bluuebunny/crossref_metadata_2025_split huggingface dataset:
INCREASED CALCIUM SEQUESTRATION BY SARCOPLASMIC RETICULUM IN SMALL MUSCULAR ARTERIES IN YOUNG SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Toyoda Yasuaki , Shima Hiroki , Sasajima Hisashi , Nishio Ichiro 
Published: June 2007

Summary1. Sarcoplasmic reticulum (SR) in small resistance arteries plays a role in the regulation of the cytosolic free calcium concentration by sequestration of calcium from cytoplasm.2. To examine the contribution of calcium (Ca2+) sequestration by the SHR to both contraction and relaxation in young spontaneously hypertensive rats (SHR), we measured evoked tension before and after depletion of SR Ca2+ stores in the rings of the first branch of superior mesenteric artery in 5 week old SHR and age‐matched Wistar‐Kyoto (WKY) rats. Contractile responses were induced by 40 mmol/L potassium and 10 mmol/L caffeine before and after the treatment with ryanodine or thapsigargin, which depletes SR calcium stores.3. The magnitude of potassium‐induced contraction was almost the same in both strains.4. Ryanodine and thapsigargin did not affect the resting tension and almost decreased caffeine‐induced contraction in both strains.5. After the treatment with ryanodine or thapsigargin, the magnitude and the rate of potassium‐induced contraction were augmented greatly in SHR, but not in WKY.6. The relative relaxation rate after exposure of potassium was significantly slowed in SHR by ryanodine or thapsigargin, but only slightly in WKY.7. These results suggest that Ca2+ sequestration by the SR in SHR was greater than in WKY. Therefore, it is concluded that SR plays an important role in preventing the development of hypertension in SHR via a buffering effect on the elevation of cytosolic free Ca2+.
EXPRESSION OF SARCOPLASMIC RETICULUM Ca2+‐ATPase mRNA IN THE HYPERTROPHIED HEART OF YOUNG SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Ohta Kensuke , Kim Shokei , Hamaguchi Akinori , Miura Katsuyuki , Yukimura Tokihito , Iwao Hiroshi 
Published: June 2007

Summary1. Recent evidence indicates that cardiac hypertrophy induced by pressure overload is associated with a decrease in sarcoplasmic reticulum (SR) Ca2+‐ATPase of myocytes, which may contribute to a diastolic dysfunction of the heart by causing intracellular Ca2+ overload. To elucidate whether or not this is also the case in genetic hypertension, we examined cardiac mRNA levels of SR Ca2+‐ATPase in 11 week old spontaneously hypertensive rats (SHR) by northern blot analysis.2. Furthermore, to test the effects of short‐term inhibition of the renin‐angiotensin system on its expression, we treated 10 week old SHR with angiotensin‐converting enzyme inhibitors (alacepril and imidapril) or an AT1 receptor antagonist (SC‐52458) for 7 days.3. Though the left ventricular weight of SHR was significantly higher than that of Wistar‐Kyoto (WKY) rats (277 ± 6 vs 237 ± 4mg/100g bodyweight, respectively, P < 0.05), the level of SR Ca2+‐ATPase mRNA showed no difference between SHR and WKY at this age.4. Moreover, the aforementioned three drugs did not at all affect the SR Ca2+‐ATPase expression of SHR.5. Thus, the expression of SR Ca2+‐ATPase was not down‐regulated in the heart of 11 week old SHR, and seemed not to be mediated by angiotensin AT1 receptor at this age. Since some evidence on pressure‐overloaded cardiac hypertrophy indicate that the decrease in SR Ca2+‐ATPase expression occur in prominent hypertrophy and in the failured heart, further studies on cardiac SR Ca2+‐ATPase expression in more aged SHR will be required.
NERVE GROWTH FACTOR, VESSEL INNERVATION AND HYPERTENSIVE PROGRESSION IN THE INBRED DAHL SS/Jr AND SR/Jr RATS
Authors: Tuttle Jeremy B. , Stewart Jeanine S. , Spitsbergen John M. , McCarty Richard M. 
Published: June 2007

