bluuebunny/crossref_metadata_2025_split huggingface dataset:
FOREBRAIN PATHWAYS MEDIATING STRESS‐INDUCED RENIN SECRETION
Authors: Van de Kar Louis D. 
Published: June 2007

SUMMARY1. All stressors tested so far increase plasma renin levels; among these are exposure to foot‐shock, immobilization, forced swimming, head‐up tilt, exercise, hypotension haemorrhage and conditioned fear.2. In old rats (22 months old), conditioned fear stress fails to increase plasma renin concentrations to the same level as in young rats (7 months old).3. Destruction of cells in the paraventricular hypothalamic nucleus (PVH), either electrolytically or with the cell‐selective neurotoxin ibotenic acid, prevents the effect of conditioned fear stress, but not of immobilization, on plasma renin concentration.4. Ibotenic acid‐induced lesions in the central amygdaloid nucleus inhibit conditioned fear stress‐induced increases in plasma renin concentrations, but do not reduce the renin response to immobilization. Lesions in lateral amygdaloid nuclei do not reduce the renin response to stressors.5. Although lesions in the bed nucleus of the stria terminalis (BNST) reduce the adrenocortical response to conditioned fear stress, they do not reduce the effect of stress on plasma renin concentration.6. Destruction of catecholaminergic terminals in the PVH prevents the effect of conditioned fear stress on plasma renin concentration.7. Electrolytic lesions in the dorsal raphe nucleus, which is a major site of origin of ascending serotonergic pathways, also inhibit the effect of conditioned fear stress on plasma renin concentration.8. Activation of serotonin1A (5HT1A) receptors with the anti‐anxiety drugs buspirone and ipsapirone reduces the firing rate of serotonergic neurons in the dorsal raphe nucleus in the midbrain and decreases the effect of stress on plasma renin concentrations. In contrast, the benzodiazepine anxiolytic drugs, chlordiazepoxide and midazolam, are ineffective in inhibiting the renin response to stress.9. Chemical sympathectomy combined with adrenal medullectomy does not prevent the effect of conditioned fear stress on plasma renin concentration, suggesting that the sympathetic system is not the sole mediator of the message from the brain to the kidneys.10. Combined, these observations suggest that aversive information from the cortex is transmitted via the amygdala to catecholaminergic cells in the medulla and to serotonergic cells in the dorsal raphe that stimulate the PVH to increase the release of renin.
INTEGRATIVE ROLE OF THE LAMINA TERMINALIS IN THE REGULATION OF CARDIOVASCULAR AND BODY FLUID HOMEOSTASIS
Authors: Johnson Alan Kim , Cunningham J Thomas , Thunhorst Robert L. 
Published: June 2007

SUMMARY1. Cardiovascular and body fluid homeostasis depends upon the activation and co‐ordination of reflexes and behavioural responses. In order to accomplish this, the brain receives and processes both neural and chemical input. Once in the brain, information from sources signalling the status of the cardiovascular system and body fluid balance travels, and is integrated, throughout a widely distributed neural network. Recent studies using neuroanatomical and functional techniques have identified several key areas within this neural network. One major processing node is comprised of structures located along the lamina terminalis.2. Structures associated with the lamina terminalis include the median preoptic nucleus (MePO) and two sensory circumventricular organs (SCVO), the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Current evidence indicates that blood‐borne signals, such as angiotensin II (AngII), reach SCVO (e.g. SFO) where they are transduced. This information is then carried via neural pathways to brain nuclei (e.g. MePO) where it is integrated with other inputs, such as those derived from systemic arterial blood pressure and volume receptors.3. Because of their receptive and integrative functions, lamina terminalis structures are essential for the normal control of hormone release (e.g. vasopressin), sympathetic activation and behaviours (thirst and salt appetite), which collectively contribute to maintenance of cardiovascular and body fluid homeostasis.
CARDIOVASCULAR EFFECTS OF ORAL HYPOGLYCAEMIC DRUGS
Authors: Howes Laurence Guy , Sundaresan Purnima , Lykos Denise 
Published: June 2007

