Abstract
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.
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