Summary1. To test whether the inbred Dahl salt‐sensitive hypertensive rat strain shares disturbed vessel innervation with the spontaneously hypertensive rat (SHR) model, highly innervated and sparsely innervated tissues from the SR/Jr and SS/Jr strains at several ages were assayed for tissue norepinephrine (NE) content and nerve growth factor (NGF).2. Only two significant differences were found: (i) 1 week old SS/Jr rat kidneys had more NGF than SR/Jr kidneys; and (ii) six week old mesenteric arteries from SS/Jr contained significantly more NE than those in the SR/Jr animals.3. The differences are in the expected direction for vessel hyperinnervation as a consequence of high vessel NGF, but the data do not support the hypothesis of a central role for vessel NGF and innervation in the hypertensive progression of the Dahl strain, The vessels of young Dahl inbred rat strains do not display the same degree of vessel hyperinnervation associated with hypertension as found in the young SHR compared to WKY strains.4. The Dahl strain may lack the disturbed NGF metabolism of the SHR. This might suggest that the Dahl inbred strains and the SHR represent two distinct genetic mechanisms that predispose to hypertension via essentially independent processes and that all forms will evidence at least mildly altered vessel innervation.
PHARMACOLOGICAL CHARACTERIZATION AND AUTORADIOGRAPHIC LOCALIZATION OF DIHYDROPYRIDINE‐TYPE CALCIUM CHANNELS IN THE KIDNEY OF SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Amenta Francesco , Liu Aiping , Sabbatini Maurizio 
Published: June 2007

Summary1. The pharmacological profile and the microanatomical localization of Ca2+ channels of the L‐type were analysed in sections of the kidney of Wistar‐Kyoto (WKY) rats and of spontaneously hypertensive rats (SHR) of different ages.2. [3H]‐Nicardipine was used as a ligand. It was bound to sections of rat kidney in a manner consistent with the labelling of Ca2+ channels of the L‐type. The density of [3H]‐nicardipine binding sites was similar in WKY rats of different ages and in SHR of 2 and 4 months, but was significantly increased in SHR of 6 months.3. Light microscope autoradiography revealed the highest density of binding sites in the tubular portion of the nephron and to a lesser extent within smooth muscle of renal arteries and renal corpuscles. In SHR of 4 and 6 months the density of [3H]‐nicardipine binding sites was increased within the epithelium of proximal tubules and of the loop of Henle and decreased in renal corpuscles in comparison with WKY rats or 2 month old SHR.4. These results show that the density of Ca2+ channels of the L‐type increases with the worsening of hypertension in SHR. The observation of a different sensitivity to hypertension of Ca2+ channels located in the various portions of the nephron indicates the usefulness of light microscope autoradiography for assessing hypertension‐related changes of Ca2+ channels in the kidney.
DIFFERENT CHOLESTEROL DEPOSITION IN AORTA OF DAHL SALT‐SENSITIVE RATS AND SPONTANEOUSLY HYPERTENSIVE RATS FED A HIGH‐CHOLESTEROL DIET
Authors: Yamaguchi Y. , Kitagawa S. , Kwon Y. , Shinozuka K. , Kunitomo M. 
Published: June 2007

Summary1. We compared the serum and aortic lipid levels in spontaneously hypertensive rats (SHR) and Dahl salt‐sensitive rats (DSR) fed a high‐cholesterol (HC) diet.2. In SHR fed the HC diet, the serum cholesterol level significantly increased, but no aortic cholesterol deposition was observed.3. The serum cholesterol level in DSR fed the HC diet markedly increased compared to that in DSR fed the basal diet, and this change was greater with the diet containing 8% NaCl than 0.4% NaCl. A significant increase in the content of aortic cholesterol, notably cholesteryl ester, was observed in only DSR fed the HC diet containing 8% NaCl.4. These results suggest that the combination of hyper‐cholesterolaemia with salt‐induced hypertension acts as a greater risk factor for atherosclerosis than that with genetic hypertension.
PATHOGENESIS OF LACUNA‐LIKE CYST FORMATION AND DIFFUSE DEGENERATION OF THE WHITE MATTER IN THE BRAIN OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Hazama Fumitada , Chue Chin‐Hui , Kataoka Hideo , Sasahara Maskiyo , Amano Shigeru 
Published: June 2007

