title: Glomerular dimensions in spontaneously hypertensive rats: effects of AT1 antagonism.
abstract: OBJECTIVE
  A reduction in glomerular number and/or size has been implicated in the development of hypertension. This study investigated whether differences in glomerular number and/or size occur during the development of hypertension in the spontaneously hypertensive rat (SHR) and whether angiotensin II is responsible for any glomerular differences.
  
  
  METHODS
  SHR (n=6) and Wistar-Kyoto (WKY) rats (n=6) were administered the angiotensin II type I receptor antagonist TCV-116 from 4 to 10 weeks of age. At 10 weeks of age, the kidneys from these rats and those from untreated SHR (n=6) and WKY rats (n=6) controls were perfusion fixed at physiological pressures and analysed using unbiased stereological techniques.
  
  
  RESULTS
  There were no significant differences in glomerular number, glomerular volume or total glomerular volume between SHR and WKY rats. Treatment of SHR with TCV-116 significantly lowered systolic blood pressure but had no significant effect on glomerular number or volume or total glomerular volume. Treatment of WKY rats with TCV-116 reduced systolic blood pressure, body weight, glomerular volume and total glomerular volume; however, total glomerular volume per body weight of treated WKY rats was not significantly different from that of untreated WKY rats.
  
  
  CONCLUSIONS
  There were no differences in glomerular number or volume in SHR compared with WKY rats at 10 weeks of age. We therefore conclude that glomerular changes are not responsible for the development of hypertension in SHR. Angiotensin II, via the type 1 receptor, does not contribute to glomerular growth during the development of hypertension in the SHR.
authors.affiliation: Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria, Australia.
authors.forename: M M
authors.initials: MM
authors.lastname: Kett
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: D057911:Angiotensin Receptor Antagonists; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001562:Benzimidazoles / Q000037:antagonists & inhibitors; D001713:Biphenyl Compounds / Q000037:antagonists & inhibitors; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004336:Drug Antagonism; D007678:Kidney Glomerulus / Q000187:drug effects*; D008297:Male; D008955:Models, Cardiovascular; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; D014654:Vascular Patency / Q000187:drug effects / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; C077793:candesartan cilexetil