bluuebunny/crossref_metadata_2025_split huggingface dataset:
Proceedings of the Symposium ‘Angiotensin AT1Receptors: From Molecular Physiology to Therapeutics’: ANGIOTENSIN II AND THE ADRENAL
Authors: Giacchetti G. , Opocher G. , Sarzani R. , Rappelli A. , Mantero F. 
Published: September 2010

SUMMARYAngiotensin II (AngII) evokes a variety of physiological responses in the adrenal gland. It is the major regulator of aldosterone secretion, in the medulla it enhances catecholamine release and it exerts trophic effects in the adrenal and stimulates growth factor secretion.Angiotensin II acts via binding to specific receptors, located on the plasma membrane. Two pharmacologically distinct AngII receptor subtypes, type 1 (AT1) and type 2 (AT2) receptors, have been identified using the non‐peptide antagonists Dup753 and PD 123177, respectively, and cDNA encoding each type have been identified.In the adrenal, the AT1receptor modulates all the known biological effects of AngII. The expression of the AT1receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up‐regulate AT1receptor mRNA levels and binding and increase aldosterone secretion.A tissue renin‐angiotensin system has been found in the adrenal, suggesting an important paracrine role for AngII in aldosterone regulation.The possible involvement of AT1receptors in human disease has been investigated by examining the role of AngII receptors in adrenal tumours. Binding and gene expression studies have shown that AngII receptors are abundantly expressed in aldosterone‐producing adenoma (APA).Densitometric analysis of AT1expression in APA showed no significant differences compared with normal and nontumorous adrenal. In addition, no mutations in the coding sequence of the AT1receptor have been found to date in adrenal tumours.
Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: STRUCTURAL CHANGES IN THE RENAL VASCULATURE IN THE SPONTANEOUSLY HYPERTENSIVE RAT: NO EFFECT OF ANGIOTENSIN II BLOCKADE
Authors: Kett Michelle M , Anderson Warwick P , Bertram John F , Alcorn Daine 
Published: September 2010

SUMMARY

There is strong evidence for a renal basis to the development of hypertension in the spontaneously hypertensive rat (SHR). Alterations of the SHR renal vasculature, including the glomerulus, may be involved in the initiation and maintenance of hypertension in this animal model.
The arterial walls of pre‐glomerular vessels of the SHR are hypertrophied compared with WKY vessels. Unlike other vascular beds in the SHR, this hypertrophy is independent of angiotensin II (AngII).
Glomerular number and volume are similar between SHR and the normotensive Wistar‐Kyoto (WKY) rats. These results provide no support for the theory that a reduced filtration surface area within the kidneys of the SHR contributes to the elevated blood pressure in these animals.
Intrarenal hypertrophy may have similar haemodynamic consequences to clipping of the main renal artery, as in Goldblatt hypertension. Further analysis of the role of pre‐glomerular arterial hypertrophy is warranted to determine its involvement in the initiation and maintenance of hypertension in the SHR.
Proceedings of the Symposium ‘Angiotensin AT1Receptors: From Molecular Physiology to Therapeutics’: PRESENCE OF ANGIOTENSIN II AT2RECEPTOR BINDING SITES IN THE ADVENTITIA OF HUMAN KIDNEY VASCULATURE
Authors: Zhuo Jialong , Dean Rachael , MacGregor Duncan , Alcorn Daine , Mendelsohn Frederick AO 
Published: September 2010

