Neuser D, Schulte-Brinkmann R, Kazda S
Department of Pharmacology, BAYER AG, Pharma Research Center, Wuppertal, F.R.G.
J Cardiovasc Pharmacol. 1990 Dec;16(6):971-4. doi: 10.1097/00005344-199012000-00017.
We have investigated the role of the parathyroid gland (PTG) in the long-term development of blood pressure (BP) in stroke prone spontaneously hypertensive rats (SHR/SP) and Wistar Kyoto (WKY) rats. After ablation of their own PTGs, SHR/SP animals received PTGs from WKY rats and vice versa. Transplantation resulted in a normal calcium and parathyroid hormone status without signs of hypoparathyroidism. All animals received a high salt diet (8% NaCl) for 4 weeks after transplantation of PTGs. In SHR/SP, which received PTGs from WKY, development of high BP was clearly attenuated when compared to sham-operated SHR/SP rats. WKY rats with PTGs from SHR/SP rats became hypertensive, while WKY sham-operated animals remained normotensive. PTGs from SHR/SP rats are able to induce hypertension in normotensive WKY rats.
我们研究了甲状旁腺（PTG）在易患中风的自发性高血压大鼠（SHR/SP）和Wistar Kyoto（WKY）大鼠血压（BP）长期发展中的作用。在切除自身的PTG后，SHR/SP动物接受来自WKY大鼠的PTG，反之亦然。移植导致钙和甲状旁腺激素状态正常，无甲状旁腺功能减退的迹象。在PTG移植后，所有动物接受高盐饮食（8%氯化钠）4周。在接受来自WKY的PTG的SHR/SP中，与假手术的SHR/SP大鼠相比，高血压的发展明显减弱。接受来自SHR/SP大鼠的PTG的WKY大鼠变得高血压，而假手术的WKY动物仍保持血压正常。来自SHR/SP大鼠的PTG能够在血压正常的WKY大鼠中诱发高血压。
