Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma
potassium alterations in acute
alkalosis. Respiratory and metabolic
alkalosis were induced by
hyperventilation and intravenous NaHCO3 or
tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced
alkalosis provoked decreases in plasma
potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced
alkalosis elicited an increase in plasma
potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01).
Hypokalemia in
respiratory alkalosis was associated with a decrease in the plasma
norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of
epinephrine,
insulin,
glucagon,
cortisol, and
aldosterone. However, this
hypokalemia was not affected by
phentolamine. Also,
somatostatin did not modify the hypokalemic response. NaHCO3-induced
hypokalemia was associated with a decline in the plasma
aldosterone and
norepinephrine concentrations. The decline in plasma
norepinephrine in NaHCO3-induced
alkalosis followed the decrease in plasma
potassium. In Tris-induced
alkalosis, plasma
insulin increased but
norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma
potassium alterations in bilaterally nephrectomized dogs with acute
alkalosis.