Temporary occlusion of the middle cerebral artery (MCA) causing damage to brain tissue occurs in the majority of human stroke victims. Reflex cardiovascular responses during static exercise were attenuated following transient MCA occlusion (MCAO) and reperfusion, mediated via alteration of the neuronal nitric oxide synthase (nNOS) protein isoform within the rostral (RVLM) and caudal (CVLM) ventrolateral medulla (Ally, A., Nauli, S.M., Maher, T.J. 2005. Molecular changes in nNOS protein expression within the ventrolateral medulla following transient focal ischemia affect cardiovascular functions. Brain Res. [1055, 73-82]. We hypothesized that the endothelial NOS (eNOS) isoform within the RVLM and CVLM might also play a role in integrating cardiovascular function. Thus, we compared cardiovascular responses to static muscle contraction and eNOS expression within the four quadrants, i.e., left and right sides of both RVLM and CVLM in sham operated rats and in rats with a temporary 90-minute one-sided MCAO followed by 24 hour reperfusion. Increases in arterial pressure during a muscle contraction were attenuated in MCAO rats when compared to sham rats. Left-sided MCAO significantly decreased the expression of eNOS in the ipsilateral side but not contralateral RVLM, and to both RVLM quadrants in sham-operated rats. In contrast, compared to sham rats and the right CVLM quadrant of MCAO rats, eNOS expression was significantly increased in the left ipsilateral CVLM quadrant in left-sided MCAO rats. These data suggest that attenuation of cardiovascular responses during muscle contraction in MCAO rats may be partly due to a reduction in eNOS expression within the ipsilateral RVLM and an overexpression of eNOS within the ipsilateral CVLM. Results demonstrate that the eNOS protein within the medulla may play a significant role in mediating cardiovascular responses during static exercise in pathophysiological conditions, such as stroke.