Summary1. In an attempt to clarify the developmental mechanisms of lacuna and diffuse degeneration of the white matter in the brain in chronic hypertension, we investigated histologically the cerebral changes and histochemically, as well as biochemically, the lysosomal enzymes in the brain of stroke‐prone spontaneously hypertensive rats (SHRSP).2. The most prominent advanced lesions observed in SHRSP were cyst formation in the cortex and subcortical white matter, and diffuse degeneration of the white matter. On the other hand, the early cerebral changes were all related to blood‐brain barrier dysfunction. The localization of cystic lesions and degeneration of the white matter corresponded very well with the extent of brain oedema demonstrated by immunostaining for leaked fibrinogen. All lysosomal enzyme activities in the adult SHRSP, both in the cortex and white matter, were higher than those in the controls. Histochemical investigation showed that SHRSP had an increased number of cells, reactive astrocytes and microglial cells, with positive reaction to lysosomal enzymes in the oedematous portion.3. These findings suggest that chronic oedema due to blood‐brain barrier dysfunction causes cystic changes as well as diffuse degeneration of the white matter, and that activated lysosomal enzymes in the reactive astrocytes and microglia play an important role in the development of such hypertensive lesions.
GENE EXPRESSION OF PROSTACYCLIN RECEPTOR IN THE HYPERTROPHIED HEART OF SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Nakagawa O. , Sasaki Y. , Tanaka I. , Usui T. , Sando T. , Muro S. , Mori K. , Itoh H. , Yoshimasa T. , Narumiya S. , Nakao K. 
Published: June 2007

Summary1. Prostacyclin elicits potent vasodilation and inhibition of platelet aggregation through binding to its membrane receptor. The impairment of prostacyclin receptor activity is implicated in various human cardiovascular diseases. We recently succeeded in molecular cloning of cDNA for the mouse, rat, and human prostacyclin receptors.2. In the present study, we examined the mRNA expression of the prostacyclin receptor in various rat tissues, and further investigated its gene expression in the hypertrophied cardiac ventricles of stroke‐prone spontaneously hypertensive rats (SHRSP).3. In rat tissues, a single RNA band of approximately 3.7 kb was detected by northern blotting analysis using rat prostacyclin receptor cDNA as a probe. In adult Wistar rats, abundant mRNA expression was observed in the aorta, lung and spleen. Substantial amounts of transcript were expressed in the heart, pancreas, thymus and stomach. In contrast, no mRNA expression was detected in the brain.4. We further examined the mRNA expression of the prostacyclin receptor in the ventricles of 21 week old SHRSP. The ventricles of SHRSP showed remarkable hypertrophy, compared with those of age‐matched Wistar‐Kyoto (WKY) rats. The expression of prostacyclin receptor mRNA in the hypertrophied ventricles of SHRSP was almost equivalent to that in the ventricles of WKY.5. The present study revealed the gene expression of the prostacyclin receptor in various rat tissues, and further demonstrated the receptor mRNA expression in hypertensive cardiac hypertrophy. The present study will give a clue to investigate the clinical implication of prostacyclin and its receptor.
EPIDEMIOLOGICAL INVESTIGATION OF INSULIN RESISTANCE SYNDROME (SYNDROME X) IN A CITY IN JAPAN
Authors: Imamura Minoru , Kishitani Yuzuru , Saika Toyohiko , Iio Kazuya , Ikami Hitoshi , Kagita Atushi , Nishimura Akiyoshi , Masuda Katuhiko , Ohno Yasuhiro , Aoki Norihiko 
Published: June 2007

