Gastrin/cholecystokinin type B receptors (CCK_BRs) can be found on parietal cells and smooth muscle cells and are the predominant brain CCK receptors. Recent cloning studies indicate that this receptor type might also be expressed in the kidney.

We used Northern blot analysis in guinea pig. kidney and reverse transcriptase polymerase chain reaction (RT‐PCR) in several murine kidney cell lines to evaluate this organ for the expression of the CCK_BRs. The receptor was pharmacologically characterized by displacement experiments using [¹²⁵I]‐BH‐CCKs and various agonists and antagonists. Polyclonal antibodies vs. the CCK_BRs were raised in chicken, and immunohistochemistry on tissue sections was used to localize the receptor within the organ. The effect of gastrin on renal cell growth was measured using proximal tubulus (MCT) cells, which were cultured with gastrin (10⁻⁹ M) for 24–72 h. Cell counts and [³H]‐thymidine incorporation experiments were performed.

CCK_BR transcripts can be detected in kidney RNA (tubules > glomeruli > interstitium). RT‐PCR revealed CCK_BR transcripts in proximal tubules (MCT cells) and in mesangium (MMC). The medullary thick ascending limb of Henle's loop and several control tissues such as liver and muscle were negative. Displacement experiments using [¹²⁵I]‐BH‐CCK and various agonists and antagonists identified binding sites with typical CCK_BR pharmacology. CCK_BRs were localized in the proximal tubulus, distal collecting ducts and mesangium cells. Treatment of rested MCT cells with gastrin 17‐1 induced cell proliferation and [³H]‐thymidine incorporation by at least 40% compared with normal growth (P < 0.05).

These results show for the first time that CCK_BRs are present in selected areas of the kidney, and strongly confirm our previous observation that this organ expresses binding sites for [¹²⁵I]‐gastrin. Furthermore, gastrin might act as a growth factor in the kidney.