Sowers J R, Resch G, Tempel G, Herzog J, Colantino M
Acta Endocrinol (Copenh). 1979 Jan;90(1):1-7. doi: 10.1530/acta.0.0900001.
A hypothalamic role in the aetiology of hypertension in the spontaneously hypertensive rat (SHR) has been suggested by prior observations. In an attempt to determine whether the central control of prolactin (PRL) release is altered in the SHR we have compared the PRL response to immobilization stress, thyrotrophin releasing hormone (TRH), haloperidol, and L-DOPA in the SHR and in normotensive Wistar control rats. Carotid artery catheters were inserted 48 h prior to the PRL response studies and the catheters were maintained patent with heparinized saline. Timed blood samples were obtained in SHR and control rats weighing 180-225 g. The SHR demonstrated elevated basal serum levels of PRL and greater PRL responses to stress. However, administration of L-DOPA resulted in a similar suppression of serum PRL in the SHR and in the normotensive controls. These findings suggest alteration in the central control of PRL release in the SHR. Observations of elevated basal PRL, exaggerated PRL in response to L-DOPA in SHR are consistent with normal pituitary responsiveness to dopamine suppression of PRL release, but defective hypothalamic metabolism of dopamine. Alterations in central dopamine control mechanisms in the SHR may play a role in the pathogenesis of essential hypertension in these animals.
先前的观察结果提示，下丘脑在自发性高血压大鼠（SHR）高血压病因学中发挥作用。为了确定SHR中催乳素（PRL）释放的中枢控制是否改变，我们比较了SHR和正常血压的Wistar对照大鼠对固定应激、促甲状腺激素释放激素（TRH）、氟哌啶醇和左旋多巴（L-DOPA）的PRL反应。在进行PRL反应研究前48小时插入颈动脉导管，并用肝素化盐水保持导管通畅。对体重180 - 225克的SHR和对照大鼠采集定时血样。SHR的基础血清PRL水平升高，对应激的PRL反应更强。然而，给予L-DOPA后，SHR和正常血压对照大鼠的血清PRL受到类似程度的抑制。这些发现提示SHR中PRL释放的中枢控制发生改变。SHR基础PRL升高、对L-DOPA反应性PRL增强的观察结果，与垂体对多巴胺抑制PRL释放的正常反应性一致，但下丘脑多巴胺代谢存在缺陷。SHR中枢多巴胺控制机制的改变可能在这些动物原发性高血压的发病机制中起作用。
