Clinical and experimental pharmacology & physiology. Supplement最新文献_第9页

Intestinal calcium absorption and response of calcium regulating hormones in the stroke-prone spontaneously hypertensive rat as a model of osteoporosis. 卒中易发自发性高血压大鼠肠道钙吸收及钙调节激素反应作为骨质疏松模型。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02899.x

S Fukuda, S Tsuchikura, H Iida, K Ikeda, Y Nara, Y Yamori

引用次数: 5

Influence of hypertensive vascular changes in intratesticular arteries on spermatogenesis in SHRSP. 睾丸内动脉高血压血管改变对SHRSP患者精子发生的影响。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02852.x

N Itoh, K Akagashi, Y Kumamoto, T Suzuki, Y Ohta

引用次数: 8

Receptor density in the rat heart following ischaemia and prolonged reperfusion. 缺血和长时间再灌注后大鼠心脏受体密度的变化。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02916.x

W de Jong, L Lukovic, C R Jones, M A Petty

引用次数: 4

Mechanisms for preserved cerebrovascular autoregulation during hypertension in rats after sinoaortic denervation. 主动脉去神经后大鼠高血压期间保留的脑血管自身调节机制。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02978.x

W T Talman, D N Dragon

{"title":"Mechanisms for preserved cerebrovascular autoregulation during hypertension in rats after sinoaortic denervation.","authors":"W T Talman, D N Dragon","doi":"10.1111/j.1440-1681.1995.tb02978.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02978.x","url":null,"abstract":"1. Cerebral blood flow (CBF) and cerebrovascular resistance (CVR) autoregulate to higher levels of arterial pressure (AP) in rats after sinoaortic denervation (SAD) than in intact rats. 2. Potential mechanisms for this phenomenon were studied by monitoring CBF by laser flowmetry while increasing AP in rats after: (i) SAD; (ii) SAD plus bilateral removal of the superior cervical ganglia; (iii) SAD plus interruption of all renal vessels and nerves (renal isolation); (iv) SAD plus sympathectomy and renal isolation; and (v) intravenous treatment with the nitric oxide synthase inhibitor L-nitroarginine (LNA). 3. Compared to intact control rats autoregulation persisted to higher absolute levels of AP in SAD rats with isolation of the kidneys and resistance did not fall significantly below that in rats with SAD alone. 4. Effects of SAD on autoregulation were not altered by combining renal isolation with an interruption of sympathetics. 5. LNA did not affect the baroreflex but blocked a breakthrough of autoregulation even at a maximal mean AP (MAP) of 189 +/- 2 mmHg. 6. Breakthrough occurred in animals pretreated with LNA plus L-arginine but not in animals given LNA plus D-arginine. 7. These data are consistent with a role of the baroreflex in the expression of breakthrough and suggest that breakthrough may result from release of nitric oxide or a nitric oxide donor.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S77-9"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02978.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Effects of a high-salt diet on tissue noradrenaline concentrations in Dahl salt-resistant and -sensitive rats. 高盐饮食对达尔盐抗性和敏感大鼠组织去甲肾上腺素浓度的影响。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02886.x

