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June 1973, Vol 106, No. 6 >
ARTICLE | June 1973

Renal Inactivation of Endogenous Gastrin in Dogs

Robert A. D. Booth, FRCS; David D. Reeder, MD; Ulf B. Hjelmquist, MD; Edward N. Brandt, MD; James C. Thompson, MD
Arch Surg. 1973;106(6):851-854. doi:10.1001/archsurg.1973.01350180085024.
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Concentrations of gastrin in the renal artery, renal vein, and urine of dogs were determined by radioimmunoassay. Renal blood flow was determined by flowmeters. These measurements allowed calculation of the mass of gastrin lost from blood flowing through the kidney. No loss of gastrin was detected during the basal state or during suppression of endogenous gastrin release by antral acidification. When circulating levels of gastrin were elevated by irrigating the antrum with acetylcholine, a significant mass of gastrin was removed on transit of the kidney. Excretion of gastrin in the urine was minuscule in comparison with the total mass lost. The kidney therefore possesses the power to inactivate stimulated levels of endogenous gastrin. Failure of inactivation of basal levels may be due to a threshold concentration or to a difference in the molecular form of gastrin released on stimulation.

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