The present study was designed to assess whether or not changes in genomic expression of cyclooxygenases (COX-1, COX-2), nitric oxide synthase (eNOS), prostanoid synthases in the endothelium and of prostanoid receptors in vascular smooth muscle contribute to the occurrence of endothelium-dependent contractions during aging and hypertension. Gene expression was quantified by real-time PCR using isolated endothelial and smooth muscle cells (SMC) from the aorta of Wistar Kyoto and spontaneously hypertensive rats. Genes for all known prostanoid synthases and receptors were present in endothelial and SMC, respectively. Aging caused over-expression of eNOS, COX-1, COX-2, thromboxane synthase, hematopoietic-type prostaglandin D synthase, membrane prostaglandin E synthase-2, prostaglandin F synthase in endothelial cells and COX-1, EP4-receptors in SMC. Hypertension augmented the expression of COX-1, prostacyclin synthase, thromboxane synthase, hematopoietic-type prostaglandin D synthase in endothelial cells and DP-, EP3- and EP4-receptors in SMC. The increase in genomic expression of endothelial COX-1 explains why in aging and hypertension, the endothelium has greater propensity to release cyclooxygenase-derived vasoconstrictive prostanoids. The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1 derived endoperoxides are transformed into prostacyclin, substantiating the role of prostacyclin as an endothelium-derived contracting factor. The expression of thromboxane synthase was increased in the cells of aging or hypertensive rats, explaining why the prostanoid can contribute to endothelium-dependent contractions. It is uncertain whether the gene modifications caused by aging and hypertension directly contribute to endothelium-dependent contractions or rather to vascular aging and the vascular complications of the hypertensive process.