Q H Chen, H Morita, Y Nishida, H Hosomi

{"title":"Effects of a high-salt diet on tissue noradrenaline concentrations in Dahl salt-resistant and -sensitive rats.","authors":"Q H Chen, H Morita, Y Nishida, H Hosomi","doi":"10.1111/j.1440-1681.1995.tb02886.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02886.x","url":null,"abstract":"1. We measured systolic arterial pressure (SAP) and tissue noradrenaline concentrations (tNA) of 16 organs (heart, kidney, aorta, brain stem, pancreas, spleen, stomach, jejunum, ileum, colon, lung, muscle, cerebrum, liver, bone, salivary gland) in Dahl salt-resistant (DSR) and -sensitive rats (DSS) fed 0.4 (0.4%) or 8% salt diet (8%) from 5 weeks old until the age of 5, 7, 9 and 11 weeks. 2. SAP increased in DSS with the 8% salt diet. An increased rate of SAP of DSS with the 0.4% salt diet was larger than DSR with the 0.4% diet. In DSR with 0.4%, tNA tended to increase from 5 weeks old except in the bone, which may have been the result of ageing. In DSS with 0.4%, tNA did not increase from 5 weeks old. DSS showed salt-sensitivity even to 0.4%. 3. tNA of the heart and kidney of both DSS and DSR with 8% were lower than 0.4%. These organs are high-salt-sensitive organs. tNA of the aorta, spleen, stomach, jejunum, ileum, and colon of DSS with 8% were lower than 0.4%, but not DSR. These organs are medium salt-sensitive organs. tNA of the pancreas of DSS with 8% was lower than 0.4% which was not different from DSR with 0.4 and 8%. The pancreas is a low salt-sensitive organ. tNA of the lung, muscle, cerebrum, liver, bone and salivary gland did not show any differences between 0.4 and 8% in DSS as well as DSR. These organs are not salt-sensitive organs. 4. There were large organ differences in tNA among organs studied. There were large organ differences in decrease rate of tNA in response to a high-salt diet. The organ function and the period of salt diet influence tNA.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S209-11"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02886.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Effects of recombinant human erythropoietin on blood pressure and renal function in SHR with chronic renal failure. 重组人促红细胞生成素对SHR合并慢性肾功能衰竭患者血压和肾功能的影响。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02865.x

M Kohzuki, M Yasujima, M Kanazawa, K Yoshida, T Sato, K Abe

{"title":"Effects of recombinant human erythropoietin on blood pressure and renal function in SHR with chronic renal failure.","authors":"M Kohzuki, M Yasujima, M Kanazawa, K Yoshida, T Sato, K Abe","doi":"10.1111/j.1440-1681.1995.tb02865.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02865.x","url":null,"abstract":"1. The effects of chronic administration of erythropoietin (EPO) on blood pressure and renal function in rats with ablation of renal mass were assessed. 2. Spontaneously hypertensive rat were subjected to 5/6 nephrectomy (5/6Nx). Four weeks after the operation, the rats were randomly allocated to vehicle, EPO 20IU/kg i.p., or EPO 100 IU/kg i.p. (both given twice a week) for 4 weeks. 3. Marked anaemia was noted in SHR-5/6Nx. EPO caused a significant increase in haematocrit at a high dose but not at a low dose. A dose dependent relationship was noted in the EPO-induced rise in the systolic blood pressure. 4. EPO dose-dependently increased urinary protein excretion. It also increased blood urea nitrogen and serum creatinine levels. 5. These results suggest that EPO ameliorates anaemia and severely accelerates renal failure in SHR-5/6Nx. They also suggest that anaemia can be a haemodynamically favorable adaptation to chronic renal disease and that its correction may have adverse renal haemodynamic and structural consequences.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S165-6"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02865.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Lipid-regulating action of gemfibrozil in the stroke-prone spontaneously hypertensive rat. 吉非罗齐对卒中易发自发性高血压大鼠的调脂作用。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02933.x

H Ogawa, M Tasaka

{"title":"Lipid-regulating action of gemfibrozil in the stroke-prone spontaneously hypertensive rat.","authors":"H Ogawa, M Tasaka","doi":"10.1111/j.1440-1681.1995.tb02933.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02933.x","url":null,"abstract":"1. 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 hypersensitive 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 microsomal acyl-CoA:cholesterol acyltransferase. 3. Gemfibrozil markedly reduced atherogenic beta-very low density lipoprotein (beta-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.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S313-5"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02933.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20026717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Expression of protein kinase C gene in the brain and heart of spontaneously hypertensive rats. 蛋白激酶C基因在自发性高血压大鼠脑和心脏中的表达。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02884.x