Summary1. In order to study the prevalence of insulin resistance syndrome (syndrome X) in Japanese subjects, inhabitants aged above 40 years living in Osaka‐Sayama city from September 1992 through December 1993 were investigated. The population‐based study was performed on 2498 subjects (661 males and 1837 females) constituting 10.9% of the total population aged above 40 years.2. The prevalence of glucose intolerance was 8.7% (n= 218) in 2498 subjects. The prevalence of hypertension was 36.9% (n= 923) and that of hypertriglyceridaemia was 19.0% (n= 475). The prevalence of syndrome X as characterized by an association of glucose intolerance, hypertension and hypertriglyceridaemia was 1.6% (n= 39) in all subjects examined and 17.4% in subjects showing glucose intolerance.3. Fasting serum insulin levels were significantly higher in patients with syndrome X than in normal subjects. Furthermore, the levels were significantly correlated with blood levels of frucutosamine, fasting glucose and triglyceride, and with body mass index as well.4. In conclusion, insulin resistance syndrome (syndrome X) is also found among the larger Japanese population, and fasting serum insulin levels can be a useful marker of this metabolic disorder.
ANTIHYPERTENSIVE EFFECTS, DETERMINED BY A TELEMETRY METHOD, OF TRICHLOROMETHIAZIDE AND 7–O‐ETHYLFANGCHINOLINE, A DERIVATIVE OF TETRANDRINE, IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kawashima K. , Negishi T. , Amano H. , Fujimoto K. , Suzuki T. , Fujii T. 
Published: June 2007

Summary1. The antihypertensive effects of 10 mg/kg trichloromethiazide (TCM), 10 mg/kg 7–O‐ethylfangchinoline (7–O‐EFC) and the combination of these drugs given orally once daily for 2 weeks were investigated by measuring the blood pressure (BP), heart rate (HR) and activity in conscious, freely moving spontaneously hypertensive rats (SHR) fitted with a telemetry device.2. Clear diurnal rhythms of the HR and activity in synchrony with the light/dark cycle were observed during therapy, whereas the BP rhythm was obscure.3. Alone, TCM and 7–O‐EFC produced slight and insignificant reductions of 24 h mean BP, whereas in combination they produced an additive and significant BP reduction, compared with the vehicle‐treated controls, from the third day of therapy. The BP reduction induced by the combination of these drugs during the dark phase was more marked than that during the light phase.4. None of the drug therapies affected the HR and activity diurnal rhythms.5. The results of the present study demonstrate that the telemetry method is useful for monitoring the antihypertensive effects of drugs in SHR under physiological conditions with minimal stress.
EFFECTS OF (‐)‐EPIGALLOCATECHIN‐3‐O‐GALLATE (GREEN TEA TANNIN) ON THE LIFE SPAN OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Uchida S. , Ozaki M. , Akashi T. , Yamashita K. , Niwa M. , Taniyama K. 
Published: June 2007

Summary1. Effect of (‐)‐epigallocatechin‐3‐O‐gallate (EGCG), a condensed tannin isolated from green tea leaves, on the life span and hypertensive lesions in the stroke‐prone spontaneously hypertensive rat (SHRSP) was compared with that of persimmon tannin.2. Long‐term administration of either 0.5% EGCG or 0.5% persimmon tannin to SHRSP inhibited the incidence of stroke and prolonged the life span, but did not affect the blood pressure.3. These results indicate that EGCG may prevent incidence of stroke due to the radical scavenging action and inhibition of lipid peroxidation, and may result in prolonging the life span of SHRSP, as in the case of persimmon tannin.
DIETARY DOCOSAHEXAENOIC ACID (22:6n‐3) PREVENTS THE DEVELOPMENT OF HYPERTENSION IN SHRSP
Authors: Kimura S. , Minami M. , Saito H. , Kobayashi T. , Okuyama H. 
Published: June 2007

