Several vasoregulatory systems including the renin-angiotensin-system, sympathetic vasoregulation and cytokine release have been studied extensively. The aim of the present study was to establish a physiogenomic screening model for differentially expressed genes in the regulation of blood pressure which might give a hint to new vasoregulatory mechanisms. We induced acute hypotension in normotensive rats, assuming that vasoregulatory systems will counteract hypotension. Microarray transcriptome analysis was performed from kidneys six hours after the induction of acute hypotension. The results were confirmed by real-time PCR. Six functionally known genes (Igfbp1, Xdh, Sult1a1, Mawbp, Por, Gstm1) and two ESTs (BI277460 and AI411345) were significantly upregulated. Four of these genes (Igfbp1, Xdh, Por, Gstm1) have well characterized functions in the cardiovascular system. The proteins corresponding to Xdh, Por and Gstm1 are involved in the metabolism of reactive oxygen species (ROS). Since ROS can mediate endothelial dysfunction we measured the aortic dilatory capacity in thoracic aortic rings. Indeed, vasodilator potency to acetylcholine was largely diminished in hypotensive animals, while sodium nitroprusside induced equivalent vasodilations in normotensive and hypotensive animals. The vasodilator potency of the endothelium was partially restored by the superoxide scavenger tiron. Hence, acute hypotension induces a diminished vasodilator potency of the endothelium due to an accelerated degradation of NO by ROS. The present physiogenomic approach is capable of detecting vasoregulatory mechanisms and may provide deeper insight into the genetics and physiology of blood pressure regulation.