P J Gao, G S Zhao, X Y Yuan, H F Zhao, F Chen, S S Chen

{"title":"Expression of protein kinase C gene in the brain and heart of spontaneously hypertensive rats.","authors":"P J Gao, G S Zhao, X Y Yuan, H F Zhao, F Chen, S S Chen","doi":"10.1111/j.1440-1681.1995.tb02884.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02884.x","url":null,"abstract":"1. The aim of this study was to investigate protein kinase C (PKC) gene expression in spontaneously hypertensive rats (SHR). 2. Using the PKC oligodeoxyribonucleotide probes (gamma, epsilon), we detected PKC isoforms gene expression in the heart and brain of 4 and 20 week old SHR with those of age-matched Wistar-Kyoto (WKY) rats by northern blot analysis. 3. In the cerebral cortex, there were significantly increased levels of expression of the Ca2+-dependent isoform PKC-gamma in 4 and 20 weeks SHR compared with that of WKY, while Ca2+ -independent isoform PKC-epsilon did not differ between SHR and WKY. 4. In ventricular myocytes, there was a significant expression of the Ca2+-independent isoform PKC-epsilon in 4 and 20 week old SHR compared with that of WKY, while Ca2+ -dependent isoform PKC-gamma could not be detected in the same extracts of SHR or WKY. 5. We conclude that both of the Ca2+ -dependent and Ca2+ -independent PKC could be involved in the pathogenesis of SHR. Ca2+ -dependent PKC-gamma may be mainly involved in the modulation of blood pressure in the level of the central nervous system, while Ca2+ -independent PKC-epsilon could be related to the genetic myocardial hypertrophy.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S204-6"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02884.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20027122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Protective effects of manidipine on spermatogenesis in stroke-prone spontaneously hypertensive rats. 曼尼地平对卒中易发自发性高血压大鼠精子发生的保护作用。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02947.x

K Akagashi, N Itoh, Y Kumamoto, T Tsukamoto, T Suzuki, Y Ohta

{"title":"Protective effects of manidipine on spermatogenesis in stroke-prone spontaneously hypertensive rats.","authors":"K Akagashi, N Itoh, Y Kumamoto, T Tsukamoto, T Suzuki, Y Ohta","doi":"10.1111/j.1440-1681.1995.tb02947.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02947.x","url":null,"abstract":"1. 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.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S342-4"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02947.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20027129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Brief treatment of SHR with an ace inhibitor fails to cause long-term normotension but markedly increases mortality. 用ace抑制剂短暂治疗SHR不能引起长期的正常血压，但明显增加死亡率。

Clinical and experimental pharmacology & physiology. Supplement Pub Date : 1995-12-01 DOI: 10.1111/j.1440-1681.1995.tb02948.x

L Lan, R Di Nicolantonio, C Bramich, T O Morgan

{"title":"Brief treatment of SHR with an ace inhibitor fails to cause long-term normotension but markedly increases mortality.","authors":"L Lan, R Di Nicolantonio, C Bramich, T O Morgan","doi":"10.1111/j.1440-1681.1995.tb02948.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.1995.tb02948.x","url":null,"abstract":"1. We examined the effect of three doses (0.03, 0.3 and 3 mg/kg per day) of the angiotensin converting enzyme (ACE) inhibitor, perindopril, on the long-term blood pressure of spontaneously hypertensive rats (SHR) of the Okamoto strain after treatment during the developmental stage of hypertension development. 2. While the 0.03 mg/kg per day dose, given between the ages of 4-10 weeks of age, failed to lower blood pressure, the two higher doses resulted in normotension over this treatment period as did the highest dose given between the ages of 4-20 weeks of age. 3. Only the 0.3 mg/kg per day dose resulted in a moderate (17%) long-term fall in blood pressure upon cessation of treatment when compared to untreated SHR controls. The highest dose, given over the 4-20 week period resulted in a significant rebound hypertension above the blood pressure level of untreated, control SHR. 4. The 3 mg/kg per day dose, whether given over the 4-10 or 4-20 week treatment period, resulted in 100% mortality in these groups by 52 weeks of age. There were no deaths in the groups receiving the two lower doses. 5. We conclude that treatment of SHR with perindopril during the developmental phase of hypertension development results in only a modest fall in long-term blood pressure upon cessation of treatment and that the relationship between the dose of this ACE inhibitor and long-term blood pressure is not linear. The 100% mortality in the two groups receiving the highest dose of perindopril may be due to either a toxic action of this drug or vascular rupture due to insufficient hypertrophy for the rapid rise in blood pressure upon cessation of treatment.","PeriodicalId":75710,"journal":{"name":"Clinical and experimental pharmacology & physiology. Supplement","volume":"22 1","pages":"S345-6"},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.1995.tb02948.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20027130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7