{"title":"Analysis of effect of renal nerve on kidney functions during sodium restriction by using a mathematical model","authors":"F. Karaaslan","doi":"10.1109/BIYOMUT.2014.7026383","DOIUrl":null,"url":null,"abstract":"In our previous study, the hypothesis that during sodium restriction an increased renal sympathetic nerve activity (RSNA) contributes to decreased sodium excretion was tested by using a cardiovascular model with two kidneys [1]. The RSNA of the left kidney was fixed at its normal steady state value while allowing RSNA in the right kidney to change normally in response to the decreased sodium intake. The results demonstrated that the kidney with intact RSNA excreted less sodium than the RSNA fixed kidney. In this study, the effect of an increased RSNA on kidney functions during a long-term decrease in sodium intake is analyzed by using the same mathematical model. There is no difference between blood flows, afferent and efferent arteriolar resistances, renal vascular resistances, glomerular hydrostatic pressures, glomerular filtration rates, afferent arteriolar pressures, myogenic responses, release of nitric oxide, filtered sodium in the intact and the fixed-RSNA kidneys during sodium restriction. However, it is seen that proximal tubule sodium reabsorption and renin secretion from the intact kidney is more than the fixed-RSNA kidney. Thus, the reason why the intact kidney excretes less sodium than the fixed-RSNA kidney is that sodium reabsorption from the intact kidney is more than the other one.","PeriodicalId":428610,"journal":{"name":"2014 18th National Biomedical Engineering Meeting","volume":"86 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2014-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"2014 18th National Biomedical Engineering Meeting","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1109/BIYOMUT.2014.7026383","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In our previous study, the hypothesis that during sodium restriction an increased renal sympathetic nerve activity (RSNA) contributes to decreased sodium excretion was tested by using a cardiovascular model with two kidneys [1]. The RSNA of the left kidney was fixed at its normal steady state value while allowing RSNA in the right kidney to change normally in response to the decreased sodium intake. The results demonstrated that the kidney with intact RSNA excreted less sodium than the RSNA fixed kidney. In this study, the effect of an increased RSNA on kidney functions during a long-term decrease in sodium intake is analyzed by using the same mathematical model. There is no difference between blood flows, afferent and efferent arteriolar resistances, renal vascular resistances, glomerular hydrostatic pressures, glomerular filtration rates, afferent arteriolar pressures, myogenic responses, release of nitric oxide, filtered sodium in the intact and the fixed-RSNA kidneys during sodium restriction. However, it is seen that proximal tubule sodium reabsorption and renin secretion from the intact kidney is more than the fixed-RSNA kidney. Thus, the reason why the intact kidney excretes less sodium than the fixed-RSNA kidney is that sodium reabsorption from the intact kidney is more than the other one.