Electrolyte and Blood Pressure最新文献_第10页

Mechanisms of the effects of acidosis and hypokalemia on renal ammonia metabolism. 酸中毒和低钾血症对肾氨代谢影响的机制。

Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI: 10.5049/EBP.2011.9.2.45

Ki-Hwan Han

引用次数: 24

ACE2 and Angiotensin-(1-7) in Hypertensive Renal Disease. 高血压肾病中的ACE2和血管紧张素-(1-7)

Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI: 10.5049/EBP.2011.9.2.41

Ju-Young Moon

{"title":"ACE2 and Angiotensin-(1-7) in Hypertensive Renal Disease.","authors":"Ju-Young Moon","doi":"10.5049/EBP.2011.9.2.41","DOIUrl":"https://doi.org/10.5049/EBP.2011.9.2.41","url":null,"abstract":"The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-[Angiotensin-(1-7)(Ang-(1-7)]-Mas receptor axis has an opposing function to that of the ACE-Angiotensin II (Ang II)-Angiotensin type 1 (AT1) receptor axis. Ang-(1-7) is present in the kidneys at concentrations comparable to those of Ang II and is associated with vasodilation, modulation of sodium and water transport, and stimulation of nitric oxide (NO) synthase. Ang-(1-7) also acts as a physiological antagonist of Ang II by counterbalancing the Ang II-mediated intracellular signaling pathway. In a hypertensive model, increased ACE and decreased ACE2 along with a higher ACE/ACE2 ratio in hypertensive kidneys appeared to favor Ang II generation, leading to hypertensive renal damage. In addition, the administration of a selective Ang-(1-7) receptor blocker or an ACE2 inhibitor was associated with worsening of hypertension and renal function. Ang-(1-7)-mediated increases in renal blood flow were abolished by blockade of the Mas receptor and by inhibition of prostaglandin release and NO in spontaneously hypertensive rats and in Wistar-Kyoto controls. Further research on the function of the ACE2-Ang-(1-7)-Mas receptor axis could lead to a novel target for inhibiting kidney disease progression.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"9 2","pages":"41-4"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/20/1d/ebp-9-41.PMC3302904.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30520679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Volume control by using the body composition monitor in a puerperal patient on hemodialysis. 利用体成分监测仪控制产褥期血液透析患者的体积。

Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI: 10.5049/EBP.2011.9.2.63

Wookyung Chung, Shung Han Choi, Jiyoon Sung, Eul Sik Jung, Dong Su Shin, Ji Yong Jung, Jae Hyun Chang, Hyun Hee Lee, Seung-Ho Lee, Sejoong Kim

引用次数: 0

V2 receptor antagonist; tolvaptan. V2受体拮抗剂;tolvaptan。

Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI: 10.5049/EBP.2011.9.2.50

Joo-Hark Yi, Hyun-Jong Shin, Ho-Jung Kim

引用次数: 16

Effects of dietary salt restriction on puromycin aminonucleoside nephrosis: preliminary data. 饮食盐限制对嘌呤霉素氨基核苷肾病的影响:初步数据。

Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI: 10.5049/EBP.2011.9.2.55

Chor Ho Jo, Sua Kim, Joon-Sung Park, Gheun-Ho Kim

{"title":"Effects of dietary salt restriction on puromycin aminonucleoside nephrosis: preliminary data.","authors":"Chor Ho Jo, Sua Kim, Joon-Sung Park, Gheun-Ho Kim","doi":"10.5049/EBP.2011.9.2.55","DOIUrl":"https://doi.org/10.5049/EBP.2011.9.2.55","url":null,"abstract":"Proteinuria is a major promoter that induces tubulointerstitial injury in glomerulopathy. Dietary salt restriction may reduce proteinuria, although the mechanism is not clear. We investigated the effects of dietary salt restriction on rat kidneys in an animal model of glomerular proteinuria. Male Sprague-Dawley rats were used and divided into 3 groups: vehicle-treated normal-salt controls, puromycin aminonucleoside (PA)-treated normal-salt rats, and PA-treated low-salt rats. PA was given at a dose of 150 mg/kg BW at time 0, followed by 50 mg/kg BW on days 28, 35, and 42. Sodium-deficient rodent diet with and without additional NaCl (0.5%) were provided for normal-salt rats and low-salt rats, respectively. On day 63, kidneys were harvested for histopathologic examination and immunohistochemistry. PA treatment produced overt proteinuria and renal damage. Dietary salt restriction insignificantly reduced proteinuria in PA-treated rats, and PA-treated low-salt rats had lower urine output and lower creatinine clearance than vehicle-treated normal-salt controls. When tubulointerstitial injury was semiquantitatively evaluated, it had a positive correlation with proteinuria. The tubulointerstitial injury score was significantly increased by PA treatment and relieved by low-salt diet. ED1-positive infiltrating cells and immunostaining for interstitial collagen III were significantly increased by PA treatment. These changes appeared to be less common in PA-treated low-salt rats, although the differences in PA-treated normal-salt versus low-salt rats did not reach statistical significance. Our results suggest that renal histopathology in PA nephrosis may potentially be improved by dietary salt restriction. Non-hemodynamic mechanisms induced by low-sodium diet might contribute to renoprotection.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"9 2","pages":"55-62"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2011.9.2.55","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30521686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Alkali therapy in patients with metabolic acidosis. 代谢性酸中毒患者的碱治疗。

