Regulation of sodium balance in hypertension.

Abstract

SUMMARY Pressure natriuresis, defined as the relationship between sodium excretion and mean arterial pressure (MAP), was assessed during graded reduction of arterial pressure with nltroprusside in 12 uncomplicated essential hypertensives. In all patients, sodium excretion fell linearly with reductions in arterial pressure (r > 0.71; p < 0.05). The percent change of sodium excretion from control per mm Hg change in MAP (AUN.V/AMAP) was less in patients with resting MAP above 120 mm Hg than in those with lower BP (1.4% ± 0.1% versus 3.2% ± 0.3%; p < 0.001), but the pressure at which urine flow extrapolated to zero (77 ± 4 mm Hg) was not significantly different in the two groups. Further, there was a significant correlation between AUN.V/AMAP and resting MAP (r = - 0.65, p < 0.05), suggesting that the sensitivity of pressure natriuresis was, in part, determined by the level of resting arterial pressure. This attenuation of pressure natriuresis might reduce sodium loss and thereby preserve body fluid volume in the face of persistent hypertension. The slope of the relationship between sodium excretion and arterial pressure was also significantly correlated (r = 0.70; p < 0.05) with plasma volume (PV). Thus, two mechanisms might be activated in essential hypertension to avoid dangerous sodium and volume depletion: 1) attenuation of pressure natriuresis at higher levels of arterial pressure, and 2) blunting of pressure natriuresis by volume contraction. Therefore, hypovolemia might be, at the same time, the consequence of hypertension and a limiting factor for pressure natriuresis. By this hypothesis, the lower slope of pressure natriuresis is secondary to hypertension rather than its cause. (Hypertension 2: 515-523, 1980)