Abstract
Evidence has been presented which demonstrates that infusions of SKF 525-A into the renal artery produce a marked increase in the urinary excretion of sodium and in urine volume without significantly affecting glomerular filtration rate. These effects were found to be very brief in duration. In practically all experiments, it was found that the excretion of potassium increased concomitantly with increases in the excretion of sodium.
"Stop-flow" experiments suggest that SKF 525-A administered at rates of 8 to 10 mg/minute is capable of inhibiting distal tubular reabsorption of sodium and possibly proximal tubular reabsorption of this ion. At rates of administration of 4 mg/minute, only proximal tubular sodium samples were altered.
The natruretic action of SKF 525-A is not markedly influenced by alterations in acid-base balance. Denervation of the kidney is also without strong influence on the natruretic response.
Footnotes
- Received October 3, 1961.
- Accepted November 13, 1963.
- The Williams & Wilkins Company
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