Abstract
Quantification of aortic androgen and estrogen receptor content and distribution in AXC/SSh rats established that the total androgen receptor content in intact young mature males (mean +/- SD, 55 +/- 13 fmol/mg DNA) was indistinguishable (P greater than 0.05) from that in proestrous females (50 +/- 3 fmol/mg DNA). However, 60% of male aortic androgen receptors were in the nuclear fraction, whereas all proestrous female aortic androgen receptors were in the cytoplasmic fraction. The total aortic estrogen receptor content of intact young mature males (70 +/- 16 fmol/mg DNA) was indistinguishable (P greater than 0.05) from that of proestrous (92 +/- 12) or diestrous (77 +/- 4) females. However, 50% of proestrous female aortic estrogen receptors were in the nuclear fraction, whereas male or diestrous female aortic estrogen receptors were restricted to the cytoplasmic fraction. To assess estrogen receptor function, we characterized aortic cytoplasmic progesterone receptors and established that the receptor content of intact male aortae (101 +/- 3 fmol/mg DNA) was not significantly different (P greater than 0.05) from that of diestrous female aortae (100 +/- 11). 17 beta-Estradiol injection of intact males failed to affect aortic progesterone receptor content (93 +/- 17 fmol/mg DNA). However, injection of orchiectomized males with 17 beta-estradiol significantly (P less than 0.05) increased progesterone receptor content to 208 +/- 24 fmol/mg DNA. This value is twice that of intact males and is not significantly different (P greater than 0.05) from the aortic cytoplasmic progesterone receptor content (190 +/- 32 fmol/mg DNA) of 17 beta-estradiol-injected oophorectomized females. These studies establish that intracellular distribution of aortic androgen and estrogen receptors of male or female AXC/SSh rats is regulated by endogenous hormones. The observation that 17 beta-estradiol modulates aortic progesterone receptor content indicates that rat aortic estrogen receptors are physiologically functional. Our data imply that steroid hormones directly regulate aspects of rat cardiovascular cell function and that sexually dimorphic differential regulation may characterize male and female aortic metabolism.
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