High sodium intake enhances renal nerve and antinatriuretic responses to stress in spontaneously hypertensive rats.

Abstract

The effects of high sodium intake (drinking 0.9% NaCl for 15 days) on the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from stressful environmental stimulation (air jet to head) were examined in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). On a normal sodium intake in SHR, air stress increased renal sympathetic nerve activity 77% and decreased urinary sodium excretion 28% without altering effective renal plasma flow or glomerular filtration rate. By contrast, in conscious SHR on high sodium intake, the same air stress caused a greater increase in renal sympathetic nerve activity (103%) and a greater antinatriuresis (42%) along with reductions in effective renal plasma flow and glomerular filtration rate. Surgical renal denervation prevented the antinatriuretic responses to air stress in other conscious SHR on high or normal sodium intake. In conscious WKY, air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion, regardless of normal or high sodium intake. We conclude that the enhanced renal sympathetic nerve activity and antinatriuretic responses to air stress in conscious SHR on high sodium intake are dependent on a centrally mediated facilitation of sympathetic neural outflow to the kidney. The greater antinatriuretic response to air stress in conscious SHR than in WKY may reflect a greater genetic predisposition in SHR to increase renal sympathetic nerve activity during air stress.