Enhanced sympathetic control of renal function in rats congenic for the hypertension‐related region on chromosome 1

Recent studies suggest that a quantitative trait locus (QTL) for blood pressure (BP) on rat chromosome 1 is associated with exaggerated sympathetic nervous activity. The aim of the present study was to examine whether this QTL can affect BP by altering sympathetic control of renal function. Male stroke-prone spontaneously hypertensive rats of Izumo origin (SHRSP/Izm), Wistar-Kyoto rats (WKY/Izm) and rats from a WKY/Izm congenic strain that contains an SHRSP/Izm chromosomal segment between D1Wox29 and D1Arb21 (WKYpch1.0) were used. Clearance and micropuncture experiments were performed in anaesthetized rats after acute unilateral renal denervation (DN). Mean BP in sham-operated WKYpch1.0 was significantly higher than that in WKY/Izm. The DN procedure elicited a greater reduction in renal noradrenaline levels in SHRSP/Izm and WKYpch1.0 than in WKY/Izm. In both SHRSP/Izm and WKYpch1.0, DN decreased renal vascular resistance and filtration fraction, whereas it increased renal blood flow and urinary and fractional excretion of sodium. Unilateral renal denervation did not affect these parameters in WKY/Izm. Unilateral renal denervation decreased the tubuloglomerular feedback (TGF) responsiveness only in SHRSP/Izm, whereas it increased the non-perfused early proximal flow rate in SHRSP/Izm and WKYpch1.0. The results of the present study indicate that the renal sympathetic nervous system exerts enhanced tonic control of the renal vasculature and tubular function in SHRSP/Izm and WKYpch1.0, but not in WKY/Izm. Neural impact on the TGF response in WKYpch1.0 is indiscernible. Thus, a gene or genes in the QTL may influence BP, at least in part, through renal vasoconstriction and sodium retention mediated by the enhanced activity of the renal sympathetic nerves.