['Testosterone (T) and the androgen receptor (AR) are involved in mechanisms associated with hypertension and vessel reactivity.', 'To investigate T and the AR on blood vessel reactivity, testicular feminized male (TFM; AR deficient males) and normal androgen receptor (NAR) male rats were used. Therefore, if the functional AR is necessary for plasma T to regulate vessel responsiveness, TFM males will exhibit altered vessel function compared to NAR males.', 'Adult (16 weeks of age) TFM or NAR males were assigned to the following treatment groups: gonadal intact controls (CONT), castrate (CAST), or castrate with T replacement (CAST+T) with (n=8-10/group).', 'Plasma T followed a consistent pattern with CAST+T elevated compared to CONT and CAST TFM and NAR males. In addition, CAST plasma T was significantly decreased compared to CONT and CAST+T in TFM and NAR males. In a similar manner for systolic blood pressure (SBP), CAST lowered SBP compared to CONT in both NAR and TFM. Following 8 weeks of treatment, second-order mesenteric artery responses to changes in intraluminal pressure (myogenic reactivity) were analyzed using a pressure arteriograph system. Both TFM (P < 0.05) and NAR (P < 0.05) CAST groups revealed a decrease in myogenic reactivity compared to CONT. Following T treatment the TFM CAST+T myogenic reactivity returned to CONT levels, whereas the NAR CAST+T myogenic reactivity increased a further 10%.'] Does testosterone increase myogenic reactivity of second-order mesenteric arteries in both defective and normal androgen receptor adult male rats?