SUMMARY1. There is increasing evidence that sulfonylurea and biguanide oral hypoglycaemic drugs have cardiovascular effects and influence risk factors for cardiovascular disease in patients with non‐insulin‐dependent diabetes because of actions that are unrelated to alterations in glycaemic control.2. While sulfonylureas may have anti‐arrhythmic effects following myocardial ischaemia, there is concern that their action on vascular ATP‐sensitive potassium channels may contribute to elevated blood pressure and enhanced vascular responsiveness.3. In contrast to sulfonylureas, metformin (a biguanide) appears to reduce blood pressure and have beneficial effects on plasma lipoproteins by reducing low‐density lipoprotein cholesterol and possibly increasing high‐density lipoprotein cholesterol levels.4. The pharmacological basis and clinical significance of these effects of sulfonylureas and biguanides require further investigation.
EFFECTS OF CELERY EXTRACT AND 3‐N‐BUTYLPHTHALIDE ON LIPID LEVELS IN GENETICALLY HYPERCHOLESTEROLAEMIC (RICO) RATS
Authors: Tsi D. , Tan BKH 
Published: June 2007

SUMMARY1. Aqueous celery extract was administered intraperitoneally to genetically hypercholesterolaemic (RICO) and normochol‐esterolaemic (RAIF) rats via Alzet osmotic pumps over a 13 day period.2. The serum cholesterol concentration of the celery extract‐treated RICO rats was found to be significantly lower (P<0.05) than the control rats. Aqueous celery extract was effective in preventing the rise of cholesterol level in the RICO rats. However, no such observation was seen in the RAIF rats. The serum triglyceride level was unchanged in both strains of rats.3. When 3‐n‐butylphthalide (BuPh), a unique component in celery, was administered in the same manner to the RICO and RAIF rats, it did not produce significant changes in the serum and liver lipid profiles of these rats. The activities of hepatic 3‐hydroxy‐3‐methylglutaryl CoA reductase in both strains of rats were also not significantly different from their respective controls.4. Together with our recently reported thin‐layer chroma‐tography findings that BuPh was not detected in the aqueous celery extract, this study suggests that the effect of celery extract on serum cholesterol levels in the RICO rats could be attributed to chemical constituents other than BuPh.
RELATIONSHIP BETWEEN NIFEDIPINE SENSITIVITY OF AORTAE AND BLOOD PRESSURE OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Jiang Guang‐Chi , Iwanov Victor , Moulds Robert FW 
Published: June 2007

SUMMARY1. We have previously described an increased sensitivity to inhibition by nifedipine of noradrenaline‐induced contractures of blood vessels in hypertension. In this study we have investigated whether changes in blood pressure (BP) change the sensitivity to nifedipine and K+ of aortic rings from normotensive (Wistar‐Kyoto rats, WKY) and stroke‐prone spontaneously hypertensive rats (SHRSP).2. SHRSP were treated with: hydralazine plus hydrochloro‐thiazide; captopril plus hydrochlorothiazide; hydralazine plus guanethidine; or captopril alone. WKY rats were treated with deoxycorticosterone acetate (DOCA) and NaCl. Treatment commenced from 5 weeks of age and continued until 13–15 weeks.3. The SHRSP treatments produced similar reductions in BP, and the BP of all the treated groups were significantly lower than the mean BP of untreated SHRSP (201.0 ± 7.7 mmHg). The mean BP of the treated WKY rats (134.2 ± 7.6 mmHg) was significantly higher than the mean BP of the untreated WKY rats (86.8 ± 7.4 mmHg).4. An area‐under‐curve (AUC) analysis of the inhibitory effects of nifedipine on responses of aortae to noradrenaline showed no differences between treated and untreated SHRSP groups (overall mean 40.6 ± 1.9% and 43.4 ± 3.4% inhibition of control AUC, respectively), or between DOCA‐salt treated WKY and untreated WKY groups (58.8 ± 5.9 and 64.8 ± 2.3, respectively). Noradrenaline‐induced contractures of aortae from all SHRSP groups were significantly more sensitive to inhibition by nifedipine than aortae from both WKY groups.5. The molar concentration of agonist required to evoke 50% of the maximum response (EC50) values for potassium chloride (KCI) were significantly increased in the aortae of all treated SHRSP groups in comparison to those from untreated SHRSP (treated SHRSP groups, 15.53 ± 0.68 mmol/L vs untreated SHRSP group, 11.36 ± 1.10 mmol/L). The EC50 values for KC1 for the aortae from the DOCA‐treated WKY rats were significantly less than those from aortae of the untreated WKY (11.80 ± 0.80 and 17.08 ± 1.50 mmol/L, respectively).6. We conclude that reduction (in SHRSP) or increase (in WKY) of the BP has no effect on the sensitivity of aortic smooth muscle to the inhibitory effects of nifedipine on responses to noradrenaline, suggesting that alterations in voltage‐dependent Ca2+ mechanisms may be a primary phenomenon in the SHRSP. In contrast, the fact that sensitivity to KC1 changes in the treated SHRSP and WKY aortae suggests such sensitivity is secondary to the BP and thus a separate phenomenon from voltage‐dependent Ca2+ mechanisms.
GENDER DIFFERENCES IN RESPONSE TO ENDOTHELIN‐1 IN CORONARY ARTERIES: TRANSCRIPTION, RECEPTORS AND CALCIUM REGULATION
Authors: Miller Virginia M. , Barber Dustan A. , Fenton Alexis M. , Wang Xiaofang , Sieck Gary C. 
Published: June 2007

