title: Renal vascular resistance properties and glomerular protection in early established SHR hypertension.
abstract: OBJECTIVE
  To characterize the in vivo vascular properties of the spontaneously hypertensive rat (SHR) renal vascular bed by examining vascular conductance/resistance responsiveness to vasoactive agents in vivo and determining whether the filtration surface area of glomerular capillaries is reduced.
  
  
  METHODS
  in vivo renal blood flow responses to intrarenally administered angiotensin II, phenylephrine and acetylcholine were compared in 10-week-old SHR and Wistar-Kyoto (WKY) rats using a wide range of doses from near threshold to near maximal effect. Unbiased stereological techniques and high-resolution light microscopy were used to estimate the surface area and length of glomerular capillaries, and evidence of capillary damage.
  
  
  RESULTS
  The SHR renal bed demonstrated significantly enhanced dose-vascular resistance responses to vasoconstrictors. For vascular conductance and calculated radius of resistance vessels, the SHR curves were significantly lower across the full dilator-constrictor range examined, but the dose-related changes were similar to those of WKY rats. There were only modest enhancements of the renal blood flow responses in the SHR, evident only when renal blood flow was reduced by more than 50% SHR and WKY rats did not differ in mean glomerular capillary surface area (0.13+/-0.02 mm2 and 0.14+/-0.02 mm2, respectively) or length (5.76+/-0.85 mm and 5.48+/-0.90 mm, respectively) nor was there evidence of glomerular capillary damage in either strain.
  
  
  CONCLUSIONS
  The renal vascular bed of the SHR in vivo exhibits reduced vascular conductance across a wide vasomotor range, compatible with findings in other vascular beds. We have further shown no evidence of reduced glomerular capillary surface area or damage. These findings are compatible with the hypothesis that the reduced conductance of the SHR pre-glomerular vasculature increases the aorta-capillary pressure gradient thus protecting the glomerular capillaries from systemic hypertension at this age.
authors.affiliation: Department of Physiology, Monash University, VIC, Australia. michelle.kett@med.monash.edu.au
authors.forename: M M
authors.initials: MM
authors.lastname: Kett
authors.forename: G
authors.initials: G
authors.lastname: Bergström
authors.forename: D
authors.initials: D
authors.lastname: Alcorn
authors.forename: J F
authors.initials: JF
authors.lastname: Bertram
authors.forename: W P
authors.initials: WP
authors.lastname: Anderson
mesh_terms: D000818:Animals; D002196:Capillaries / Q000473:pathology; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000098:blood supply / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY; D012079:Renal Circulation / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents