Testosterone Increases Myogenicity in Defective and Normal Androgen Receptor Male Rats.

Testosterone (T) acting through the androgen receptor (AR) is involved in a number of mechanisms in the development of hypertension, thereby potentially altering vessel responsiveness. To study the relationship of T, AR, and blood vessel resistance, a testicular feminized male (Tfm) hybrid was used. This hybrid stain consists of the Tfm or AR deficient males, as well as their normal AR (NAR) male siblings. Therefore, if the AR is necessary for T to play an integral role in vessel function, the Tfm should not respond to T manipulation. To test this hypothesis, 8 week old Tfm or NAR hybrid males were studied in the following treatments: intact control, castrate (cast), and castrate with T replacement (cast+T) with (n=6–10/group). Upon termination, the mesenteric arteriole response to changes in intraluminal pressure (myogenicity) were analyzed using a pressure arteriograph system. Both Tfm (F=3.4, p<0.05) and NAR (F=11, p<0.01) cast groups showed decreased myogenicity compared to controls. However, following T treatment the Tfm cast+T myogenicity returned to control levels; while the NAR cast+T myogenecity increased a further 30% (F=11.1, p<0.01). The results of this study indicate that T independent of the AR may be responsible for changes in vessel myogenicity, since both Tfm and NAR males responded to T treatment.