SUMMARY1. Experiments were designed to determine how sex hormonal status may influence production and response to endothelins.2. Circulating concentrations of endothelin‐1 were not different between sexually mature male and female pigs and did not differ between females of low‐ and high‐oestrogen status.3. Expression of messenger RNA for preproendothelin was not different in aortic endothelial cells derived from sexually mature male and female pigs.4. Endothelin‐1, endothelin‐3 and sarafotoxin S6c caused concentration‐dependent contractions of rings of coronary arteries suspended for the measurement of isometric force. Only in response to endothelin‐1 were contractions greater in arteries from female than in male pigs. This difference was not related to oestrogen levels in females.5. The intrinsic force‐calcium relationship defined in smooth muscle cells permeabilized with either triton‐X or β‐escine was not different in coronary arteries from male and female pigs. The calcium sensitivity was increased to the same extent by endothelin‐1 in smooth muscle from male and female pigs.6. Competitive inhibition of radiolabelled endothelin‐1 by unlabelled endothelin‐1 was not different in membranes prepared from coronary arteries from male and female pigs. However, competitive inhibition of radiolabelled endothelin‐1 by unlabelled endothelin‐3 showed two binding sites. The affinity of the high affinity binding site was increased only in females with high oestrogen levels.7. These results suggest that there are gender differences in contractions of porcine coronary arteries to endothelin‐1. These differences may not relate to transcriptional regulation for the production of the peptide in endothelial cells, to the regulation of the number or affinity of endothelin receptors or to intrinsic calcium‐sensitivity of the contractile proteins. Rather they are probably due to differences in the regulation of intracellular calcium.
ACTION OF CHOLINESTERS ON SENSORY NERVE ENDINGS IN SKIN AND MUSCLE
Authors: Carr RW , Proske U. 
Published: June 2007

SUMMARY1. This is a review of the literature on the subject of the effects of cholinesters and their agonists on sensory nerve endings.2. The present‐day view is that acetylcholine (ACh) has an excitatory action on some cutaneous receptors. Responses appear to be limited to receptors served by small myelinated and un‐myelinated axons where responsiveness is multimodal; that is, the receptors are activated by noxious thermal and mechanical stimulation.3. The possible role played by acetylcholine in sensory transduction processes is discussed, as are other explanations for the presence of nicotinic cholinergic receptors on the terminals of cutaneous receptors.4. The excitatory action of ACh and succinylcholine (SCh) on muscle spindles is described. Two possible mechanisms are considered: a direct depolarizing action on the nerve terminals and indirect excitation, brought about by a contracture of the intrafusal fibres on which the sensory endings lie.5. The technique of using SCh in combination with fusimotor stimulation is described. This has provided new information about the internal workings of muscle spindles. Brief mention is also made of the action of SCh on tendon organs and joint receptors.6. It is concluded that a direct action by cholinesters is restricted to receptors served by small axons with multimodal functions. The precise role of such an action remains the subject of speculation. Possible clinical significance is discussed.
EFFECT OF 8‐SULFOPHENYL THEOPHYLLINE ON ENDOGENOUS NORADRENALINE RELEASE FROM SYMPATHETIC NERVES OF THE RABBIT EAR ARTERY
Authors: Ishii Reiko , Shinozuka Kazumasa , Kunitomo Masaru , Hashimoto Takao , Takeuchi Koichi 
Published: June 2007

SUMMARY1. The release of endogenous noradrenaline (NA) and adenyl purine (ATP, ADP, AMP and adenosine) from the rabbit ear artery, evoked by electrical stimulation (ES; 16Hz), was examined.2. ES evoked a significant release of NA and adenyl purine; the ratio of the amount of total purine released to NA released was approximately 180 on a molar base.3. ES‐evoked purine release was significantly reduced by the denudation of the endothelium and abolished by the α1‐adrenoceptor antagonist, prazosin (1 μmol/L).4. ES‐evoked NA release was significantly reduced by a P1‐purinoceptor antagonist, 8‐sulfophenyl theophylline (8SPT). Purine release was slightly reduced by 8SPT.5. These results suggest that endogenous NA released by ES results in the release of a large amount of purine, which may, in turn, increase the release of NA by acting on prejunctional purinoceptors on sympathetic nerve terminals.
DEHYDROEPIANDROSTERONE DOES NOT PREVENT ADRENOCORTICOTROPHIN‐INDUCED HYPERTENSION IN CONSCIOUS RATS
Authors: Li Ming , Wen Cheng , Martin Allison , Whitworth Judith A 
Published: June 2007

