EFFECT OF INCREASED RENAL VENOUS PRESSURE ON RENAL FUNCTION
- 1 April 1949
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 157 (1), 1-13
- https://doi.org/10.1152/ajplegacy.1949.157.1.1
Abstract
The effect of increased renal venous pressure on renal function was studied in anesthetized dogs by means of clearance techniques. Renal function was measured separately and simultaneously in the 2 kidneys but the pressure was raised in the left renal vein only, by means of a specially designed clamp. Venous pressure was measured with a saline manometer through a venous catheter which had been passed into the left renal vein. Control values for the functions of the left kidney were obtained before and after elevation of venous pressure and were comparable to controls obtained from the right kidney. Under the stated conditions moderate elevation of the left renal venous pressure up to 350 mm. saline caused in that kidney a significant decrease in water and Na excretion without any change in the renal plasma flow, glomerular filtration on rate, glucose Tm or diodrast Tm. The reduction in water and sodium excretion was due to an increase in the reabsorption rate of these substances by the renal tubule cells. This effect also occurred when the Na load was low, for example in one expt. in which the serum Na was 127 MEq/l. Greater elevation of venous pressure to 550 mm. saline decreased renal blood flow and filtration rate, but the results were not sufficient to state whether filtration fraction was significantly altered. The mechanism for the increased reabsorption of sodium and water ascribed to increased venous pressure was not obvious. It was local, i.e., confined to the kidney in which the venous pressure was raised and consequently was not related to release of pituitary, adrenal and hepatic hormones. It probably was mechanical rather than the result of any alteration in specific metabolic processes of the tubular cells since there were no associated changes in glucose Tm or diodrast Tm. Some of the implications of these results with respect to the pathogenesis of edema in cardiac failure are discussed.Keywords
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