| pubmed-article:2184674 | pubmed:abstractText | The ability to regulate renal sodium excretion after an acute reduction of total body sodium by peritoneal dialysis (PD) and subsequent dietary sodium repletion was investigated in 12 [6 intact, 6 chronically cardiac denervated (CD)] conscious, chronically instrumented dogs. For 10 days, balance experiments were performed with daily measurements of mean arterial blood pressure (MABP), right atrial pressure (RAP), and heart rate (HR). The prepared diet contained 0.5 (days 1-3 after PD) or 2.5 mmol Na.kg body wt-1.day-1 (control day and days 4-9 after PD). Control values were all similar in both groups except higher fasting plasma renin activities (PRA) were observed in the CD dogs [2.6 +/- 0.4 vs. 1.0 +/- 0.2 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.05]. Days 1-4 after PD, RAP fell in both groups by 2-3 cmH2O, and renal sodium excretion decreased abruptly. PRA increased to 22.8 +/- 4.1 (intact) and 29.9 +/- 4.9 ng ANG I.ml-1.h-1 (CD dogs) (day 3 after PD). Both groups continued to retain sodium, and when it was available again, PRA decreased. After the amount of sodium lost by PD was regained, the intact dogs remained in a balanced equilibrium. In the CD dogs, PRA was still above control, and they retained sodium in excess (+ 1.9 +/- 0.1 mmol/kg body wt). We conclude that the cardiac nerves are not essential for stimulating PRA and sodium retention after an acute sodium deficit. However, the inhibition of PRA and the rapid adjustment of sodium balance during sodium repletion is impaired after cardiac denervation. | lld:pubmed |
