Role of the gonads in hypertension-prone rats
Role of the gonads in hypertension-prone rats
复制标题
性腺在高血压易感大鼠中的作用
DOI：
--
复制
发表时间：
1975
影响因子：
15.3
通讯作者：
R. Tuthill
中科院分区：
文献类型：
--
作者：
L. Dahl;K. Knudsen;E. Ohanian;M. Muirhead;R. Tuthill
在遗传性高血压倾向（S）大鼠品系中，先前观察到雄性大鼠在高盐饮食下通常比雌性大鼠更快地发展高血压，尽管最终压力在两种性别中相似。一项遗传学研究表明，设定血压水平与性别无关，因此人们认为性腺可能与此有关。在目前的研究中，雄性动物的阉割对血压没有影响，但在雌性动物中，无论是高盐饮食还是低盐饮食，都会导致血压升高，这种升高与雄性动物的血压无法区分。阉割导致女性比对照组更大的增长，而它在男性中有相反的效果。据推测，这些变化是由于阉割对垂体生长激素的影响，增加了雌性生长激素的净输出（或增强受体对生长激素的敏感性），而雄性则相反。从其他人的工作中，有一些数据与这种解释相符。在实验中，生长激素会导致大鼠高血压。因此，可以想象生长激素参与了在这些去势雌性动物中观察到的高血压增加。由于在接受高和低NaCl饮食的去势雌性动物中均观察到对血压的影响，因此认为血压影响不太可能仅仅是由于食物中NaCl摄入量增加与生长速度加快相关。有人认为，这种伴随卵巢功能停止的血压升高可能与尚未解决的妇女“绝经期”高血压问题有关：在遗传易感个体中，与绝经期卵巢功能下降相关的生长激素增加可能比其他情况提前几年刺激高血压的出现。
In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought that the gonads might be involved. In the present work, castration of males had no effect on blood pressure but in the females it caused a rise in pressure that could not be distinguished from that in males, both on a high and low salt diet. Castration resulted in greater growth in females than in controls, whereas it had the opposite effect in males. It was speculated that these changes were due to influences on pituitary growth hormone with castration increasing the net output of growth hormone (or enhancing receptor sensitivity to it) in the female and the opposite in the male. From the work of others, there are some data compatible with such an interpretation. Experimentally, growth hormone will induce hypertension in rats. Therefore, it is conceivable that growth hormone is involved in the increment in hypertension observed in these castrate females. Because the effect on blood pressure was observed in castrate females on both high and low NaCl diets, it was considered unlikely that the blood pressure effect was simply due to increased NaCl intake in the food associated with greater growth. It was suggested that this rise in blood pressure with cessation of ovarian function might bear on the unsettled question of "menopausal" hypertension in women: in the genetically susceptible individual an increase in growth hormone associated with declining ovarian funtion in the menopause could provide the stimulus for the appearance of hypertension some years earlier than would otherwise have been the case.