofibrils, dilatation of sarcoplasmic reticulum and endothelial swelling) were also diminished.3. It is concluded that treatment with a Ca2+‐antagonist is beneficial to the heart exposed to environmental stress.
ACUTE MANNITOL AND SALINE VOLUME EXPANSION IN THE RAT: EFFECT ON TRANSEPITHELIAL POTENTIAL DIFFERENCE IN PROXIMAL TUBULES
Authors: Sugo E. , Györy Á. Z. 
Published: June 2007

SUMMARY1. Transepithelial potential difference (PDte) of proximal tubules was measured in rats under control conditions (C), and mannitol‐saline and saline extracellular fluid volume expansion (MVE, SVE, respectively) under conditions of normal net lumen to basal sodium transport.2. PDte was measured in kidneys bathed with Hartmann's solution or covered with mineral oil under both volume‐expanded conditions together with their controls.3. PDte was significantly lower in kidneys bathed with Hartmann's solution than in those covered with oil.4. In MVE rats, with mineral oil covering the kidneys, PDte (expressed as mean and s.e.m.) was for the control 2.20 ± 0.05 (n= 45) mV and MVE 1.97 ± 0.04 (n= 36) mV, lumen positive, a significant reduction of 10% (P<0.001). In SVE rats, with mineral oil covering the kidneys, PDte was for C = 2.42 ± 0.05 (n= 74) mV and SVE = 1.93 ± 0.03 (n= 67) mV, a significant reduction (P<0.001) of 20%.5. According to thermodynamic considerations, neither of these changes is sufficient to explain the 50% inhibition of Na transport measured previously during MVE and SVE with autologous tubular fluid. The present results offer further evidence supporting the idea that the inhibition of Na transport during MVE and SVE is largely due to inhibition of the active Na transporting step.
BODY GROWTH AND POLYCYTHAEMIA IN HYPOXIC ALBINO RATS OF FIRST AND SECOND GENERATION
Authors: Quatrini U. , Licciardi A. , Morici G. 
Published: June 2007

SUMMARY1. In our study we followed the growth rate and the haematologic changes occurring in albino rats of Wistar strain when living in a hypoxic environment. Two generations of hypoxic rats were observed for changes in their erythrocytes (RBC), haematocrit (Hct) and haemoglobin (Hb): the first generation (H1) and the second generation (H2). A few hours after birth, the H1 rats were placed and raised in a normobaric hypoxic environment (10% O2 in N2). The H2 rats were born and raised in the environment previously described. The control group had a normoxic environment. The H1 and H2 rats had inferior growth rates in respect to their controls, but H2 were found to have a larger growth rate than the H1 group. The RBC, Hct and Hb had values significantly greater for both H1 and H2 when compared with their controls. However, we did find that the values of H2 were significantly lower than H1. We believe that these results are in relation to the degree of development of the adaptive processes to the hypoxic environment of the H2 rats.
CHANGES OF ADP‐RIBOSYLATION OF GTP‐BINDING PROTEIN BY PERTUSSIS TOXIN IN HUMAN PLATELETS DURING LONG‐TERM TREATMENT OF MANIC DEPRESSION WITH LITHIUM CARBONATE
Authors: Watanabe Y. , Morita H. , Imaizumi T. , Takeda M. , Hariguchi S. , Nishimura T. , Yoshida H. 
Published: June 2007

SUMMARY1. The study was done to determine whether long‐term treatment with lithium carbonate affected the guanosine triphosphate (GTP)‐binding protein in platelet membranes from patients with manic depression.2. It was found that adenosine diphosphate (ADP)‐ribosylation of inhibitory G‐proteins (40–41 kDa) by pertussis toxin, islet‐activating protein in the cell membranes increased about 45% when long‐term treatment with lithium carbonate was stopped.3. These results support the idea that one site for the therapeutic effects of lithium ions is G‐proteins.
EFFECT OF ETHAMSYLATE ON CARRAGEENAN‐INDUCED RAT PAW OEDEMA: A COMPARISON WITH INDOMETHACIN
Authors: Gard P. R. , Trigger D. J. 
Published: June 2007

