Gap junctional coupling of renin producing cells is of major functional importance for the control of renin synthesis and release. This study was designed to determine the relevance of the vascular gap junction protein connexin 45 (Cx45) for the control of renin expression and secretion. By crossbreeding mice which drive Cre recombinase expression under the control of the endogenous renin promoter with mice harbouring floxed Cx45 gene alleles we generated viable mice with a deletion of Cx45 in the renin cell lineage. These mice were normotensive and renin cells in their kidneys were normal with regard to localization and number. Sodium deficiency induced typical recruitment of renin producing cells along afferent arterioles, and regulation of renin secretion by perfusion pressure, catecholamines and angiotensin-II in isolated kidneys of mice with renin cell specific deletion of Cx45 were normal. Cx45 promoter activity in cells of the preglomerular arteriolar tree was analyzed by using mice driving the reporter gene LacZ under the control of the Cx45 promoter. In these mice we found strong staining in smooth muscle cells of the media, whereas renin expressing cells were almost devoid of LacZ staining. Conversely, renin producing cells, but not vascular smooth muscle cells expressed the gap junction protein Cx40. These findings suggest that connexin 45 plays no major functional role in renin producing cells, probably because the expression of Cx45 is downregulated in these cells. Since renin producing cells in the adult kidney can reversibly transform into vascular smooth muscle cells and vice versa, our findings on connexin expression indicate that these phenotype switches are paralleled by characteristic reciprocal changes of the transcriptional activity of Cx40 and Cx45 genes.