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Acute Isolated Increased Renal Venous Pressure and Kidney Functions in an Experimental Rat Model
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- Author / Creator
- Huang, Xiaohua
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Increased renal venous pressure is a recognized risk factor for kidney dysfunction. It is not rare in clinical settings with venous congestion, such as heart failure, and is associated with worsening kidney function and increased mortality. However, the underling mechanisms are not well understood. In addition, advanced kidney dysfunction might result in sodium and fluid retention, which exacerbates the congestive state. Sodium handling at high renal venous pressure has not been well addressed. In this thesis, we first review principal mechanisms governing renal hemodynamics and sodium handling. Then we investigate how these mechanisms would relate to increased renal venous pressure. Pathophysiologically, both intravascular and extravascular factors can lead to an increased renal venous pressure. Limited data could be found regarding a comprehensive understanding of how increased renal venous pressure contributes to kidney dysfunction in disease states. Thus, it is not well understood how increased renal venous pressure contributes to renal dysfunction. It is therefore that we embarked on a number of studies to define the role of increased renal venous pressure on renal function. Increased renal venous pressure forms a physical factor that directly decreases renal blood flow. However, neurohumoral factors are likely involved in mediating effects of increased renal venous pressure on renal blood flow, glomerular filtration rate and sodium handling. To separate the role of renal venous pressure from the role of a congestive state as a whole, we adapted a model of isolated increased renal venous pressure in the rat. The acute isolated increase in renal venous pressure results in decreases in RBF, renal vascular conductance, glomerular filtration rate and heart rate. Two very powerful modulators are the renin-angiotensin system and renal sympathetic nerve activity. The roles of these two mechanisms in the renal response to increased renal venous pressure are not clearly delineated. Moreover, it has been suggested that the intrinsic mechanism intended to maintain renal blood flow and glomerular filtration rate stable upon fluctuations in renal perfusion pressure, renal autoregulation, is compromised by increased renal venous pressure, but this has hardly been studied in this context. Our data indicate that other than renal sympathetic nerve activity, renin-angiotensin system and autoregulation, have primary roles in vasoconstrictive response to renal venous pressure elevation. Furthermore, the supression of renal sympathetic nerve activity and inappropriate activation of the renin-angiotensin system contribute to the impact on heart rate and mean arterial pressure. Increased renal venous pressure also modulates the sodium handling. The inappropriate activation of renin-angiotensin system is also responsible for the sodium retention in renal venous pressure elevation. Increased renal venous pressure also tend to incease the tubular pressure, which might affect the tubular sodium tansport.In conclusion, increased renal venous pressure impairs kidney function, which involves potential modulators such as the renal sympathetic nerve activity, the renin-angiotensin system and others. This report describes an initial exploration of this area, with emphasis on the renin-angiotensin system, renal nerves and renal autoregulation.
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- Graduation date
- Spring 2019
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- Type of Item
- Thesis
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- Degree
- Doctor of Philosophy
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- License
- Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.