bluuebunny/crossref_metadata_2025_split huggingface dataset:
INTERACTION BETWEEN ENDOTHELIN AND ANGIOTENSIN II
Authors: Phillips Paddy A 
Published: March 2003

1. Angiotensin II (AngII) and endothelin (ET) stimulate cardiac hypertrophy in vitro and in vivo. Also AngII stimulates ET production.2. In order to investigate whether AngII produces its cardiac hypertrophic effects through stimulating ET production which acts on the ETA receptor, male Sprague‐Dawley rats (6–8 weeks of age) received an intravenous infusion of AngII at 0, 100 or 200 ng/kg per min via Alzet osmotic minipumps and jugular venous catheters for 7 days (n = 12 per dose). Half of the rats in each group received the selective ETA receptor antagonist BMS 193884 25 mg/kg per orally and the other half received the vehicle daily.3. Telemetrically measured mean arterial pressure (MAP) rose with the 200 ng/kg per min dose of AngII (P = 0.0001). The ETA receptor blockade lowered MAP in all groups (P = 0.011). Left ventricular weights increased only in the 200 ng/kg per min AngII infusion rats (P = 0.04). There was no effect of ETA receptor blockade on left ventricular weights.4. These results suggest that AngII causes left ventricular hypertrophy not only in association with a pressor response but also when MAP was lowered with ETA blockade to control levels, suggesting a non‐pressor effect of AngII on cardiac hypertrophy. Also, ET, acting via ETA receptors, does not mediate the hypertrophic effect of AngII in this model.
EFFECT OF STEROID HORMONES ON BLOOD PRESSURE
Authors: Dodic M , Wintour Em , Whitworth * JA , Coghlan Jp 
Published: March 2003

1. There is considerable evidence to support the idea that steroid hormones have the potential to increase blood pressure that may not always be via ‘classical’ mineralocorticoid or glucocorticoid action.2. Epidemiological studies, together with the evidence from studies in animals, proposed the link between an adverse intra‐uterine environment (i.e. undernutrition or excess exposure to glucocorticoids) and the early onset of cardiovascular and metabolic diseases later in life.3. We tested this by treating pregnant ewes (and foetuses) with excess steroid early in pregnancy. The mean ages at which the prenatal exposure to glucocorticoid (dexamethasone 0.48 mg/h for 48 h) occurred were 22±0.4 to 29±0.4 days (prenatal treatment group 1; PTG1) and 59±2 to 66±2 days (PTG2), respectively. Basal blood pressures and hormones and the vascular responsiveness to graded doses of angiotensin II and noradrenaline, or to a 5‐day adrenocorticotropin hormone treatment (ACTH), in lambs at 4, 10 and 19 months of age were studied.4. Basal mean arterial pressure in PTG1 group (80±1 mmHg at 4 months; 83±1 mmHg at 10 months; and 89±1 mmHg at 19 months; n = 6) was significantly different (P < 0.05 in all groups) from that in the control group of lambs (74±2 mmHg at 4 months; 76±1 mmHg at 10 months; and 81±1 mmHg at 19 months; n = 7). Prenatal glucocorticoid exposure did not alter vascular responsiveness to noradrenaline, angiotensin II and ACTH in these sheep at any of the ages studied.5. These results suggest that foetal exposure to maternal dexamethasone during defined developmental stage or ‘window’ programmes elevated blood pressure, which persists later in life.
Troponin T In The Coronary Sinus And Percutaneous Transluminal Coronary Angioplasty Related Myocardial Injury
Authors: Katoh Harumi , Shimada Toshio , Sano Kazuya , Inoue Shin‐ichi , Kitamura Jun , Sakane Takeshi , Murakami Yo , Ishibashi Yutaka , Karino Kenji , Masuda Junichi 
Published: March 2003

SUMMARY1. Myocardial injury has been shown to be associated with successful percutaneous transluminal coronary angioplasty (PTCA). The present study was designed to determine whether uncomplicated successful PTCA results in myocardial injury by measuring coronary sinus (CS) cardiac troponin T (cTnT).2. We measured cTnT in the CS and the femoral vein (FV) in 16 patients with stable angina pectoris who underwent uncomplicated PTCA for stenotic lesions of the left anterior descending artery. Blood samples were drawn from both the CS and FV before and immediately after PTCA and every 4 h for the next 12 h.3. All patients had chest pain and electrocardiographic ST segment elevation or depression during balloon inflation and higher peak elevation of cTnT in the CS than in the FV (0.054±0.059 vs 0.036±0.022 ng/mL; P < 0.05). However, all CS cTnT levels were within the normal range over the 12 h period.4. The fact that CS cTnT measurements showed no evidence of uncomplicated PTCA‐related myocardial injury led us to conclude that uncomplicated successful PTCA does not cause myocardial injury.
RENOMEDULLARY INTERSTITIAL CELLS: A TARGET FOR ENDOCRINE AND PARACRINE ACTIONS OF VASOACTIVE PEPTIDES IN THE RENAL MEDULLA
Authors: Zhuo Jia Long 
Published: March 2003

