Figure 113

Nitric oxide in mediation of pressure natriuresis. Several recent studies have demonstrated that nitric oxide also directly affects tubular sodium transport and may be an important mediator of the changes induced by arterial pressure in sodium excretion, as described in Figure 1-5 [9,24]. Increases in arteriolar shear stress caused by increases in arterial pressure stimulate production of nitric oxide. Nitric oxide may exert direct effects to inhibit tubule sodium reabsorptive mechanisms and may elicit vasodilatory actions. Nitric oxide increases intracellular cyclic GMP (cGMP) in tubular cells, which leads to a reduced reabsorption rate through cGMP-sensitive sodium entry pathways [24,25]. When formation of nitric oxide is blocked by agents that prevent nitric oxide synthase activity, sodium excretion is reduced and the pressure natriuresis relationship is markedly suppressed. Thus, nitric oxide may exert a critical role in the regulation of arterial pressure by influencing vascular tone throughout the cardiovascular system and by serving as a mediator of the changes induced by the arterial pressure in tubular sodium reabsorption. (Adapted from Navar [3].)

Filtered NA+ load = Plasma Na x Glomerular filtration rate = 140 mEq/L x 0.120 L/min = 16.8 mEq/min x 1440 min/d = 24,192 mEq/min Urinary Na+ excretion = 200 mEq/d Fractional Na excretion = 0.83% Fractional Na reabsorption = 99.17%
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