Electrolyte and Blood Pressure Pub Date : 2011-06-01 Epub Date: 2011-06-30 DOI: 10.5049/EBP.2011.9.1.38

Viktor Rosival

引用次数: 0

The authors reply: alkali therapy in patients with metabolic acidosis. 作者回复:碱治疗代谢性酸中毒。

Electrolyte and Blood Pressure Pub Date : 2011-06-01 Epub Date: 2011-06-30 DOI: 10.5049/EBP.2011.9.1.39

Yun Kyu Oh

引用次数: 0

Hyponatremia associated with bupropion. 安非他酮所致低钠血症。

Electrolyte and Blood Pressure Pub Date : 2011-06-01 Epub Date: 2011-06-30 DOI: 10.5049/EBP.2011.9.1.23

Chang Seong Kim, Joon Seok Choi, Eun Hui Bae, Soo Wan Kim

引用次数: 14

The role of proximal nephron in cyclophosphamide-induced water retention: preliminary data. 近端肾元在环磷酰胺诱导的水潴留中的作用:初步数据。

Electrolyte and Blood Pressure Pub Date : 2011-06-01 Epub Date: 2011-06-30 DOI: 10.5049/EBP.2011.9.1.7

Sua Kim, Chor Ho Jo, Joon-Sung Park, Ho Jae Han, Gheun-Ho Kim

{"title":"The role of proximal nephron in cyclophosphamide-induced water retention: preliminary data.","authors":"Sua Kim, Chor Ho Jo, Joon-Sung Park, Ho Jae Han, Gheun-Ho Kim","doi":"10.5049/EBP.2011.9.1.7","DOIUrl":"https://doi.org/10.5049/EBP.2011.9.1.7","url":null,"abstract":"Cyclophosphamide is clinically useful in treating malignancy and rheumatologic disease, but has limitations in that it induces hyponatremia. The mechanisms by which cyclophosphamide induces water retention in the kidney have yet to be identified. This study was undertaken to test the hypothesis that cyclophosphamide may produce water retention via the proximal nephron, where aquaporin-1 (AQP1) and aquaporin-7 (AQP7) water channels participate in water absorption. To test this hypothesis, we gave a single dose of intraperitoneal cyclophosphamide to male Sprague-Dawley rats and treated rabbit proximal tubule cells (PTCs) with 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide. In the short-term 3-day rat study, AQP1 protein expression was significantly increased in the whole kidney homogenates by cyclophosphamide administration at 48 (614 ± 194%, P < 0.005), and 96 (460 ± 46%, P < 0.05) mg/kg BW compared with vehicle-treated controls. Plasma sodium concentration was significantly decreased (143 ± 1 vs. 146 ± 1 mEq/L, P < 0.05) by cyclophosphamide 100 mg/kg BW in the long-term 6-day rat study. When primary cultured rabbit PTCs were treated with 4-HC for 24 hours, the protein expressions of AQP1 and AQP7 were increased in a dose-dependent manner. Quantitative polymerase chain reaction revealed no significant changes in the mRNA levels of AQP1 and AQP7 from cyclophosphamide-treated rat renal cortices. From these preliminary data, we conclude that the proximal nephron may be involved in cyclophosphamide-induced water retention via AQP1 and AQP7 water channels. Further studies are required to demonstrate intracellular mechanisms that affect the expression of AQP proteins.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"9 1","pages":"7-15"},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2011.9.1.7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30206439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Orthorexia nervosa with hyponatremia, subcutaneous emphysema, pneumomediastimum, pneumothorax, and pancytopenia. 伴低钠血症、皮下肺气肿、纵隔气胸、全血细胞减少症的神经性缺氧。

Electrolyte and Blood Pressure Pub Date : 2011-06-01 Epub Date: 2011-06-30 DOI: 10.5049/EBP.2011.9.1.32

Sang Won Park, Jeong Yup Kim, Gang Ji Go, Eun Sil Jeon, Heui Jung Pyo, Young Joo Kwon

引用次数: 73