title: Renomedullary interstitial cell lipid droplet content is increased in spontaneously hypertensive rats and by low salt diet.
abstract: OBJECTIVE
  To compare the volumes of renomedullary interstitial cell (RMIC) lipid droplets (putative source of vasodepressor substance) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats on high and low salt diets as an indication of whether the renomedullary vasodepressor system of the SHR is defective.
  
  
  METHODS
  Ten-week-old male SHR and WKY rats received a low (0.05% w/w) or high salt (5.0%) diet for 21 days. Conscious mean arterial pressure (MAP) was measured and the renal papilla perfusion fixed with a high osmolarity fixative. Using electron microscopic stereological techniques, the volume density of lipid in RMIC (VVLipid,RMIC) and the total volumes of lipid (VLipid) and RMIC (VRMIC) in papilla were measured.
  
  
  RESULTS
  MAP of SHR (high 155 +/- 3 mmHg; low 151 +/- 3 mmHg) was significantly greater than WKY rats (high 126 +/- 2 mmHg; low 129 +/- 2 mmHg; P< 0.001), however salt diet had no significant effect on MAP. The VLipid of rats on the low salt diet was approximately 2.5 times greater than in rats on the high salt diet (P < 0.01). SHR had significantly greater VLipid than WKY rats irrespective of salt diet (P< 0.05; SHR-low 0.245 +/- 0.031 mm3, SHR-high 0.093 +/- 0.007 mm3; WKY-low 0.126 +/- 0.032 mm3, WKY-high 0.051 +/- 0.020 mm3). Similar differences were seen for VVLipid,RMIC, however VRMIC was not different between rat strains or salt diet groups.
  
  
  CONCLUSIONS
  SHR and WKY rats responded similarly to the altered salt diets, and SHR demonstrated greater volumes of stored RMIC lipid droplets irrespective of the level of salt intake. These results indicate that SHR hypertension is not due to a deficiency in the amount of lipid droplets, the putative source of the renomedullary vasodepressor substance and that the renomedullary vasodepressor system of the SHR is capable of responding normally to the physiological stimulus of altered salt intake.
authors.affiliation: Department of Physiology, Monash University, Clayton, Victoria, Australia. m.kett@med.monash.edu.au
authors.forename: M M
authors.initials: MM
authors.lastname: Kett
authors.forename: B L
authors.initials: BL
authors.lastname: Heideman
authors.forename: J F
authors.initials: JF
authors.lastname: Bertram
authors.forename: W P
authors.initials: WP
authors.lastname: Anderson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004039:Diet, Sodium-Restricted; D007679:Kidney Medulla / Q000166:cytology / Q000378:metabolism*; D050356:Lipid Metabolism; D008297:Male; D008863:Microspheres; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY / Q000502:physiology