SUMMARY1. The renal medulla plays an important role in regulating body sodium and fluid balance and blood pressure homeostasis through its unique structural relationships and interactions between renomedullary interstitial cells (RMIC), renal tubules and medullary vasculature.2. Several endocrine and/or paracrine factors, including angiotensin (Ang)II, endothelin (ET), bradykinin (BK), atrial natriuretic peptide (ANP) and vasopressin (AVP), are implicated in the regulation of renal medullary function and blood pressure by acting on RMIC, tubules and medullary blood vessels.3. Renomedullary interstitial cells express multiple vasoactive peptide receptors (AT1, ETA, ETB, BK B2, NPRA and NPRB and V1a) in culture and in tissue.4. In cultured RMIC, AngII, ET, BK, ANP and AVP act on their respective receptors to induce various cellular responses, including contraction, prostaglandin synthesis, cell proliferation and/or extracellular matrix synthesis.5. Infusion of vasoactive peptides or their antagonists systemically or directly into the medullary interstitium modulates medullary blood flow, sodium excretion and urine osmolarity.6. Overall, expression of multiple vasoactive peptide receptors in RMIC, which respond to various vasoactive peptides and paracrine factors in vitro and in vivo, supports the hypothesis that RMIC may be an important paracrine target of various vasoactive peptides in the regulation of renal medullary function and long‐term blood pressure homeostasis.
Time‐Course Of Changes In Hepatic Lipid Peroxidation And Glutathione Metabolism In Rats With Carbon Tetrachloride‐Induced Cirrhosis
Authors: Cabré M , Camps J , Paternáin Jl , Ferré N , Joven J 
Published: March 2003

SUMMARY1. The aims of the present study were to assess: (i) the temporal relationships between hepatic lipid peroxidation, changes in the glutathione detoxification system and the onset/development of cirrhosis in CCl4‐treated rats; and (ii) the effects of oral zinc administration on these parameters.2. Cirrhosis was induced in 120 rats by intraperitoneal injections of CCl4 twice a week over 9 weeks. One hundred and twenty additional animals were used as controls. Both groups were further subdivided to receive either a standard diet or one supplemented with zinc. Subsets of 10 animals each were killed at weeks 1, 2, 3, 5, 7 and 9 from the start of the study.3. Induction of cirrhosis produced a decrease in the components of the hepatic glutathione anti‐oxidant system: glutathione transferase activity decreased from week 1, the concentration of reduced glutathione (GSH) decreased from week 5 and glutathione peroxidase (GPx) activity decreased from week 7. This impairment was chronologically related to an increase in free radical generation. Hepatic lipid peroxidation was significantly correlated with GPx activity (r = – 0.47; P < 0.001) in CCl4‐treated rats. Zinc administration did not produce any significant improvement of the hepatic glutathione system.4. In conclusion, cirrhosis induction in rats by CCl4 administration produced a decrease in the hepatic glutathione anti‐ oxidant system that was related to an increase in free radical production. Furthermore, zinc supplementation produced a reduction in the degree of hepatic injury and a normalization of lipid peroxidation, but not an improvement of the hepatic GSH anti‐oxidant system.
Capillary Network Patterning During Angiogenesis
Authors: Hansen‐Smith Fay M 
Published: March 2003

