Previously, we showed that estrogen, topically applied to the spinal cord, attenuated the exercise pressor reflex in female cats. The attenuation was gender specific and partly opioid dependent. Our finding that the µ and opioid antagonist, naloxone, was only able to partially restore estrogen's attenuating effect on the pressor response to contraction suggested that estrogen effected an additional pathway, involving the dorsal root ganglion (DRG). Estrogen has been described to stimulate transcription within 10 minutes of its application to the DRG, raising the possibility that rapid genomic effects on neurotransmitter production may have contributed to its effect on the exercise pressor reflex. This prompted us to test the hypothesis that the estrogen modulated the pressor response to static contraction by influencing gene expression of the neurotransmitters released by the thin fiber muscle afferents that evoke the exercise pressor reflex. We confirmed in decerebrated female rats that topical application of estrogen (0.01 µg/ml) to the lumbosacral cord attenuated the pressor response to contraction (from 10 ± 3 to 1 ± 1 mmHg; P<0.05). GeneChip analysis of the DRG revealed that neither estrogen nor contraction alone changed mRNA expression of substance P, NK-1 receptor, CGRP, NGF, P2X3 receptor, GABA A and B receptor, the 5-HT 3A and 3B receptor, NMDA and non-NMDA receptors, opioid receptors and opioid receptor like receptor. Surprisingly however, contraction stimulated the expression of neuropeptide Y in the DRG in the presence and absence of estrogen. We conclude that estrogen does not attenuate the exercise pressor reflex through a genomic effect in the DRG.