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3 Kidney Blood Vessel Development

The morphogenesis of kidney arterioles is not well understood. Experiments from several laboratories, including ours, indicate that these blood vessels originate from mesenchymal precursors within the renal blastema. Thus, all progenitors of the renal preglomerular arterioles including smooth muscle, endothelial and renin-producing cells are present in the embryonic kidney before assembly of the arterioles has been initiated. Upon proper stimulation and the right environmental conditions, those vascular precursors form the kidney arterioles. We have recently shown an association between renin-expressing cells and branching of the aforementioned vessels. In fact, disruption of the renin-angiotensin system, by either gene targeting or pharmacological means, results in marked alterations in nephrovascular development, including the presence of fewer, shorter and thicker renal arterioles. Our data suggest that lack of angiotensin results in concentric proliferation of immature smooth muscle cells and recruitment of renin-containing cells along the outside layer of the arteriolar walls. These studies demonstrate that the renin-angiotensin system is intimately linked to the differentiation of the renal arterial tree. Similarly, a number of transcription factors, including the ETS gene family of transcriptional regulators, seem to regulate many of the downstream genes involved in vascular formation. Mice with targeted null mutations of the ETS-1 or Tel genes have severe kidney abnormalities and/or lethal angiogenic defects. Current work in our laboratories suggests that these genes are crucial for the development of the renal arterioles.

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