Effects of norepinephrine and angiotensin on total and venous resistance in the kidney

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Abstract
The intact kidney of anesthetized dogs was perfused at constant blood flow. Small vein pressure (SVP) was measured from a catheter which was passed through the main renal vein deep into the kidney. Perfusion pressure (PP), tissue pressure (TP), and inferior vena caval pressure also were recorded. Norepinephrine and angiotensin administered intra-arterially produced large increases in PP and small increments in SVP. The rise in SVP was usually accompanied by an increase in TP. Evidence indicated that augmentation in venous resistance was caused by a direct stimulatory action of the agents on venous smooth muscle. Tissue pressure appears to be increased secondarily to SVP because of an increased intravascular volume and decreased tubular reabsorption. Sympathetic nerve stimulation produced small changes in SVP for large increments in PP as did the exogenous administration of norepinephrine. These results indicate that the arterial side of the kidney possesses a much greater constrictor capacity compared to the venous side and that renal vasomotor adjustments are made mainly on the arterial side of the bed.