SUMMARY1. Although much is known of signalling events associated with angiogenesis, starting with a sprout, less is known of how an intact microvascular network is correctly formed following the initiation of sprouting. The aim of the present report is to evaluate some of the factors that could be involved in directing the patterning of the resulting microvascular bed.2. Hypothetical ‘patterning rules’ are discussed and considered in the context of data obtained from studies of angiogenesis. The guidelines suggest that both tissue‐ and stimulus‐specific regulators are involved in directing patterning.3. Examples of ‘patterned’ and ‘non‐patterned’ angiogenesis in rat mesentery are given, with evidence to support stimulus‐related differences in angiogenesis patterns.4. Skeletal muscle angiogenesis follows metabolic patterns within the muscle, as discerned through traditional histochemical evaluation. However, further examination, using confocal microscopy and new patterning assays, indicates that branching patterns differ according to stimulus. Patterning guidelines within the tissue may be important in preventing the growth of sinusoidal vessels.5. The concept of ‘angiotypes’ is proposed to direct future studies towards understanding how therapeutic angiogenesis or angiostasis applications can be used to obtain correctly patterned microvascular networks. Angiogenesis via ‘branching’ compared with ‘non‐branching’ angiotypes will involve different signalling pathways. Both sprouting and dividing of capillaries are found in the ‘branching’ angiotype, with each pattern having several subtypes that would be expected to be mediated via different signalling mechanisms.
Effect Of Temperature On Responses Of Dog Isolated Lingual And Mesenteric Arteries To Vasoactive Substances
Authors: Tsukada Miyoko , Chiba Shigetoshi 
Published: March 2003

SUMMARY1. The effects of temperature on submaximal vasoconstriction to an intraluminal administration of noradrenaline (NA), phenylephrine, tyramine and KCl were investigated in canine isolated and perfused lingual and mesenteric arteries, using the cannula‐inserting method.2. In lingual arteries, cooling (from 37 to 27°C) caused significant depression of vasoconstriction to the four vasoactive substances used. Rewarming (to 37°C) induced a significant augmentation of constriction by NA, phenylephrine and KCl, but not tyramine.3. In mesenteric arteries, cooling depressed tyramine‐ and KCl‐induced constrictions, but had no effect on NA‐ and phenylephrine‐induced vasoconstriction. Only in the case of KCl‐induced constrictions did rewarming induce a potentiation of the vasoconstrictor response.4. We conclude that: (i) cooling induces a depression of voltage‐dependent Ca2+ channels and rewarming may induce a potentiation of Ca2+ channels in both arteries; (ii) α1‐ adrenoceptor‐operated Ca2+ channels are depressed by cooling in lingual arteries but not in mesenteric arteries; and (iii) cooling may induce an attenuation of the re‐uptake function in sympathetic nerve terminals in both arteries and this attenuation may be not rapidly restored by acute rewarming.
Effects Of Tachykinins On Uterine Smooth Muscle
Authors: Patak EN , Story ME 
Published: March 2003

SUMMARY1. Sensory nerves supplying the mammalian uterus have been shown to contain substance P (SP) and neurokinin (NK)A. This review presents some of the advances that have led to a greater understanding of the effects of tachykinins on uterine smooth muscle.2. The cell‐surface peptidase neprilysin (EC.3 24.11, endopeptidase 24.11, enkephalinase, CALLA, CD10) has been shown to play a major role in regulating the actions of tachykinins on both rat and human myometrium. Because this peptidase is known to be regulated by steroids and pregnancy, its effects may be of physiological relevance.3. Tachykinins produce contractions of isolated myometrial preparations from non‐pregnant rats and mice. The NK2 receptor mediates these effects in rat uterus, while the NK1 receptor may mediate these effects in the mouse uterus.4. The effects of tachykinins have been examined on myometrial preparations obtained at Caesarean section from near‐term pregnant women. In the presence of the peptidase inhibitors (thiorphan, captopril and bestatin), the mammalian tachykinins SP, NKA and NKB produced concentration‐dependent uterine contractions.5. The order of agonist potency NKA > SP = NKB suggested that NK2 receptors mediate uterine contractions in the human. This was confirmed using the stable analogues [Sar
9,Met(O2)
11]SP, [Lys
5MeLeu
9Nle
10]NKA(4–10) and [N‐MePhe
7]NKB, which are NK1, NK2 and NK3 receptor selective, respectively. Only [Lys
5MeLeu
9Nle
10]NKA(4–10) produced concentration‐related contractions of human uterine smooth muscle.6. The experimental findings described in the present review, taken together with results published previously in the literature, indicate that tachykinin peptides may play a physiological or pathophysiological role in regulating uterine smooth muscle activity. However, more extensive research will be required to confirm such a role for these peptides.
Effect Of Organic Cations On The Renal Tubular Secretion Of Pseudoephedrine In The Rat
Authors: Strindelius Lena C , Nation Roger L , Evans Allan M , Cabot Juanita L , Corbett Kathryn M 
Published: March 2003

