Renal vascular morphology and haemodynamics in Dahl salt-sensitive rats onhigh salt-low potassium diet: neural and genetic influences

Objective A dietary combination of high salt and tow potassium (HS-LK) exac erbates hypertension in Dahl salt-sensitive (DS) rats and renders Dahl salt -resistant (DR) rats hypertensive. In both strains, the hypertension is acc ompanied by remodelling of the renal resistance vasculature, and is attenua ted by peripheral chemical sympathectomy. In the current study, we sought t o determine whether the sympathetic nervous system is causally involved in mediating the renal vascular and haemodynamic alterations associated with H S-LK feeding in Dahl rats. Design Two groups each of DS and DR rats were maintained on HS-LK diet (8% NaCl, 0.2% KCl) for 8 weeks. One group of DS (n = 9) and DR (n = 8) were tr eated with 6-hydroxydopamine (6-OHDA) in 0.001 N HCl vehicle to chemically ablate peripheral sympathetic nerve terminals. The two remaining groups (n = 8 each) received equivalent injections of vehicle. Methods At the end of the dietary regimen, arterial blood pressure (ABP), g lomerular filtration rate (GFR) and renal blood flow (RBF) were measured, a nd the structure of intra-renal resistance vessels was examined by planar m orphometric analysis of coronal sections prepared from perfusion-fixed kidn eys. Results Both 6-OHDA-treated and untreated DS rats presented a greater degre e of intrarenal vessel remodelling characterized by reduced lumen diameter in the absence (eutrophic) or presence (hypertrophic) of cross-sectionaIare aexpansion, higher renal vascular resistance (RVR) and lower GFR and RBF th an DR rats. Chemical sympathectomy increased lumen diameters and reduced va scular wall expansion, resulting in a decrease in RVR and a concomitant inc rease in RBF and GFR in both strains; however, the effect was more prominen t in the DS rats. Conclusions We conclude that HS-LK-induced changes in int ra-renal vessel structure and renal haemodynamic function in Dahl rats are, at least in part, dependent on the activity of the sympathetic nervous sys tem. J Hypertens 2000, 18:783-793 (C) Lippincott Williams & Wilkins.