title: Evidence for decreased structurally determined preglomerular resistance in the young spontaneously hypertensive rat after 4 weeks of renal denervation.
abstract: OBJECTIVE
  To study the effects of denervation of the kidney on renal vascular resistance at maximal dilatation and renal function during the development of hypertension in the spontaneously hypertensive rat (SHR).
  
  
  METHODS
  SHR aged 6 weeks were subjected to left renal denervation or a sham-operation (n = 18 denervated, n = 13 sham). When they were aged 10 weeks, pairs of denervated and sham-operated left kidneys were perfused with 2% dextran in Tyrode's solution and pressure-flow and pressure-glomerular filtration rate (GFR) relationships at maximal vasodilation were established. The awake mean arterial blood pressure, in-vivo renal function and renal noradrenaline content were also measured.
  
  
  RESULTS
  There were no significant differences between the pressure-flow relationships for denervated and sham-operated kidneys. However, there was a marked, parallel, shift leftwards in the pressure-GFR relationship (P < 0.001). Thus, the denervated kidneys commenced filtering at a lower threshold perfusion pressure than did the sham-operated ones. In-vivo renal plasma flow and GFR were significantly greater in the denervated left kidneys of SHR than they were in the contralateral kidneys. The noradrenaline content in denervated kidneys was 5 +/- 3% of that in innervated kidneys. The awake mean arterial pressure was 135 +/- 1 and 138 +/- 2 mmHg in the denervated and sham-operated groups respectively.
  
  
  CONCLUSIONS
  Denervation of the kidney of SHR aged 6 weeks of age altered the pressure-GFR but not the pressure-flow relationship for these rats 4 weeks later. The results are compatible with there having been an increase in average preglomerular and a decrease in post-glomerular vessel lumen diameters. These changes suggest that the renal nerves affect the structural development of the renal vasculature in SHR.
authors.affiliation: Department of Physiology, Monash University, Clayton, Victoria, Australia.
authors.forename: F
authors.initials: F
authors.lastname: Tomoda
authors.forename: G
authors.initials: G
authors.lastname: Bergström
authors.forename: R G
authors.initials: RG
authors.lastname: Evans
authors.forename: W P
authors.initials: WP
authors.lastname: Anderson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002851:Chromatography, High Pressure Liquid; D003714:Denervation; D004195:Disease Models, Animal; D005919:Glomerular Filtration Rate; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D012077:Renal Artery / Q000294:innervation*; D017595:Renal Plasma Flow; D014655:Vascular Resistance / Q000502:physiology*
chemical_list: D009638:Norepinephrine