SUMMARYAngiotensin II (AngII) receptor subtypes in adult human kidney were pharmacologically characterized byin vitroautoradiography using the AngII receptor subtype‐selective antagonists, losartan and PD 123319, and the sensitivity to the reducing agent, dithiothreitol.High densities of AngII AT1receptor binding occur in the glomeruli and the inner stripe of the outer medulla, while a moderate AT1receptor binding is localized in the proximal convoluted tubules.AT2receptor binding is observed predominantly in the intrarenal large blood vessels, including the arcuate, inter‐ and intra‐lobular arteries, and in the renal capsule.In the major renal artery, AT1receptor binding is abundant in the media and adventitia, while AT2receptor binding is observed mainly in the adventitia.At the light microscopic level using emulsion autoradiography, AT1receptors are localized in the glomeruli and juxtaglomerular apparatus, as expected. However, in larger renal blood vessels, including the arcuate arteries, inter‐ and intra‐lobular arteries, intense AT2receptor labelling occurs primarily in the adventitia, while the endothelium and vascular smooth muscle layers contain only low levels of AngII receptor binding.These results indicate that the adult human kidney displays two pharmacologically distinct AngII receptor subtypes, with AT1predominating in the glomeruli, juxtaglomerular apparatus, proximal tubules and the inner stripe of the outer medulla, while AT2predominates in the adventitia of the arcuate and interlobular arteries and the renal capsule. The functional significance of AT2receptor binding sites in the adventitia of adult human kidney vessels remains to be elucidated.
COMPARISON OF LOW and HIGH DOSES OF CARVEDILOL ON RESTORATION OF CARDIAC FUNCTION and CALCIUM‐HANDLING PROTEINS IN RAT FAILING HEART
Authors: Sun Yi‐Lan , Hu Shen‐Jiang , Wang Li‐Hong , Hu Ying , Zhou Jian‐Ying 
Published: September 2010

SUMMARY1. The β‐adrenoceptor antagonist carvedilol reverses cardiac dysfunction in the failing heart. A recent study showed that β‐adrenoceptor antagonists indirectly normalize Ca2+‐regulatory proteins. The relationship between these two phenomena and the suitable dosage of carvedilol remains unclear.2. We investigated the change in left ventricular (LV) remodelling and function in a rat model of heart failure due to myocardial infarction (MI) with or without carvedilol (30 or 2 mg/kg per day) treatment for 6 weeks. The expression of mRNA and proteins of sarcoplasmic reticulum Ca2+‐ATPase (SERCA) and phospholamban (PLB) in cardiomyocytes was also measured.3. There was significant LV remodelling and cardiac contractile dysfunction in MI rats. The expression of SERCA mRNA and protein were downregulated (P < 0.01), but the expression of PLB mRNA and protein were upregulated (P < 0.01) in MI rats compared with sham‐operated rats. After treatment with carvedilol, LV remodelling and cardiac contractile dysfunction were clearly improved. Low‐dose carvedilol was better at improving some parameters of LV remodelling and function than the high dose. Carvedilol partially restored the low expression of SERCA (P < 0.05), but had no effect on PLB expression (P > 0.05). Moreover, low‐dose carvedilol induced a more significant improvement in SERCA expression than did the high dose (P < 0.05).4. The results of the present study suggest that carvedilol is effective in improving LV remodelling and cardiac contractile dysfunction after MI. This may be related to the normalization of SERCA expression.
EFFECT OF PERINATAL HYPOXIA ON CARDIAC TOLERANCE TO ACUTE ISCHAEMIA IN ADULT MALE AND FEMALE RATS
Authors: Netuka Ivan , Szarszoi Ondrej , Maly Jiri , Besik Josef , Neckar Jan , Kolar Frantisek , Ostadalova Ivana , Pirk Jan , Ostadal Bohuslav 
Published: September 2010

