Blood pressure and hemodynamic responses to an acute sodium load in humans

The purpose of this study was to investigate the acute blood pressure (BP) and hemodynamic effects of sodium chloride (3% intravenous solution). Although many studies link a change in dietary sodium to a change in BP, few consider the effects of sodium concentration in the blood on BP. We hypothesized that an intravenous sodium load would increase BP, and we quantified alterations in cardiac output ((Q) over dot c) and peripheral vascular resistance (PVR). Thirteen subjects (age 27 +/- 2 yr) underwent a 60-min 3% saline infusion (0.15 ml center dot kg(-1) center dot min(-1)). BP was assessed on a beat-to-beat basis with a Finometer, (Q) over dot c was assessed via the CO2 rebreathing technique, and PVR was derived. Serum sodium and osmolality increased, and hematocrit declined during the infusion (ANOVA, P < 0.01). Mean arterial pressure (MAP) increased continuously during the infusion from 81.8 +/- 3.4 to 91.6 +/- 3.6 mmHg (ANOVA, P < 0.01). BP responsiveness to sodium was expressed as the slope of the serum sodium-MAP relationship and averaged 1.75 +/- 0.34 mmHg center dot mmol(-1) center dot l(-1). BP responsiveness to the volume change was expressed as the slope of the hematocrit-MAP relationship and averaged -2.2 +/- 0.35 mmHg/%. The early change in MAP was mediated by an increase in (Q) over dot c and the late change by an increase in PVR (P < 0.05), corresponding to a 30% increase in plasma norepinephrine. In conclusion, an acute infusion of hypertonic saline was effective in increasing BP, and both sodium and volume appear to be involved in this increase; acute BP responsiveness to serum sodium can be quantified using a MAP-sodium plot.