Modification of renal and tissue cation transport by cholecystokinin octapeptide in the rabbit.

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Abstract
1. Reports that gastric sodium loads cause a greater natriuresis than those administered intravenously, suggest that a gastric or portal sodium monitor exists which releases a humoral natriuretic factor. To determine whether cholecystokinin octapeptide (CCK‐8) had direct renal natriuretic effects (and was therefore a candidate for this gut‐derived natriuretic factor) we compared the natriuretic response to CCK‐8 infused intravenously with that infused directly into the renal artery of six conscious male rabbits. 2. CCK‐8 produced a significant log dose‐dependent decrease in the fractional excretions of calcium (P less than 0.05) and magnesium (P less than 0.005) and a log dose‐dependent increase in fractional sodium excretion (P less than 0.025). The significant decreases in the fractional excretions of calcium and magnesium were accompanied by log dose‐dependent falls in their plasma levels (calcium, P less than 0.05, and magnesium, P less than 0.005), indicating movement of calcium and magnesium to extravascular sites. Studies of tissue calcium and magnesium levels in response to CCK‐8 infusion showed that calcium accumulated in kidney and skeletal muscle. 3. We conclude that CCK‐8 has direct renal natriuretic effects at the tubular level and could be the gut‐derived natriuretic factor. In addition to its effects on sodium excretion, CCK‐8 causes renal retention and increased gut absorption of calcium and magnesium with movement of these ions to extravascular sites.