SUMMARY

The number of adult patients undergoing surgery for congenital cyanotic defects in childhood has increased significantly. Therefore, the aim of the present study was to examine the effect of perinatal hypoxia on the tolerance of the adult myocardium to acute ischaemia–reperfusion injury.
Pregnant Wistar rats were exposed to intermittent hypobaric hypoxia 7 days before delivery; pups were born under normoxic conditions and exposed to hypoxia again for 10 postnatal days. After the last hypoxic exposure, all animals were kept for an additional 3 months under normoxic conditions. All experiments were performed on 90‐day‐old rats.
Ventricular arrhythmias were assessed on isolated perfused hearts during 30 min occlusion of the left anterior descending coronary artery. Infarct size was measured on isolated hearts (40 min regional ischaemia and 120 min reperfusion) and on open‐chest animals (20 min regional ischaemia and 3 h reperfusion).
Perinatal exposure to hypoxia significantly increased cardiac tolerance to ischaemic injury in adult females, as evidenced by the lower incidence and severity of ischaemic ventricular arrhythmias, compared with the normoxic group. The effect of perinatal hypoxia on ischaemic arrhythmias in males was quite the opposite. Myocardial infarct size measured in open‐chest animals only was significantly smaller in normoxic females compared with normoxic males. Perinatal exposure to hypoxia had no effect on infarct size in either setting or sex.
The results of the present study support the hypothesis that perinatal hypoxia is a primary programming stimulus in the heart that may lead to sex‐dependent changes in cardiac tolerance to acute ischaemia in later adult life. This would have important implications for patients who have experienced prolonged hypoxaemia in early life.
BEHAVIOUR OF THE ANTI‐OXIDANT DEFENCE SYSTEM AND HEME OXYGENASE‐1 PROTEIN EXPRESSION IN FRUCTOSE‐HYPERTENSIVE RATS
Authors: Polizio Ariel H , Gonzales Soledad , Muñoz Marina C , Peña Clara , Tomaro María L 
Published: September 2010

SUMMARY

Addition of fructose to a rat diet for various periods of time leads to hypertension, hyperinsulinaemia and dyslipidaemia and provides a model for testing oxidative stress parameters in the animals.
In the present study, oxidative stress generation, the soluble and enzymatic defence system and heme oxygenase‐1 (HO‐1) protein expression were investigated in the heart, liver and kidney of rats fed fructose for a period of 1 or 8 months.
Compared with the control group, fructose‐hypertensive rats showed increased in lipid peroxidation only in the heart after both 1 and 8 months of fructose treatment. Changes in the behaviour of the soluble and enzymatic defence system and HO‐1 protein expression were different depending on the organ. Increased or unaltered activities of anti‐oxidant enzymes were found in the liver and kidney, respectively. Induction of HO‐1 prevented the generation of oxidative stress in the liver, where the activity of anti‐oxidant defence enzymes was not reduced. Increased expression of HO‐1 protein was not able to prevent the generation of oxidative stress in the heart, where fructose treatment diminished the activity of anti‐oxidant enzymes.
The results of the present study demonstrate that upregulation of HO‐1 may prevent the generation of oxidative stress only when the anti‐oxidant defence system is still operative.
CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE¶
Authors: Chen Sheng‐Hsien , Niu Ko‐Chi , Lin Mao‐Tsun 
Published: September 2010

SUMMARYThe aim of the present review is to summarize clinical observations and results of animal models that advance the knowledge of the attenuation of cerebrovascular dysfunction in the setting of heat stroke. It is a narrative review of selected published literature from Medline over the period 1959–2005.All heat‐stressed rodents, even under general anaesthesia, have hyperthermia, systemic inflammation, hypercoagulable state, arterial hypotension and tissue ischaemia and injury in multiple organs. These findings demonstrate that rodent heat stroke models can nearly mirror the full spectrum of human heat stroke. Experimental heat stroke fulfills the empirical triad used for the dignosis of classical human heat stroke, namely hyperthermia, central nervous system alterations and a history of heat stress.These physiological dysfunctions and survival during heat stroke can be improved by whole‐body or brain cooling therapy adopted immediately after the onset of heat stroke.However, in the absence of body or brain cooling, these heat stroke reactions can still be reduced by the following measures: (i) fluid replacement with 3% NaCl solution, 10% human albumin or hydroxyethyl starch; (ii) intravenous delivery of anti‐inflammatory drugs, free radical scavengers or interleukin‐1 receptor antagonists; (iii) hyperbaric oxygen therapy; or (iv) transplantation of human umbilical cord blood cells.In addition, before initiation of heat stress, prior manipulations with one of the following measures was found to be able to protect against heat stroke reactions: (i) systemic delivery of α‐tocopherol, mannitol, inducible nitric oxide synthase inhibitors, mu‐opioid receptor antagonists, endothelin ETAreceptor antagonists, serotoninergic nerve depletors or receptor antagonists, or glutamate receptor antagonists; or (ii) heat shock portein 72 preconditioning.There is compelling evidence that cerebrovascular dysfunction is an attractive target for therapy in heat stroke.
CHRONIC FLUVASTATIN TREATMENT ALTERS VASCULAR CONTRACTION BY INHIBITING THE RHO/RHO‐KINASE PATHWAY
Authors: Kansui Yasuo , Fujii Koji , Goto Kenichi , Oniki Hideyuki , Iida Mitsuo 
Published: September 2010

