The anti-pressor effect of oral potassium supplementation to salt loading induced blood pressure increasing

Objective: To estimate the possible existing anti-pressor effect of oral potassium chloride supplementation for short term chronic salt loading induced blood pressure rising through diet intervention. Methods: Essential hypertensive families and subjects are selected as participants, then baseline study followed by dietary intervention including 7 days low salt diet (50 mmol NaCL each day), 7 days high salt diet(340 mmol NaCL each day) and 7 days high salt with potassium supplementation( 60 mmol each day) will be carried out. Blood pressure and body weight will be measured; urinal sodium and potassium excretion will be determined. Result: 49 people from 14 families were enrolled in this one month study. The average blood pressure of all subjects presented a fluctuating change. 13 of all the participants were deemed as salt sensitive (SS), 36 were defined as non-salt sensitive (NSS). The blood pressures in SS showed significant decreasing during low salt diet (8.7 7.7/5.3 4.7 mmHg), then increasing after salt loading (9.9 5.2/5.1 2.8 mmHg), and declining again as a result of potassium mending (9.6 7.4/5.6 4.8 mmHg). The blood pressures in NSS mainly significantly decreased during low salt diet, further declining of DBP after salt loading and dropping of SBP after potassium mending were found, MBP had little change or had no obvious change at the two later stages. During high salt with potassium supplementation, the 24 hour urinary sodium excretion in SS were significantly increased than in NSS(P 0.01). Conclusion: Salt restriction lowered BP while salt loading elevated BP of partial subjects (SS), and potassium mending declined it again. So it is concluded that oral potassium chloride supplementation, through interaction with sodium can promote urinary sodium excretion, have an anti-pressor effect for short term chronic salt loading which induced blood pressure rising in Chinese people who are salt sensitive.