Persson A E, Boberg U
Department of Physiology and Biophysics, University of Lund, Sweden.
J Cardiovasc Pharmacol. 1988;12 Suppl 3:S27-35.
Renal regulation of extracellular fluid volumes via the tubuloglomerular feedback control (TGF) has been studied in rat experiments. Important modulation of the TGF mechanism was achieved from arterial blood pressure level and extracellular fluid volume via renal interstitial pressure changes. This volume-regulating mechanism has been studied in spontaneously hypertensive rats of the Milan strain (MHS) and compared with Milan normotensive rats (MNS). During development of hypertension, the TGF mechanism was highly sensitive and activated to reduce glomerular filtration rate and retain electrolytes and water. When blood pressure was increased in the adult MHS animals the TGF mechanism was normalized. It could be speculated that the cause of the increased TGF mechanism was dependent on an increased Na-K-2 Cl cotransport into the macula densa cells. In SHR rats compared to Wistar-Kyoto rats, the TGF sensitivity was also increased but, in contrast, the TGF mechanism was not activated in these animals to retain fluid. Some other mechanism for the development of hypertension in these rats has to be proposed.
通过肾小管-肾小球反馈控制（TGF）对细胞外液量的肾脏调节已在大鼠实验中进行了研究。通过肾间质压力变化，从动脉血压水平和细胞外液量实现了对TGF机制的重要调节。已在米兰品系自发性高血压大鼠（MHS）中研究了这种容量调节机制，并与米兰正常血压大鼠（MNS）进行了比较。在高血压发展过程中，TGF机制高度敏感并被激活，以降低肾小球滤过率并保留电解质和水分。当成年MHS动物的血压升高时，TGF机制恢复正常。可以推测，TGF机制增加的原因取决于进入致密斑细胞的Na-K-2 Cl共转运增加。与Wistar-Kyoto大鼠相比，SHR大鼠的TGF敏感性也增加，但相反，这些动物的TGF机制未被激活以保留液体。必须提出这些大鼠高血压发展的其他一些机制。
