title: Impact of renal transplantation on small vessel reactivity.
abstract: BACKGROUND
  The function of large arteries is altered after renal transplantation. Whether transplantation also induces agonist-dependent functional changes in small arterial renal and extrarenal vessels has not yet been studied.
  
  
  METHODS
  Chronic rejection was induced by grafting Lewis rats with kidneys from Fischer rats (FL). Rats that underwent transplantation were bilaterally nephrectomized. Rats that underwent syngeneic transplantation, uninephrectomized rats, uninephrectomized rats with denervated kidneys or with kidneys made ischemic, and native rats served as controls. All animals were treated with cyclosporine for 10 days. Eighteen weeks after surgery, the reactivity of small arteries (220-270 microm) was tested by myography.
  
  
  RESULTS
  Weight gain, glomerular filtration rate, and arterial pressure were similar in all groups, whereas proteinuria was elevated in FL. Only kidneys from FL showed glomerular lesions, tubular atrophy, and vasculopathy. Responsiveness of coronary, mesenteric, and femoral resistance vessels to both constrictor and dilator agonists was similar in transplanted and nontransplanted animals. Resistance vessels obtained from both allogeneically and syngeneically transplanted kidneys were more sensitive to norepinephrine, phenylephrine, angiotensin II, and vasopressin than renal vessels from weight-matched controls. Vasodilation in response to acetylcholine and sodium nitroprusside was mitigated in transplanted versus nontransplanted kidneys.
  
  
  CONCLUSIONS
  In rat renal transplantation, renal resistance vessel responsiveness to constrictor or dilator stimuli is altered. Extrarenal small vessel function is not affected. The changes in function of renal resistance vessels are not explained by reduction of nephron mass, denervation, ischemia, or chronic rejection.
authors.affiliation: Medizinische Klinik und Poliklinik D, Universitätsklinikum Münster, Münster, Germany. gabrie@uni-muenster.de.
authors.forename: Gert
authors.initials: G
authors.lastname: Gabriëls
authors.forename: Christian
authors.initials: C
authors.lastname: August
authors.forename: Olaf
authors.initials: O
authors.lastname: Grisk
authors.forename: Martin
authors.initials: M
authors.lastname: Steinmetz
authors.forename: Markus
authors.initials: M
authors.lastname: Kosch
authors.forename: Karl Heinz
authors.initials: KH
authors.lastname: Rahn
authors.forename: Eberhard
authors.initials: E
authors.lastname: Schlatter
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D001158:Arteries; D001808:Blood Vessels / Q000187:drug effects / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology; D005263:Femoral Artery / Q000503:physiopathology; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation; D008297:Male; D008638:Mesenteric Arteries / Q000503:physiopathology; D008833:Microcirculation; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011916:Rats, Inbred F344; D012079:Renal Circulation; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D001127:Arginine Vasopressin; D010656:Phenylephrine; D009638:Norepinephrine