SUMMARY

In the present study, we investigated the effects of chronic treatment of stroke‐prone spontaneously hypertensive rats (SHRSP) with the statin fluvastatin on vascular Rho/Rho‐kinase pathway mediated contraction, which has been shown to be upregulated in hypertension.
Contribution of the Rho/Rho‐kinase pathway to noradrenaline‐induced contraction of arteries from SHRSP was assessed by the inhibitory effect of Y‐27632, a Rho/Rho‐kinase inhibitor. Stroke‐prone spontaneously hypertensive rats were treated with fluvastatin (10 mg/kg per day) for 1 month.
Treatment with fluvastatin tended to attenuate the contraction to noradrenaline and significantly decreased the Y‐27632‐sensitive component of the contraction in controls compared with fluvastatin‐treated rats.
RhoA, as assessed by western blotting, was also reduced by fluvastatin treatment.
These findings suggest that chronic treatment with fluvastatin reduces the contractile response associated with Rho/Rho‐kinase in arteries of hypertensive rats.
EFFECTS OF PERINDOPRIL AND HYDROCHLOROTHIAZIDE ON SELECTED INDICES OF OXIDATIVE STRESS IN THE BLOOD OF ELDERLY PATIENTS WITH ESSENTIAL HYPERTENSION
Authors: Kȩdziora‐Kornatowska Kornelia , Czuczejko Jolanta , Szewczyk‐Golec Karolina , Motyl Jadwiga , Szadujkis‐Szadurski Leszek , Kornatowski Tomasz , Pawluk Hanna , Kȩdziora Józef 
Published: September 2010

SUMMARY

The aim of the present study was to determine the effect of hypotensive therapy with a diuretic (hydrochlorothiazide) and an angiotensin‐converting enzyme inhibitor (perindopril) on selected oxidative stress parameters in the blood of elderly patients with essential hypertension.
Studies were performed in 45 elderly patients with essential hypertension at baseline and after the 45th day of perindopril (n = 25) or hydrochlorothiazide (n = 20) therapy, as well as in 25 young and 25 elderly normotensive subjects. The following parameters were measured: systolic and diastolic blood pressure, nitric oxide (NO), carbonyl groups and malondialdehyde (MDA) concentrations, as well as the activity of ceruloplasmin (Cp) oxidase, Cu‐Zn superoxide dismutase (SOD‐1) and catalase (CAT).
The activity of SOD‐1 and NO levels were reduced with age.
Compared with elderly controls, hypertensive subjects showed increases in baseline MDA, carbonyl group concentrations and Cp oxidase activity and decreases in NO levels and SOD‐1 and CAT activities.
Treatment with perindopril, but not hydrochlorothiazide, resulted in significant increases in SOD‐1 and CAT activities and decreases in MDA concentration and Cp oxidase activity. Both therapies decreased the level of carbonyl groups and increased NO levels.
Angiotensin‐converting enzyme inhibitor therapy has significant anti‐oxidant effects that may be important in the treatment of elderly patients with essential hypertension.
REDUCED SINOATRIAL cAMP CONTENT PLAYS A ROLE IN POSTNATAL HEART RATE SLOWING IN THE RABBIT
Authors: Yang Zhi‐Fang , Sun Yun , Li Ci‐Zhen , Wang Hong‐Wei , Wang Xi‐Jun , Zheng Yan‐Qian , Liu Kai , Liu Yuan‐Mou 
Published: September 2010

