Sodium restriction increases renal vascular reactivity to adrenergic stimuli

We have shown that chronic sodium restriction up-regulates renal α₁-adrenoceptors (AR) in rats. The present experiments were designed to lest the functional significance of renal a,-AR after long-term altered NaCl intake. SpragueDawley rats were fed with ahigh salt (HS, 1.5% NaCl), normal salt (NS, 0.3% NaCl), or low salt (LS, 0.03% NaCl) diet for 4 weeks. The left kidney was isolated and perfused with a physiologic salt solution at a constant flow rate during each experiment α-AR were activated via perivascular renal nerve stimulation (RNS) and by addition of norepinephrine (NE) to the perfusate. Increases in perfusion pressure (PP. mmHg) indicated renal vasoconstriction. *ignifies p<0.05 compared to NS. RNS(Hz) 0 1 2 4 8 16 PP HS 50 M.U02 52 1±0.4 55.0±0.6 680±2.1 74.1±32 NS 50 M 1±0 1 52.8±0.3 56.1±0.8 64.6±1 8 69.3±1.9 LS 50 52.7±03 54.1±04 59.4±1.4 76.9±3.2* 85.1±35* NE(μM) 0 0.1 0.2 0.3 0.4 0.5 0.6 PP HS 50 56±2 62±3 67±4 73±5 79±4 87±5 NS 50 58±5 64±7 69±8 74±8 78±8 84±8 LS 50 57±3 64±5 74±7 88±11 109±15 144±24* Both RNS and NE infusion induced renal vasoconstriction was blocked by the α₁-AR antagonist prazosin but not by the α₂-AR antagonist rauwolscine. Addition of 50 mM KC1, as a non-specific vasoconstrictor, to the perfusate increased PP from 50 mmHg tol95±28,212±21, and 213±11 mmHg in LS, NS, and HS rats, respectively. These results suggest that the up-regulation of renal α₁-AR in sodium restricted rats enhances sympathetic neural control of renal vascular function.