Omvik P
Acta Med Scand Suppl. 1981;646:77-89. doi: 10.1111/j.0954-6820.1981.tb02625.x.
Pressure natriuresis, defined as the relationship between sodium excretion and mean arterial pressure (MAP), was assessed during graded reduction of arterial pressure with nitroprusside in 16 essential hypertensives (EH). In all patients, sodium excretion fell linearly with reductions in arterial pressure (r greater than 0.68; p less than 0.05). The per cent change of sodium excretion from control per mmHg change in MAP (delta UNaV/delta MAP) was less in patients with resting MAP above 120 mmHg than in those with lower blood pressure (1.4 +/- 0.1 versus 3.0 +/- 0.3; p less than 0.001), but the pressure at which urine flow extrapolated to zero (75 +/- 3 mmHg) was not significantly different in the two groups. The slope of the relationship between sodium excretion and arterial pressure was significantly correlated with resting MAP (r = -0.67; p less than 0.05) and with plasma volume (r = 0.61; p less than 0.05). Furthermore, the ratio delta UNaV/delta MAP also rose in concert with body fluid volumes when a salt load of 8 g of sodium chloride was added to the regular diet. Thus, the sensitivity of pressure natriuresis was determined by level of resting arterial pressure and body fluid volumes. These experiments suggest tht two mechanisms might be activated in EH 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. By this hypothesis, the lower slope of pressure natriuresis is secondary to hypertension rather than its cause.
压力性利钠作用定义为钠排泄与平均动脉压(MAP)之间的关系,在16例原发性高血压(EH)患者中,用硝普钠逐渐降低动脉压时对其进行了评估。在所有患者中,钠排泄量随动脉压降低呈线性下降(r>0.68;p<0.05)。静息MAP高于120 mmHg的患者,MAP每变化1 mmHg时钠排泄量相对于对照的变化百分比(δUNaV/δMAP)低于血压较低的患者(1.4±0.1对3.0±0.3;p<0.001),但两组中尿流外推至零时的压力(75±3 mmHg)无显著差异。钠排泄与动脉压之间关系的斜率与静息MAP显著相关(r = -0.67;p<0.05),与血浆容量也显著相关(r = 0.61;p<0.05)。此外,当在常规饮食中添加8 g氯化钠的盐负荷时,δUNaV/δMAP比值也随体液量同步升高。因此,压力性利钠作用的敏感性由静息动脉压水平和体液量决定。这些实验表明,在原发性高血压中可能激活了两种机制以避免危险的钠和容量耗竭:1)在较高动脉压水平时压力性利钠作用减弱,2)容量收缩使压力性利钠作用减弱。根据这一假设,压力性利钠作用较低的斜率是高血压的结果而非原因。