SUMMARY1. We tested the hypothesis that dehydroepiandrosterone (DHEA), which prevents dexamethasone‐induced hypertension in rats, may block adrenocorticotrophin (ACTH) hypertension, which has been presumed due to corticosterone excess. The blood pressure and metabolic effects of DHEA (18 mg/kg per day) were examined in sham and ACTH‐treated (0.5 mg/kg per day) conscious Sprague‐Dawley rats (n= 20).2. ACTH but not sham injection increased blood pressure, water intake and urine output and decreased bodyweight.3. DHEA administration for 10 days did not alter blood pressure or metabolic effects in either sham or ACTH‐treated rats.4. DHEA, which is known to block dexamethasone‐induced hypertension, did not modify ACTH‐induced hypertension in the rat. This suggests either that ACTH‐induced hypertension is not simply a consequence of glucocorticoid activity or that the action of DHEA in dexamethasone hypertension is not through blocking the glucocorticoid receptor.
DOSE DEPENDENT IN VIVO INHIBITION OF HUMAN COLORECTAL CANCER (LoVo) BY THE GASTRIN RECEPTOR ANTAGONIST, CI‐988
Authors: Romani Rossana , Howes Laurence G , Morris David L 
Published: June 2007

SUMMARY1. The dose‐response relationship of a new, potent and selective cholecystokinin B receptor antagonist, CI‐988, on the growth of LoVo, a human colon cancer cell line, was studied in vivo.2. We have previously shown the growth of LoVo to be inhibited both in vitro and in vivo by CI‐988.3. LoVo was grown for 10 days in nude mice that were then treated with CI‐988 at 1,5,10,25 and 50 mg/kg per day orally for 20 days.4. CI‐988 significantly inhibited the growth of xenografts at all concentrations except the highest concentration of 50 mg/kg per day (P<0.00001; anova). The largest inhibitory activity was caused by the 10 mg/kg per day dose, causing a 47% inhibition at day 29 (P= 0.00003; Newman‐Keul's test).5. CI‐988 may be of use in inhibiting the growth of colorectal cancer.
CALCITONIN GENE‐RELATED PEPTIDE ANTAGONIZES THE PROTECTIVE EFFECT OF ADRENOMEDULLIN ON HISTAMINE‐INDUCED BRONCHCTION
Authors: Kanazawa Hiroshi , Kawaguchi Takashi , Kamoi Hiroshi , Fujii Tatsuo , Kudoh Shinzoh , Hirata Kazuto , Kurihara Naotsugu , Yoshikawa Junichi 
Published: June 2007

SUMMARY1. In the present study the possible relationship between adrenomedullin (AM) and calcitonin gene‐related peptide (CGRP) in the regulation of airway functions in anaesthetized guinea‐pigs was examined in vivo.2. We found that AM significantly inhibited histamine‐induced bronchoconstriction in a dose‐dependent manner. CGRP or the CGRP receptor antagonist (CGRP [8–37]) alone did not affect pulmonary resistance and pretreatment with CGRP or CGRP [8–37] did not significantly affect histamine‐induced bronchoconstriction. However, AM‐induced broncho‐protection was significantly inhibited by pretreatment with CGRP or CGRP [8–37] in a dose‐dependent manner.3. It is therefore possible that CGRP may be competitive, at least in part, with binding sites of AM in the guinea‐pig airway. Exogenous AM may be useful for the management of bronchial asthma, not only as a potent bronchodilator, but also as a functional antagonist of CGRP.
RELATIONSHIP BETWEEN ALTERATIONS IN LYMPHOCYTE AND MYOCARDIAL β‐ADRENOCEPTOR DENSITY IN PATIENTS WITH LEFT HEART VALVULAR DISEASE
Authors: Dzimiri Nduna , Moorji Azadali 
Published: June 2007