SUMMARY

Decreasing heart rate during development is known to be the result of parasympathetic nervous system maturation that depresses the pacemaker current (If) by acetylcholine (ACh). However, a direct effect of ACh on If has been ruled out and the involvement of other secondary messengers, such as cAMP, was verified in previous studies. Therefore, we hypothesized that reduced basal cAMP production in sinoatrial (SA) nodal cells may contribute to the slowing of heart rate after birth.
The electrocardiogram and heart rate variability (HRV) were documented and measured in vivo and in vitro (in isolated perfused Langendorff preparations) for rabbits aged 2, 4, 6, 8 and 12 weeks. Sinoatrial node action potential (AP) recording and perforated patch‐clamp analyses were used to investigate the spontaneous depolarization rate and pacemaker If currents. Concentrations of cAMP in SA nodal tissues were determined by radioimmunoassay. Relative expression of adenylate cyclases (ADCY1, 5) and phosphodiesterases (PDE1A, 4A and 8A) were quantified by real‐time reverse transcription–polymerase chain reaction.
Significantly reduced heart rate, but unchanged HRV, was observed in perfused hearts in the older age groups, accompanied with a slowed phase 4 spontaneous depolarization rate (90.5 ± 4.7 vs 49.6 ± 2.6 mV/s for 2 week vs 4 week hearts, respectively; n = 5; P < 0.05), a negative shift of the If threshold potential (−45.5 ± 3.0 vs−51.1 ± 6.0 mV for 2 week vs 4 week hearts, respectively; n = 9; P < 0.05) and decreasing basal levels of SA nodal cAMP (0.31 ± 0.05 vs 0.025 ± 0.002 µmol/L for 2 week vs 4 week hearts, respectively; n = 6; P < 0.05). Gene expression levels of PDE1A, 4A and 8A were increased in the 12 week group compared with the 2 week group 1.5‐, 2‐ and 1.8‐fold, respectively (P < 0.05), with little change in ADCY1 and 5.
These data suggest that, in addition to autonomic innervation, slowing of heart rate during postnatal maturation can be attributed to a negative shift of the If activation caused by diminished baseline cAMP content in SA nodal cells.
REGULATION OF EPITHELIAL Na+CHANNELS BY ALDOSTERONE: ROLE OF Sgk1
Authors: Lee Il‐Ha , Campbell Craig R , Cook David I , Dinudom Anuwat 
Published: September 2010

SUMMARYThe epithelial sodium channel (ENaC) is tightly regulated by hormonal and humoral factors, including cytosolic ion concentration and glucocorticoid and mineralocorticoid hormones. Many of these regulators of ENaC control its activity by regulating its surface expression via neural precursor cell‐expressed developmentally downregulated (gene 4) protein (Nedd4‐2).During the early phase of aldosterone action, Nedd4‐2‐dependent downregulation of ENaC is inhibited by the serum‐ and glucocorticoid‐induced kinase 1 (Sgk1).Sgk1 phosphorylates Nedd4‐2. Subsequently, phosphorylated Nedd4‐2 binds to the 14‐3‐3 protein and, hence, reduces binding of Nedd4‐2 to ENaC.Nedd4‐2 is also phosphorylated by protein kinase B (Akt1). Both Sgk1 and Akt1 are part of the insulin signalling pathway that increases transepithelial Na+absorption by inhibiting Nedd4‐2 and activating ENaC.
Gastric emptying scintigraphy in carcinoma of the pancreas
Authors: Kuruba Rajesh , Wig Jai Dev , Kochhar Rakesh , Mittal Bhagwant Rai 
Published: September 2010

