title: Exaggerated natriuresis in transgenic (mRen2)27 rats.
abstract: BACKGROUND
  Hypertension features an exaggerated natriuresis after acute volume expansion. In humans, the degree of exaggerated natriuresis appears to be correlated inversely to the level of angiotensin (Ang) II.
  
  
  OBJECTIVE
  To test the hypothesis that the degree of exaggerated natruresis is correlated to the level of Ang II by studying two rat models, transgenic rats (TGR) with and extra renin gene (TGR mRen2)27 and desoxycorticosterone acetate (DOCA)-salt rats, in comparison with Sprague-Dawley Hannover (SDH) rat controls.
  
  
  METHODS
  All of the rats were uninephrectomized for 1 month. DOCA-salt rats were implanted with a DOCA pallet and drank 1% saline. Rats were anesthetized and their left kidneys were instrumented with renal sympathetic nerve activity (RSNA) electrodes and laser-Doppler cortical and medullary flow probes. The glomerular filtration rate, diuresis, and natriuresis were measured for 120 min after sodium loading (5% body weight 0.9% saline administered during 3 min). Kidneys were examined histologically.
  
  
  RESULTS
  The blood pressure in TGR and DOCA-salt rats was 40-50 mmHg higher than that in SDH rats, and decreased briefly after volume expansion for all groups. The diuresis and natriuresis of TGR and DOCA-salt rats were greater than those of SDH rats. The medullary blood flow increased and the cortical blood flow in SDH decreased, whereas the cortical blood flow in TGR and DOCA-salt rats remained high. The RSNA in rats of all groups decreased; however, this decrease was greater in SDH than it was in TGR and DOCA-salt rats. The histology was affected most severely for the DOCA-salt rats.
  
  
  CONCLUSIONS
  Exaggerated natriuresis occurred in hypertensive rats regardless of their Ang II status. Both strains were characterized by a smaller decrease in RSNA and a preserved cortical blood flow in the face of volume expansion. These data do not support the notion that exaggerated natriuresis is a function of renin-level suppression for rats.
authors.affiliation: Franz Volhard Clinic, Berlin, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Schneider
authors.forename: V
authors.initials: V
authors.lastname: Gross
authors.forename: A
authors.initials: A
authors.lastname: Lippoldt
authors.forename: F C
authors.initials: FC
authors.lastname: Luft
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D030801:Animals, Genetically Modified; D001794:Blood Pressure / Q000187:drug effects; D006973:Hypertension / Q000503:physiopathology*; D007672:Kidney Cortex / Q000098:blood supply / Q000294:innervation / Q000473:pathology; D007677:Kidney Function Tests; D007679:Kidney Medulla / Q000098:blood supply / Q000294:innervation / Q000473:pathology; D017078:Laser-Doppler Flowmetry; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000235:genetics / Q000502:physiology*; D012964:Sodium / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects
chemical_list: D000804:Angiotensin II; D012964:Sodium; D012083:Renin