SUMMARY1. Pseudoephedrine is a weak organic base that undergoes renal tubular secretion. The aim of the present study was to assess whether two other commonly used weak organic bases (cimetidine and morphine) inhibit the renal tubular secretion of pseudoephedrine in the rat isolated perfused kidney.2. A total of 12 perfusions were performed with four perfusions in each of three treatment groups. In the control group, pseudoephedrine was administered as a bolus dose of [14C]‐pseudoephedrine and unlabelled pseudoephedrine to achieve an initial perfusate concentration of 0.4 μg/mL. For the treatment groups, pseudoephedrine was administered as above and cimetidine or morphine was added to the perfusion medium in increasing concentrations of 0.5–12.5 and 0.2–5.0 μg/mL, respectively.3. The mean (±SD) fraction unbound of pseudoephedrine alone in perfusate was 0.866±0.014 and was not different (P > 0.05) in the presence of cimetidine or morphine.4. In control experiments, the renal excretory clearance (CLR) of pseudoephedrine was three‐fold greater than glomerular filtration rate (GFR), yielding a ratio consistently greater than unity, which indicates extensive net tubular secretion of pseudoephedrine. The CLR and total clearance of pseudoephedrine were similar, suggesting an absence of renal metabolism of pseudoephedrine.5. The CLR/GFR ratio for pseudoephedrine was not affected by morphine, but was significantly reduced (P < 0.05) in the presence of cimetidine.6. The results indicate that cimetidine inhibits the renal tubular secretion of pseudoephedrine.
Proceedings of the Australian Neuroscience Society Symposium: Schizophrenia A REVIEW OF THE NEUROPATHOLOGY OF SCHIZOPHRENIA
Authors: Halliday Gm 
Published: March 2003

SUMMARY1. Research on the structural basis for schizophrenia was considered a graveyard for neuropathologists, largely because its aetiology has remained obscure. However, there have been several recent major reviews and studies in leading journals on the neuropathology of schizophrenia highlighting the alterations found in the brains of schizophrenic patients.2. It is clear from the evidence that schizophrenia can no longer be considered a purely functional psychosis with no structural basis. Multiple and possibly widespread neural systems are likely to participate, because diffuse ventricular enlargement and decreased cortical volume are common in schizophrenia. Interestingly, these features do not herald neuronal loss, findings similar to those obtained in alcoholic and aged populations. Impairment in judgement is common to all these subject groups.3. The frontal and temporal lobes and their thalamic relays appear particularly affected in schizophrenia and there is some evidence for significant asymmetries. These regions are also consistently affected in patients with neurodegenerative cognitive impairment, although patients with schizophrenia can be distinguished by a lack of classical tissue pathology.4. The cellular phenotypes that must be structurally compromised have yet to be definitively identified and the relationship between any neurochemical and structural abnormality remains unclear. The subtlety of these changes and their diffuse nature have evoked a consistent chorus that schizophrenia is a neurodevelopmental abnormality; however, this is hard to prove at a structural level using cross‐sectional post‐mortem analyses.
Proceedings of the Australian Physiological and Pharmacological Society Symposium: The Hypothalamus HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CARDIOVASCULAR REGULATION
Authors: Badoer Emilio 
Published: March 2003

SUMMARY1. The hypothalamic paraventricular nucleus (PVN) is an important integrative site within the brain composed of magnocellular and parvocellular neurons. It is known to influence sympathetic nerve activity.2. The parvocellular PVN contains neurons that project to the intermediolateral cell column of the thoraco–lumbar spinal cord (IML). This defines the PVN as an autonomic ‘premotor nucleus’, one of only five present within the brain.3. Another projection arising from the PVN is a prominent innervation of the pressor region of the rostral ventrolateral medulla (RVLM), also a premotor nucleus. The distribution of the PVN neurons projecting to the RVLM is similar to that of the PVN neurons that project to the IML.4. It has been found that up to 30% of spinally projecting neurons in the PVN also send collaterals to the RVLM. Thus, there are neurons in the PVN that can: (i) directly influence sympathetic nerve activity (via PVN–IML connections); (ii) indirectly influence sympathetic nerve activity (via PVN–RVLM connections); and (iii) both directly and indirectly influence sympathetic nerve activity (via neurons with collaterals to the IML and RVLM).5. In the rat, results of studies using the protein Fos to identify activated neurons in the brain suggest that neurons in the PVN with projections to the IML or RVLM may be activated by decreases in blood volume.6. In conclusion, the PVN can influence sympathetic nerve activity. Within the PVN are neurons with anatomical connections that enable them to affect sympathetic nerve activity either directly, indirectly or via both mechanisms (via collaterals). Studies that have examined the role of specific subgroups within the PVN suggest that PVN neurons with connections to the IML or to the RVLM may play a role in the reflex changes in sympathetic nerve activity that are involved in blood volume regulation.
Proceedings of the Australian Physiological and Pharmacological Society Symposium: New Frontiers in Muscle Research ‘Current’ advances in mechanically skinned skeletal muscle fibres
Authors: Posterino Giuseppe S 
Published: March 2003