Objective: In patients with unresectable carcinoma of the pancreas, the role of prophylactic gastroenterostomy is debatable. Many workers still recommend combined biliary and enteric bypass at the initial surgery despite known complications of gastroenterostomy.Method: We conducted a prospective study in 17 patients with carcinoma of the pancreas without mechanical obstruction, to evaluate the presence of functional gastroparesis by doing a radionuclide, solid‐phase scintigraphy. We tried to correlate delayed gastric emptying (DGE) with symptoms of gastric outlet obstruction, serum bilirubin level, stage of disease and intraoperative assessment.Results: Of the 17 patients, seven (41.2%) had DGE. No correlation was found between delayed emptying and symptoms, serum bilirubin level, stage of disease or intraoperative assessment for gastric outlet obstruction.Conclusion: Solid‐phase gastric emptying scintigraphy may help to detect DGE in patients with carcinoma of the pancreas preoperatively. Patients with DGE may be chosen for prophylactic gastrojejunostomy during the initial biliary bypass.
LAPAROSCOPIC RESECTION FOR COLORECTAL ADENOCARCINOMA IN PATIENTS WITH PREVIOUS ABDOMINAL SURGERY
Authors: Kwok S.Y. , Chung C.C. , Tsang W.W.C. , Chan E.S.W. , Li M.K.W. 
Published: September 2010

Objective: We compared laparoscopic colorectal resection in patients with previous abdominal surgery to those with ‘virgin abdomen’. The aim was to find out whether adhesions from previous abdominal surgery affected laparoscopic colorectal resection.Methods: We performed a retrospective review of the patients who underwent laparoscopic anterior resection (n = 91) and laparoscopic abdomino‐perineal resection (n = 30) during the period from January 1996 to May 2000. Those patients with previous abdominal surgery were compared to those without previous abdominal surgery. The operating time, blood loss, length of hospital stay, complication and conversion rate was compared.Results: Thirty‐one patients had previous abdominal surgery (study group), whereas 90 patients had no previous abdominal surgery (control group). The operating time, blood loss and length of hospitalization were similar in both groups. The complication and conversion rate were higher in the study group but the difference is not significant.Conclusion: Laparoscopic colorectal resection in patients with previous abdominal surgery is safe and gives comparable results to those without previous abdominal surgery. Previous abdominal surgery should not be considered as a contraindication for laparoscopic colorectal resection.
Cataract surgery practice and endophthalmitis prevention by Australian and New Zealand ophthalmologists
Authors: Rosha Deepinder S , Ng Jonathon Q , Morlet Nigel , Boekelaar Michelle , Wilson Shea , Hendrie Delia , Semmens James B 
Published: September 2010

AbstractPurpose:  Our aim was to examine current cataract surgery practice and the methods of chemoprophylaxis used in Australia and New Zealand, and to determine if these factors were related to self‐reported incidence rates of postoperative endophthalmitis.Methods:  All Fellows and trainees of the Royal Australian and New Zealand College of Ophthalmologists were surveyed about their cataract surgery practices and methods of chemoprophylaxis for the prevention of postoperative endophthalmitis. Associations between self‐reported incidence rates of endophthalmitis and clinical practice were examined using multivariate Poisson regression modelling.Results:  There were 731 respondents (81.6% of 896 surveyed) to the survey. Respondents reported a total of 162 120 cataract operations and 92 cases of endophthalmitis in 2003, a cumulative incidence of 0.057%. The self‐reported incidence of endophthalmitis varied from 0.034% in Victoria to 0.56% in the Northern Territory. Topical antibiotics were used preoperatively by 46.7% compared with 97.4% postoperatively; while only 44.1% used subconjunctival antibiotics. The routine use of subconjunctival antibiotic halved the self‐reported incidence of postoperative endophthalmitis (incidence rate ratio 0.53, 95% confidence interval 0.30–0.92).Conclusions:  Subconjunctival antibiotics may be beneficial in the prevention of endophthalmitis after cataract surgery.