Unchanged central hemodynamics after six months of moderate sodium restriction with or without potassium supplement in essential hypertension.

Sodium (Na) restriction and potassium (K) supplementation has been recommended as treatment of essential hypertension but the mechanism by which these may reduce blood pressure (BP) is unknown. We examined if moderately reduced Na intake, combined with a low-Na/high-K salt alternative (Pansalt: NaCl 57%, KCl 28%, MgSO4 12%) as substitute for standard table salt, induced clinically significant BP reduction in hypertensive patients and, if this therapy reduced total peripheral resistance. After a 2-month control period 40 patients aged 21-67 years with mean casual BP 156/103 mmHg were given a salt restricted diet (120 mmol Na/24 h) for 6 months. In addition, they were randomised in a double-blind manner to receive either Pansalt (P-group) or standard NaCl (S-group) as table salt in small amounts. Cardiac output was measured by dye dilution. Daily Na excretion was similarly reduced (20%) in both groups while K excretion was slightly increased in the P-group and reduced in the S-group (difference p < 0.05). No large changes occurred in 24-h ambulatory BP (by Accutracker II) or intraarterial pressure (through a brachial artery catheter) at rest or during exercise while casual BP was reduced (p < 0.05) 13/8 mmHg in the P-group and 8/5 mmHg in the S-group. While cardiac output was slightly reduced at rest and during 50W exercise in the P-group, no significant changes were seen in total peripheral resistance in either group. Thus, moderate reduction in Na intake, with or without addition of K, is not sufficient to induce significant long-term intraarterial or 24-h ambulatory BP changes in essential hypertension. Without BP changes invasively determined central hemodynamics remains remarkably stable over a 6-month period.