Abstract
IT has been noted by Winton1 and has since been confirmed many times2–5, that the renal vascular resistance is not constant but increases with increasing arterial pressure in the range 80–120 mm. mercury mean pressure. The phenomenon does not depend on an intact nerve supply to the kidney but occurs in the denervated, perfused kidney. The autoregulation of renal blood flow has been considered attributable either to an active vasomotor process3–5 or, in some recent work, to a flow-dependent separation of plasma from red cells in the renal circulation. The first of these theories appears to have been developed only by the process of elimination, and the second appears no longer tenable in the light of experiments by several groups5–7. The œdematous kidney displays a high resistance to flow which probably results from compression of vessels by extravascular fluid. This factor has not been considered important in the function of kidneys subjected to normal arterial and venous pressure, since measurements of renal tissue pressure5 indicated that it does not vary directly with renal vascular resistance.
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References
Winton, F. R., Trans. Fourteenth Congresso Internaz. de Fisiol., 264 (1932).
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Ochwadt, B., Pfluger's Arch. ges. Physiol., 262, 207 (1956).
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Thompson, D. D., Kavaler, F., Lozano, R., and Pitts, R. F., Amer. J. Physiol., 191, 493 (1957).
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Winton, F. R., Harvey Lecture, 47, 21 (1951–52).
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SCHER, A. Mechanism of Autoregulation of Renal Blood Flow. Nature 184, 1322–1323 (1959). https://doi.org/10.1038/1841322a0
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DOI: https://doi.org/10.1038/1841322a0
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