Norepinephrine (NE) is cleared from the neuroeffector junction by NE transporter (NET). NET function is reduced in the hypertensive heart; however, there is limited information about the cause of the decrease in function. The goal of this thesis was to evaluate NET in the heart of normal animals (Aims 1 & 2) and to assess the basis for reduced reuptake function with hypertension (Aim 3). Aim 1: Characterization and cellular localization of NET mRNA and protein expression in stellate ganglia and heart from normal animals. (A) This study revealed for the first time the presence of NET mRNA in heart homogenate with the atria expressing more than the ventricles. Sympathetic denervation with did not deplete NET mRNA content in the heart so the source of this mRNA is not sympathetic nerve terminals. Since NET mRNA was not in nerve terminals, there are alternative cellular sources of NET mRNA, and thus NET protein, aside from sympathetic neurons. (B) Substantial NET protein was observed in the sympathetically denervated heart supporting the notion that there are alternative sources of NET protein in the heart. NET immunoreactivity was present in cardiac-associated sensory ganglia and parasympathetic intrinsic cardiac ganglia. Aim 2: Correlation of NET protein to chamber NE content. It was expected that NET protein would positively correlate to tissue NE content since NET is present in NE-containing sympathetic nerves where it functions to clear released NE from the neuroeffector junction. However, NET protein was inversely correlated to chamber NE content. There was a high level of NET protein in the ventricles where NE is low, and a low amount of NET protein in the atria where NE is the highest. Aim 3: Changes in NET mRNA and protein in hypertension. NET mRNA in the right and left stellate ganglia were unchanged in hypertension; however, the left stellate ganglia displays an increase NET protein suggesting a post-transcriptional mechanism of NET protein