Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

Abstract

In rats fed high sodium diet, increasing renal pelvic pressure ≥3 mm Hg activates renal mechanosensory nerves, resulting in a renorenal reflex–induced increase in urinary sodium excretion. The low activation threshold of the renal mechanosensory nerves suggests a role for natriuretic renorenal reflexes in the regulation of arterial pressure and sodium balance. If so, interruption of the afferent renal innervation by dorsal rhizotomy (DRX) at T 9 -L 1 would impair urinary sodium excretion and/or increase arterial pressure during high dietary sodium intake. DRX and sham-DRX rats were fed either a high or a normal sodium diet for 3 weeks. Mean arterial pressure measured in conscious rats was higher in DRX than in sham-DRX rats fed a high sodium diet, 130±2 vs 100±3 mm Hg ( P <0.01). However, mean arterial pressure was similar in DRX and sham-DRX rats fed a normal sodium diet, 115±1 and 113±1 mm Hg, respectively. Steady-state urinary sodium excretion was similar in DRX and sham-DRX rats on high (17.9±2.2 and 16.4±1.8 mmol/24 h, respectively) and normal (4.8±0.3 and 5.0±0.4 mmol/24 h, respectively) sodium diets. Studies in anesthetized rats showed a lack of an increase in afferent renal nerve activity in response to increased renal pelvic pressure and impaired prostaglandin E 2 –mediated release of substance P from the renal pelvic nerves in DRX rats fed either a high or a normal sodium diet, suggesting that DRX resulted in decreased responsiveness of peripheral renal sensory nerves. In conclusion, when the afferent limb of the renorenal reflex is interrupted, a high sodium diet results in increased arterial pressure to facilitate the natriuresis and maintenance of sodium balance.