SUMMARY1. In skeletal muscle, excitation–contraction (E‐C) coupling describes a cascade of cellular events initiated by an action potential (AP) at the surface membrane that ultimately results in muscle contraction. Being able to specifically manipulate the many processes that constitute E‐C coupling, as well as the many factors that modulate these processes, has proven challenging.2. One of the simplest methods of gaining access to the intracellular environment of the muscle fibre is to physically remove (mechanically skin) the surface membrane. In doing so, the myoplasmic environment is opened to external manipulation.3. Surprisingly, even though the surface membrane is absent, it is still possible to activate both twitch and tetanic force responses in a mechanically skinned muscle fibre by generating an AP in the transverse tubular system. This proves that all the key steps in E‐C coupling are retained in this preparation.4. By using this technique, it is now possible to easily manipulate the myoplasmic environment and observe how altering individual factors affects the normal E‐C coupling sequence. The effect of important factors, such as the redox state of the cell, parvalbumin and the sarcoplasmic reticulum Ca2+‐ATPase, on twitch and tetanic force can now be specifically investigated independent of other factors.
Local Pulse Pressure Is A Major Determinant Of Large Artery Remodelling
Authors: Laurent Stéphane , Tropeano Anne‐Isabelle , Lillo‐Lelouet Agnès , Jondeau Guillaume , Laloux Brigitte , Boutouyrie Pierre 
Published: March 2003

SUMMARY1. The aim of the present brief review is to show that the pulsatile component of blood pressure is a stronger determinant of large artery remodelling than the steady component (i.e. mean blood pressure).2. Pulse pressure, which is a strong determinant of cardiovascular events, including coronary heart disease and stroke, is increased when large arteries stiffen. Local pulse pressure, measured with applanation tonometry in normotensives and patients with essential hypertension, explains a significant part of the variance of intima–media thickness at the site of the carotied artery, a proximal elastic artery, whereas mean blood pressure does not contribute. Local pulse pressure has no influence on intima–media thickness at the site of the radial artery, a distal muscular artery that undergoes very little stroke change in diamter.3. The decrease in carotid pulse pressure is also a major determinant of the regression of catorid intima–media thickness after antihypertensive treatment. Local pulse pressure can influence not only intima–media thickness, but also internal diameter. Indeed, there is a significant association between the lumen enlargement of the ascending aorta in patients with Marfan syndrome and pulse pressure. In addition, carotid pulse pressure is positively correlated with carotid internal diameter in normotensives and hypertensives, and the decrease in carotid internal diameter during long‐term antihypertensive treatment is influenced by the decrease in carotid pulse pressure and not by the reduction in mean blood pressure.4. We suggest that the effects of pulse pressure on large artery remodelling may explain part of its predictive value on cardiovascular events.
Coronary Dilatation Reserve In Experimental Hypertension And Chronic Heart Failure: Effects Of Blockade Of The Renin–Angiotensin System
Authors: Richer C , Domergue V , Gervais M , Fornes P , Trabold F , Giudicelli J‐F 
Published: March 2003

SUMMARY1. The aim of the present study was to investigate left and right ventricular (LV and RV, respectively) coronary vasodilatation reserve (CVR; fluorescent microsphere technique) in rats with hypertension (spontaneously hypertensive rats (SHR)) or congestive heart failure (CHF) and the effects of early and chronic renin–angiotensin system (RAS) blockade thereupon.2. In adult SHR, both LV and RV CVR were impaired, especially in the non‐hypertrophied RV, the main factor involved being coronary vascular remodelling. Blockade of the RAS normalized both LV and RV CVR, mainly through the prevention of hypertension and suppression of the resulting pericoronary fibrosis.3. In postischaemic CHF rats, there was an early and severe degradation of LV and RV CVR that developed before any significant vascular remodelling and appeared to be linked to the deterioration of cardiac hypertrophy and haemodynamics. This degradation in CVR further worsened over the longer term due to late‐developing pericoronary fibrosis and endothelial dysfunction. Blockade of the RAS had no early effects on LV and RV CVR, but improved RV CVR over the long term, mainly by limiting RV hypertrophy and by preventing the development of pericoronary fibrosis and coronary endothelial dysfunction.4. In kallikrein–kinin system‐deficient mice, CVR was not different from that of wild‐type mice, suggesting that this system is not implicated in normal CVR regulation.