Summary1. We previously reported that hypertension in stroke‐prone spontaneously hypertensive rats (SHRSP) caused renal membrane phospholipid degradation. Renal phospholipase A2 activity increased and membranous phospholipids decreased along with age in SHRSP. Membranous abnormalities induced by membrane fluidity and calcium permeability changes may contribute to the elevation of blood pressure in SHRSP. DHA, a major component of fish oil, constitutes a part of membrane phospholipid acylchains.2. The purpose of this study was to clarify the effect of DHA on the relationship between the renal function and the development of hypertension in SHRSP.3. Six week old male SHRSP were fed a semi‐purified diet supplemented with DHA (0,1 and 5%) for 14 weeks.4. The systolic blood pressure of control SHRSP (DHA 0%) significantly increased from 120.2 mmHg to 202.9 mmHg. This increase in systolic blood pressure was significantly inhibited in a dose‐dependent manner by 1 and 5% DHA diet to 167.8 and to 149.8 rnmHg, respectively.5. Serum creatinine concentration and blood urea nitrogen (BUN) were significantly lower in DHA (5%)‐treated SHRSP than in the control SHRSP.6. These results indicate that DHA prevents the development of hypertension in SHRSP, which is associated with changes in renal function.
LIPID‐REGULATING ACTION OF GEMFIBROZIL IN THE STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Ogawa Hiroshi , Tasaka Masatsuna 
Published: June 2007

Summary1. Gemfibrozil (Lopid®) is extensively used as lipid‐regulating agent in the Western World, and its beneficial effect is demonstrated in human studies such as the Helsinki Heart Study. However, the mechanism of its hypolipidaemic action is not fully understood. In the present paper, to elucidate the hypolipidaemic mechanism, we examined the effects of gemfibrozil on lipid metabolism in the normocholesterolaemic and hypercholesterolaemic stroke‐prone spontaneously hypertensive rat (SHRSP).2. Gemfibrozil effectively increased high density lipoprotein (HDL) subfraction rich in apoE (apoE‐HDL) and significantly decreased very low density lipoprotein (VLDL) in normocholesterolaemic SHRSP. In the liver of normocholesterolaemic SHRSP, gemfibrozil significantly reduced the activity of micro‐somal acyl‐CoA: cholesterol acyltransferase.3. Gemfibrozil markedly reduced atherogenic & very low density lipoprotein (β‐VLDL) and low density lipoprotein (LDL) in hypercholesterolaemic SHRSP fed a high‐fat and high‐cholesterol diet (HFC diet). On the other hand, it significantly increased the contents of apoA‐I, A‐IV and E in the HDL fraction compared with the control group, suggesting that gemfibrozil effectively increases anti‐atherogenic HDL subfractions rich in apoA‐I, A‐IV or E. In the liver of hypercholesterolaemic SHRSP, gemfibrozil markedly prevented lipid accumulation.
INSULIN‐INDUCED RENAL DYSFUNCTION IN REGULAR SABRA RATS
Authors: Bursztyn Michael , Ben‐Ishay Drori , Mekler Judith , Raz Itamar 
Published: June 2007

Summary1. We tested the effects of chronic hyperinsulinaemia on renal function. Hyperinsulinaemia, in the range of 1.5–4 times the control levels, was achieved using a sustained‐release insulin implant. Sham‐treated rats served as controls.2. Experiment 1. Acute saline loading: seven sham and seven hyperinsulinaemic rats received an acute saline load (4mL/100g). Two h post‐load urea and creatinine excretion rats were (μmol/min) 15 ± 5 and 9 ± 4, and 0.17 ± 0.05 and 0.10 ± 0.04, respectively;P < 0.05 for both.3. Experiment 2. Chronic saline loading: 12 sham‐ and 24 insulin‐treated rats drank saline for 8 weeks plus 4% NaCl in the food for 2 more weeks. By week 10 plasma creatinine (μmol/L) was 62 ± 12 and 78 ± 13, and creatinine clearance (mL/min) was 1.9 ± 0.5 and 1.5 ± 0.4, respectively; P < 0.05 for both.4. Experiment 3. Regular diet: 10 sham‐ and 14 insulin‐treated rats had, by week 8, plasma creatinine (μmol/L) of 75 ± 34 and 96 ± 37 and creatinine clearance (mL/min) of 1.260 ± 0.025 and 0.97 ± 0.22, respectively; P < 0.02 for both. Bodyweight, resting blood pressure and urinary Na+ and K+ excretion were comparable in sham‐ and insulin‐treated rats.5. In three experimental settings long‐term hyperinsulinaemia was associated with a subtle but significant renal dysfunction. This finding may be related to the aetiology of renal complications of hypertension and diabetes mellitus, both of which are insulin‐resistant and hyperinsulinaemic states.
INFLUENCE OF LONG‐TERM TREATMENT WITH THE DIHYDROPYRIDINE‐TYPE CALCIUM ANTAGONIST NICARDIPINE ON RENAL MICROANATOMICAL CHANGES IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Amenta Francesco , Abbate Francesco , Cavallotti Carlo , Ciriaco Emilia , Ferrante Fabio , Sabbatini Maurizio 
Published: June 2007