SUMMARY1. Ethamsylate (diethylammonium 2,5‐dihydroxybenzene sulfonate, DicyneneTM), a systemic haemostatic agent with an unknown mechanism of action, was tested for anti‐inflammatory activity using the carrageenan‐induced rat paw oedema test.2. Ethamsylate was shown to be an effective anti‐inflammatory agent with a time course and amplitude of effect similar to that of indomethacin, although the potency was only about 4% of that for indomethacin.3. When ethamsylate and indomethacin were co‐administered they did not show additive effects, suggesting that they do not share a common mode of action. It is proposed that ethamsylate, like indomethacin, may inhibit prostaglandin synthesis.
NICOTINIC AGONIST MODULATION OF FELINE BRONCHOMOTOR TONE
Authors: Thompson David C. , Altiere Ralph J. , Diamond Louis 
Published: June 2007

SUMMARY1. The bronchomotor actions of three nicotinic cholinoceptor agonists were investigated in anaesthetized, mechanically ventilated cats. The agonists were administered intravenously after increasing baseline airways smooth muscle tone with an infusion of 5‐hydroxytryptamine.2. Acetylcholine induced a biphasic change in lung resistance, characterized by initial bronchoconstriction followed by bronchodilation. The specific nicotinic cholinoceptor agonists, nicotine and dimethylphenylpiperazinium (DMPP), principally induced bronchodilator responses, although initial bronchoconstrictor phases were observed occasionally.3. All bronchoconstrictor phases were sensitive to muscarinic cholinoceptor block‐ age with atropine. DMPP‐induced bronchodilator responses were adrenergic in nature, whereas those induced by either nicotine or acetylcholine resulted from a combination of adrenergic and non‐adrenergic influences.4. It is concluded that intravenously administered nicotinic cholinoceptor agonists exert varying actions on feline bronchomotor tone and that these actions result from activation of different autonomic inputs.
RAT DUODENAL SMOOTH MUSCLE CONTRACTILE RESPONSES TO ANGIOTENSIN II ARE DEPENDENT ON CALMODULIN
Authors: Weekley L. Bruce 
Published: June 2007

SUMMARY1. Isolated duodenal segments were pretreated with either of the calmodulin inhibitors proadifien or trifluoroperazine and the subsequent contractile force and frequency response to angiotensin II monitored.2. Both proadifien and trifluoroperazine decreased the spontaneous contractile force and frequency in isolated perfused duodenal segments and attenuated the force generation following exposure to angiotensin II. Proadifien and trifluoroperazine also altered the qualitative behaviour of duodenal segments.3. These results suggest that the action of angiotensin II on duodenal smooth muscle motility is dependent on calmodulin. Furthermore, the change in qualitative behaviour of duodenal segments following treatment with calmodulin inhibitors suggest that the function of intrinsic intestinal neurons is also altered.
CHANGES IN SALINE AND WATER INTAKES IN BROMOCRIPTINE‐TREATED GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Tan B. K. H. , Hutchinson J. S. 
Published: June 2007

SUMMARY1. We have previously reported on the effects of a 13‐day intraperitoneal infusion of bromocriptine delivered by osmotic pump on blood pressure, plasma and pituitary PRL levels in genetically hypertensive (GH) rats and their normotensive (NT) controls. This paper reports further on that study in describing the changes in saline and water intakes in rats as a result of bromocriptine (BRC) treatment.2. In the GH rats, bromocriptine did not have any significant effect on saline or water intake.3. In the NT rats, bromocriptine significantly decreased saline intake and increased water intake.4. The saline intake in the vehicle‐treated GH rats was significantly lower than that in the vehicle‐treated NT rats while the water intake was not significantly different.5. These results indicate that differences exist between the GH and NT rats with regard to their saline and water intakes and their responses to chronic bromocriptine treatment. The changes in saline and water intakes in the GH rats seem to be different from those seen in the spontaneously hypertensive rat in another study.
SOME ALDOSTERONE‐PRODUCING ADRENAL TUMOURS ALSO SECRETE CORTISOL, BUT PRESENT CLINICALLY AS PRIMARY ALDOSTERONISM
Authors: Tunny Terry J. , Klemm Shelley A. , Gordon Richard D. 
Published: June 2007

