Control of extracellular sodium concentration by antidiuretic hormone-thirst feedback mechanism.
The effectiveness of the antidiuretic hormone (ADH)-thirst feedback mechanism to control extracellular sodium concentration was studied in dogs. The design consisted of increasing daily sodium intake from 10 to 200 meq in a group of dogs, first in the normal condition and second with a continuous 24 h/day infusion of an amount of ADH sufficient to maintain urine osmolarity at a maximal level and with fixed water intake. We were therefore able to compare the effectiveness of sodium concentration control in the same dogs with and without feedback control of the ADH-thirst mechanism, the difference in effectiveness being a quantitative measure of the control capability of the system. In the normal condition the increase in sodium intake resulted in a steady-state 2.3% elevation in sodium concentration. With the feedback control of ADH secretion and water intake blocked, the same sodium forcing produced an 11.9% increase in extracellular sodium concentration. The minimum feedback gain for the system calculated from the data is -4.2. We conclude that control of sodium concentration in the intact state is accomplished mainly by the ADH-thirst feedback mechanism.
D000818:Animals; D001794:Blood Pressure; D004231:Diuresis; D004285:Dogs; D004326:Drinking; D005110:Extracellular Space / Q000378:metabolism*; D005246:Feedback; D011188:Potassium / Q000097:blood / Q000652:urine; D012964:Sodium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D014667:Vasopressins / Q000494:pharmacology*; D014882:Water-Electrolyte Balance / Q000187:drug effects*
D014667:Vasopressins; D012964:Sodium; D011188:Potassium