Summary1. The influence of hypertension and treatment with the dihydropyridine‐type Ca2+ antagonist, nicardipine, on the structure of the kidney was assessed in spontaneously hypertensive rats (SHR) of 12 weeks of age. Treatment went for 8 weeks with a daily oral dose of 1 mg/kg of nicardipine.2. Control SHR exhibited hypertension and microanatomical vascular and glomerular changes. Vascular changes consisted of a thickening of the tunica media and decreased luminal area of medium‐ and small‐sized intrarenal artery branches. Glomerular changes included glomerulosclerosis and atrophy of varying degrees.3. Administration of nicardipine significantly reduced blood pressure. The drug also decreased the thickening of tunica media and luminal narrowing of renal artery branches as well as the degree of glomerular injury in SHR.4. These data indicate that nicardipine treatment is able to control elevated blood pressure in SHR, and to counter hypertension‐dependent microanatomical impairment of the kidney. This suggests that the compound exerts a protective effect on hypertensive kidney.
EFFECTS OF BENIDIPINE, A LONG‐ACTING CALCIUM ANTAGONIST, ON RENAL FUNCTIONS IN ANAESTHETIZED SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Nomura H. , Kusaka H. , Karasawa A. 
Published: June 2007

Summary1. The effects of benidipine, a long‐acting calcium antagonist, on renal functions were determined in anaesthetized spontaneously hypertensive rats (SHR), as compared with those of amlodipine.2. Benidipine at 3 and 10 μg/kg (i.v.) significantly increased urine volume, sodium (Na) and potassium (K) excretions with no change in creatinine clearance (C‐CRE). The increase in K excretion was relatively slight. Benidipine increased p‐amino‐hippuric acid clearance (C‐PAH) without any change in C‐CRE and, thus, decreased filtration fraction (FF).3. On the other hand, amlodipine at 300 μg/kg (i.v.) significantly increased Na and K excretions, but did not change FF.4. Thus benidipine, but not amlodipine, can dilate glomerular efferent arteriole as well as afferent arteriole in SHR. It is, therefore, expected that benidipine would not induce intraglomerular hypertension, which could result in the progression of glomerular injury.5. Benidipine at 3 μg/kg (i.v.) increased lithium clearance, while it decreased CRE concentration and increased Na concentration in the stop‐flow urine from the distal tubule.6. These results suggest that benidipine produces diuresis by the inhibition of water and Na reabsorption at both the proximal and the distal tubules.
PROTECTIVE EFFECTS OF MANIDIPINE ON SPERMATOGENESIS IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Akagashi Keigo , Itoh Naoki , Kumamoto Yoshiaki , Tsukamoto Taiji , Suzuki Tsuneyuki , Ohta Yoshio 
Published: June 2007

Summary1. We evaluated the protective effects of manidipine on spermatogenic damage induced by the hypertensive vascular changes in stroke‐prone spontaneously hypertensive rats (SHRSP).2. Blood pressure reached more than 250 mmHg in SHRSP at 15 weeks of age, and thereafter the hypertensive changes in testicular arterioles developed. Manidipine reduced both the blood pressure and the hypertensive vascular changes.3. Although immature and mature spermatids greatly diminished in SHRSP at 23 weeks of age, manidipine could preserve almost normal spermatogenesis even at 23 weeks of age. Transferrin concentration in testicular cytosol, which was considered to be indicative of the Sertoli cell function, in SHRSP with manidipine administration was significantly higher than that in SHRSP with no treatment at 23 weeks of age.4. In conclusion, manidipine could prevent the development of the hypertensive changes in intratesticular arterioles and maintain normal Sertoli cell function. As a result, manidipine protected spermatogenic damage in SHRSP.