ANDROGEN RECEPTOR AND THE TESTES INFLUENCE HYPERTENSION IN A HYBRID RAT MODEL
ANDROGEN RECEPTOR AND THE TESTES INFLUENCE HYPERTENSION IN A HYBRID RAT MODEL
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DOI：
10.1161/01.hyp.17.6.1104
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发表时间：
1991-06-01
期刊：
影响因子：
8.3
通讯作者：
JOHNSON, ML
中科院分区：
文献类型：
--
作者：
ELY, DL;SALISBURY, R;JOHNSON, ML
本研究的目的是确定雄激素受体缺陷的雄性与高血压亲本杂交时是否会发生高血压。将睾丸雌性化（Tfm）基因杂合的King-Holtzman雌性大鼠（n = 15）与自发性高血压雄性大鼠（SHR）杂交，从5-14周开始每周测量血压。大约50%的F1杂交雄性是Tfm雄性和雄激素受体缺乏，50%是正常的。在同一时期，研究人员还对金-霍尔兹曼雄性、Tfms和雌性大鼠的血压进行了跟踪调查。12周后，F1正常杂交雄鼠收缩压显著高于Tfm杂交雄鼠（分别为195 +/- 8和170 +/- 8 mm Hg） （p < 0.05）。雄性和Tfm Holtzman大鼠的血压分别为120 +/- 5 mm Hg和110 +/- 6 mm Hg。阉割使杂交雄鼠血压降低38 mm Hg， Tfm杂交雄鼠血压降低27 mm Hg。雌性F1杂交种的压力高于雌性Holtzman对照（155 +/- 6 mm Hg vs 110 +/- 6 mm Hg, p < 0.01），但低于雄性F1杂交种和Tfm杂交种。卵巢切除后植入睾酮的女性没有出现血压升高。血浆电解质、去甲肾上腺素和胆固醇在正常和Tfm杂交男性之间无显著差异。结果表明，雄激素受体和睾丸衍生因子的存在介导了杂交雄性的血压升高。这可能与Y染色体效应或性别影响位点有关，因为正常和Tfm男性的血压都明显高于其女性兄弟姐妹。
The objective of this study was to determine if males with a deficient androgen receptor would develop hypertension when crossed with a hypertensive parent. Female King-Holtzman rats (n = 15), heterozygous for the testicular feminization (Tfm) gene, were crossed with male spontaneously hypertensive rats (SHR), and blood pressure was measured weekly from 5-14 weeks in the F1 hybrid males. Approximately 50% of the F1 hybrid males were Tfm males and androgen receptor-deficient, and 50% were normal. Blood pressure in the parent King-Holtzman males, Tfms, and female rats was also followed for the same time period. The F1 normal male hybrids had a significantly higher (p < 0.05) systolic blood pressure than the Tfm hybrid males after 12 weeks (195 +/- 8 versus 170 +/- 8 mm Hg, respectively). Blood pressure in the male and Tfm Holtzman rats was 120 +/- 5 mm Hg and 110 +/- 6 mm Hg, respectively. Castration lowered blood pressure by 38 mm Hg in the hybrid males and 27 mm Hg in the Tfm hybrids. Female F1 hybrids also showed a pressure rise above that of female Holtzman controls (155 +/- 6 mm Hg versus 110 +/- 6 mm Hg, p < 0.01) but lower than the F1 males and Tfm hybrids. Ovariectomized females with testosterone implants did not show an elevation in blood pressure. Plasma electrolytes, norepinephrine, and cholesterol were not significantly different between normal and Tfm hybrid males. The results suggest that the presence of an androgen receptor and a testis-derived factor mediate the blood pressure rise in the hybrid males. A Y chromosome effect or sex-influenced locus may be involved since both the normal and Tfm males had significantly higher blood pressures than their female siblings.