SUMMARY1. We have evaluated the possibility that alterations in lymphocyte β‐adrenoceptor density may be related to changes in the myocardial population in left heart valvular diseases. Receptor density and their binding affinities were estimated using [125I]‐iodocyanopindolol.2. The lymphocyte (LC) β‐adrenoceptor density was 43.4 ± 5.6 fmol/mg protein in the controls (n= 35) and 81% lower in heart valvular patients (n= 86). In myocardial controls (n= 18), the left ventricular (LV) receptor density was 167.2 ± 29.8 fmol/mg protein, right ventricular (RV) density was 123.1 ± 14.6 fmol/mg, left atrial (LA) density was 81.6 ± 10.5 fmol/mg and right atrial (RA) 108.1 ± 14.5 fmol/mg. Compared with this group, the receptor density of the study patients (n= 47) decreased by 67, 43, 24 and 32% in the LV, RV, LA and RA, respectively. The decrease in LC was twice that of the average total myocardial receptor density.3. When patients were classified according to their left ventricular load conditions as having either left ventricular pressure overload (LVP), left ventricular volume overload, mixed lesions (MOL) and no left ventricular overload (mitral stenosis; NOL), the attenuation in LC receptor density reached statistical significance for all four groups, without showing significant difference between the individual groups. In contrast, the decrease in all chambers was predominantly due to volume overload. MOL and NOL exerted intermediate effects that were significant in the LV, while LVP did not contribute to the changes in the LA.4. Accordingly, the reduction in peripheral β‐adrenoceptor density may reflect the extent to which particularly the volume overload exerts its influence on myocardial β‐adrenoceptors in left heart valvular patients.
EXTRACELLULAR ATP INCREASES CYTOSOLIC CALCIUM IN CULTURED RAT RENAL ARTERIAL SMOOTH MUSCLE CELLS
Authors: Inscho Edward W , Belott Todd P , Mason Michael J , Smith Jeffry B , Navar L Gabriel 
Published: June 2007

SUMMARY1. Experiments were conducted on cultured renal arterial smooth muscle cells to determine the ability of extracellular ATP to alter cytosolic calcium concentration and to determine the mechanisms by which this effect occurs.2. ATP (100 μmol/L) caused the fluorescence ratio of fura‐2 to increase from a control value of 1.06±0.05 to 2.06±0.13 (P<0.01) before stabilizing at a sustained level of 1.35±0.04 (n= 8; P<0.05).3. Removal of extracellular calcium from the bathing medium resulted in an attenuation of the initial response to 100 μmol/L ATP with cell fluorescence increasing from 1.16±0.18 to 1.44±0.18 ratio units (n= 5). Furthermore, the initial increase in fluorescence ratio rapidly declined to 1.02±0.06, indicating that an influx of extracellular calcium is required to sustain the increase in fura‐2 fluorescence.4. Depletion of intracellular calcium pools with thapsigargin prevented the increase in fura‐2 fluorescence evoked by ATP.5. These data suggest that ATP‐mediated increases in cytosolic calcium in cultured renal arterial smooth muscle cells involve calcium release from the thapsigargin‐sensitive, intracellular pool in conjunction with calcium influx from the extracellular medium.
CELLULAR LOCALIZATION OF ENDOTHELIN RECEPTOR SUBTYPES IN THE RAT KIDNEY FOLLOWING IN VITRO LABELLING
Authors: Dean Rachael , Zhuo Jialong , Alcorn Daine , Casley David , Mendelsohn Frederick AO 
Published: June 2007

SUMMARY1. We have previously shown that [125I]‐endothelin (ET) receptor binding is localized almost exclusively to the fenestrated endothelial cells of glomerular capillaries and peritubular capillaries in the rat kidney following systemic administration of the radioligand in vivo. Because of the lack of specific ET receptor binding in other glomerular and tubular structures following in vivo labelling, we undertook further studies, using electron microscopic autoradiography and ET receptor subtype selective ligands, to investigate whether other renal components also contain ET receptor binding and, if so, to determine the cellular localization of the ET receptor subtypes, ETA and ETB, following in vitro labelling.2. At the electron microscopic level, ET binding sites were localized primarily to the fenestrated endothelium of glomerular and peritubular capillaries of the cortex, inner stripe of the outer medulla and the inner medulla. ET binding sites also occurred overlying renomedullary interstitial cells (RMIC) of the inner medulla.3. The ETB receptor selective agonist, sarafotoxin 6c (S6c), abolished ET binding in the vascular endothelium throughout the kidney, while the ETA receptor selective antagonist, BQ123, was without effect. Both BQ123 and S6c partially inhibited the binding in the RMIC of the inner medulla.4. These results indicate that ET receptor binding in the fenestrated endothelium in the glomerular capillaries and peritubular capillaries belongs mainly to the ETB subtype, whereas both ETA and ETB subtypes are present in the RMIC.