SUMMARY1. Two patients with angiotensin‐responsive aldosterone‐producing adenoma (APA) and one with adrenal cortical carcinoma demonstrated autonomous secretion of cortisol as well as of aldosterone.2. The response of cortisol and of aldosterone to ACTH did not differentiate between the two APA which secreted cortisol and the eight which demonstrated normal suppression with dexamethasone.3. Concurrent autonomous secretion of cortisol as well as aldosterone may occur in patients who present clinically with primary aldosteronism.4. Biochemical distinctions between adenomas may reflect differences in their cellular composition.
NALOXONE‐INDUCED ACTH RELEASE IN MAN IS INHIBITED BY CLONIDINE
Authors: Jackson Richard V. , Grice Jeffrey E. , Jackson A. Jane , Hockings Gregory I. 
Published: June 2007

SUMMARY1. Adrenergic mechanisms play an important role in regulation of ACTH release. We used the α2‐adrenergic agonist, clonidine, as a central nervous system inhibitor of ACTH release to see if it would alter naloxone‐induced ACTH secretion in normal human volunteers.2. There was a significant blunting of the mean peak level of ACTH and the mean peak change of ACTH from basal as well as the area under the ACTH‐time curve when clonidine was given prior to naloxone.3. We conclude that clonidine, by blocking central noradrenergic pathways, which stimulate corticotropin‐releasing hormone secretion, inhibits naloxone‐induced ACTH secretion. This suggests that naloxone causes ACTH release through these same central noradrenergic pathways.
HYPOTHESIS: ISCHAEMIC PLAQUE NECROSIS AS THE INITIATOR OF UNSTABLE ANGINA/ACUTE MYOCARDIAL INFARCTION?
Authors: Boyd G. W. 
Published: June 2007

SUMMARY1. Coronary atherosclerotic plaque complications are important in precipitating acute coronary events such as unstable angina and myocardial infarction.2. The hypothesis is put forward that plaque complications are initiated by increases in local coronary artery tone sufficient to cut off the vasa vasorum blood supply to the plaque and result in its ischaemic necrosis.
PREVENTION OF ARTERIAL DISEASE IN EXPERIMENTAL RENAL HYPERTENSION
Authors: Yong A. C. , Boyd G. W. 
Published: June 2007

XUMMARY1. This study examined the effect of various antihypertensive agents on the development of polyarteritis nodosa lesions along the mesenteric artery system over a 10 week period after renal artery clipping in uninephrectomized rats (lKlC).2. Of the agents, only hydralazine, enalapril and diltiazem significantly inhibited systolic blood pressure (SBP) rise over the 10 week period (P<0.001).3. All agents except hydralazine reduced the severity of arteritic lesions compared with lKlC rats, but only with enalapril (P<0.001), nifedipine (P<0.001), diltiazem (P<0.005), propranolol (P<0.001) and reserpine (P<0.05) was this reduction statistically significant.4. There was a positive correlation between the degree of arteritic change and SBP, but the correlation coefficient was neither high (r= 0.68) nor highly significant (P= 0.03, d.f. = 9). On examining the data, this was due on the one hand to nifedipine, propranolol and reserpine reducing the severity of lesions without significantly inhibiting SBP, and on the other to hydralazine reducing SBP without significantly affecting the extent of arteritic change.5. These findings suggest that factors other than mere SBP alone are involved in the pathogenesis of these arteritic lesions.
CARDIOVASCULAR EFFECTS OF NICOTINE DURING PHYSICAL ACTIVITY AND FOLLOWING MEAL CONSUMPTION
Authors: Perkins Kenneth A. , Epstein Leonard H. , Stiller Richard L. , Sexton Joan E. , Marks Bonita L. , Jacob Rolf G. 
Published: June 2007

