Abstract Body: Introduction: Neurogenic mechanisms, which increase sympathetic drive, are involved in salt-sensitive hypertension.
Hypothesis: We hypothesized that chronic high salt intake can elevate blood pressure (BP) and modulate the sympathetic nerve responses to an acute increase in blood sodium concentration.
Methods: Post-weaning male Wistar rats were assigned to a high (0.9% Na⁺, HSD) or standard (0.27% Na⁺, SSD) sodium diet for 12 weeks. In a) conscious freely moving rats (N=6), blood pressure (BP) and renal excretory responses to a 1-min IV hypertonic (3M NaCl, 1.8 mL/kg/min) infusion were recorded and b) urethane anesthetized rats (N=8-10), BP, renal (RSNA) and lumbar (LSNA) sympathetic nerve activity were recorded in response to a 3M NaCl infusion (1.8 mL/kg/min).
Results: In conscious rats, BP was elevated following HSD (BP [mmHg] 108±2.5 SSD vs. 131±1.5 HSD, p=<0.0001) and HSD rats displayed an attenuated BP increase to 3M saline (but not osmotic equivalent sorbitol) (ΔBP [mmHg] +26±3 SSD vs. +11±2 HSD, p=0.0014). Conscious HSD rats exhibited attenuated volume and sodium excretion in response to 3M NaCl (1h Na excretion [mmol] SSD 1.3±0.2 vs. HSD 0.3±0.1, p=0.0005). In anesthetized rats, BP was elevated following HSD (BP [mmHg] 100±3 SSD vs. 115±3 mmHg HSD, p=<0.0045) and 3M NaCl caused a transient increase in BP, which was not different between HSD and SSD rats. Resting SNA, assessed as % of maximal observed sympathetic drive, was smaller in the HSD group for LSNA (Resting SNA 33±3% SSD vs. 21±1.5% HSD, p=0.0022) with no detectable changes in resting RSNA. In response to 3M NaCl, LSNA displayed no change in SSD rats (8±9%) but significantly and persistently increased in HSD rats (LSNA (%) 80-min post-3M NaCl, 8±9 vs. 42±5, p=0.0038). RSNA responded to 3M NaCl with a rapid peak drop within 5 min in SSD (-39%) and HSD (-35%) which did not recover in HSD rats at the end of recording (RSNA (%) 80-min post 3M NaCl, 18±16 SSD and -23±8 HSD, p=0.0297).
Conclusion: Chronic high sodium intake post-weaning, as seen in a Western diet, evokes salt-sensitive hypertension and differential sympathetic control of SNA with a) increased LSNA driving vascular contraction at baseline and in response to acute hypernatremia and b) attenuated renal sodium handling that may be influenced by RSNA-mediated renal blood flow regulation.