Abstract
Angiotensin II is an important mediator of skeletal muscle angiogenesis induced by electrical stimulation (estim). Previous studies have shown that the low‐renin SS/Mcwi rat does not undergo angiogenesis in response to estim, while the congenic SS.BN‐(D13hmgc41‐D13Rat101), an SS/Mcwi rat with an introgressed 4.5Mbp piece of BN chromosome 13 overlapping the renin gene, has restored renin levels and the angiogenic response. In this study zinc‐finger nucleases were used to knockout the renin gene (Ren1) in each of these strains. We then tested the angiogenesis phenotype. Electrical stimulators were implanted to intermittently stimulate the peroneal nerve in one hind limb, contracting the Tibialis Anterior (TA) and Extensor Digitorum Longus (EDL) muscles for 8 hours/day for 7 days. As expected, the SS/Mcwi Ren1−/− did not undergo angiogenesis to stimulation, and the congenic SS.BN‐(D13hmgc41‐D13Rat101) Ren1−/− also did not undergo angiogenesis in response to stimulation. In both cases the infusion of AngII restored the angiogenic response. Regardless of SS or BN regulatory genes, the knockout of Ren1 eliminates the angiogenesis phenotype, indicating the gene(s) in the 4.5Mbp BN substitution responsible for the restoration of the angiogenesis phenotype on the SS/Mcwi background act through a renin dependent mechanism. Supported by NIH Heart Lung & Blood Institute 082798.
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