1. In order to confirm and investigate the hypotensive effect of a high potassium intake we compared mean arterial pressure (MAP), water and electrolyte balance, plasma and urinary noradrenaline (NA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in 20 inpatients with mild or moderate essential hypertension on a control diet (Na: 260, K: 75 mmol/day), and after high (K: 175 mmol/day) and low potassium diets (K: 25 mmol/day).
2. After potassium loading, urinary volume (UV) and urinary excretion of sodium (UNaV) and of potassium (UKV) were elevated, and MAP, body weight, plasma volume (PV), extracellular fluid volume (ECFV) and total exchangeable sodium (Nae) were reduced significantly.
3. After potassium loading, PRA, PAC, plasma and urinary NA increased and the pressor response to infused noradrenaline and angiotensin II decreased significantly.
4. The reduction of MAP after potassium loading correlated positively with PV and ECFV during the control period. In addition, significant correlations were found between ΔUV and ΔUNaV, —ΔPV and ΔU/NaV, —ΔPV and Δ plasma NA, and Δ plasma NA and Δ PRA.
5. Patients with low PRA had high PV, ECFV and Nae during the control period, and showed greater reductions of MAP, PV, ECFV and Nae after potassium loading.
6. After potassium restriction, UNaV, PRA and urinary NA decreased and PV increased, and MAP did not change significantly.
7. These results suggest that the hypotensive effect of high potassium intake may be caused by reduction of body fluid volume via augmentation of Na excretion.