SUMMARY1. In two separate studies using healthy male smokers as subjects, the acute cardiovascular effects of a measured dose of nicotine (15 μg/kg) were examined in conjunction with light physical activity and following consumption of a meal, conditions typical of nicotine intake via smoking.2. Increases in heart rate and systolic blood pressure attributable to nicotine were similar during rest, physical activity, and following eating, demonstrating additivity with the cardiovascular effects of activity and a caloric load. Diastolic blood pressure was less affected by nicotine.3. These results indicate that cardiovascular activity is acutely increased following nicotine (smoking) regardless of other influences on the cardiovascular system. Such effects may help explain increased risks of acute cardiac abnormalities due to smoking.
RELAXATION OF MESENTERIC ARTERY OF STROKE PRONE SPONTANEOUSLY HYPERTENSIVE RATS BY CALCIUM REMOVAL
Authors: Sunano S. , Shimada T. , Moriyama K. , Shimamura K. 
Published: June 2007

ABSTRACT1. The time courses of the relaxation, induced by removal of extracellular Ca2+, of K‐depolarized mesenteric artery preparations from stroke prone spontaneously hypertensive rats (SHRSP) and Wistar‐Kyoto rats (WKY) were compared.2. The time course of the decline in extracellular Ca2+ was estimated from the time course of the relaxation and the concentration‐response curve of K+‐depolarized preparations to Ca2+. The time course of the decline in the intracellular free Ca2+ concentration was also estimated from the reported relation between Ca2+ concentration and the contraction of skinned vascular smooth muscle.3. The time course of relaxation was exponential, the curve being made up of three components. The time course was slower in preparations from SHRSP, especially the first component of the relaxation curve.4. The time courses of the decline in the intracellular and extracellular Ca2+ concentrations were also exponential, being made up of three components and were also slower in the preparation made from SHRSP.5. The wall and muscle layer of the mesenteric arteries used in the present experiments were significantly thicker in the SHRSP preparations.6. Calculation of the half relaxation time, based on the diffusion of Ca2+ across the blood vessel wall, suggested that the slower relaxation in preparations from SHRSP is due largely to the thicker muscle layer, although differences in Ca2+ sequestration by the smooth muscle cells may also be involved.
THE EFFECT OF INHALED FENOTEROL AND IPRATROPIUM BROMIDE ON PROPRANOLOL INDUCED BRONCHOCONSTRICTION IN THE ASTHMATIC AIRWAYS
Authors: Latimer K. M. , Ruffin R. E. 
Published: June 2007

SUMMARY1. The provocative dose of inhaled propranolol, (PC20P, mg/mL) needed to induce a 20% reduction in the forced expired volume in 1 s (FEV1, L) was determined for 15 adult asthmatics following randomized pre‐treatment with placebo, ipratropium bromide (40, 160 μg) and fenoterol (200, 800 μg) aerosols using a double‐blind protocol.2. Fenoterol 200 μg, 800 μg increased the baseline FEV1 0.28±0.16, 0.32±0.16 L (P= 0.04, P= 0.008 respectively). Fenoterol 800 μg moved the PC20P rightwards from placebo geometric mean 10.95, 95% Confidence Intervals (95% CI) 4.43–27.22 mg/mL to mean 20.41, 95% CI 10.13 to 40.64 mg/mL (P= 0.01). Fenoterol 200 μg was not protective; mean PC20 16.22, 95% CI 7.83–34.35 mg/mL (P= 0.08). Neither 40 or 160 μg ipratropium changed the FEV1 or PC20P values compared with placebo; increase in FEV1 0.15±0.27 L (P= 0.22), 0.24±0.12 L (P= 0.14) and geometric mean PC20P 16.59±0.57 mg/mL 95% CI 8.01–34.51 mg/mL (P= 0.90), 15.48±0.66 mg/mL, 95% CI 6.72–36.05 mg/mL (P= 0.34) respectively after ipratropium treatments.3. Bronchoconstriction induced by inhaled propranolol (P) appears to be only weakly antagonized by inhaled β‐agonist and not reduced by antimuscarinic anticholinergic aerosol. This finding argues against the activation of a cholinergic reflex to explain propranolol induced bronchoconstriction (PIB).