title: Pressure control of renal renin release in Lyon hypertensive rats.
abstract: OBJECTIVE
  To assess whether the pressure-independence of renin release by isolated kidneys of Lyon hypertensive (LH) rats could result from long-term exposure to high blood pressure, sodium retention or an altered regulation of intracellular calcium through L-type voltage operated channels.
  
  
  METHODS
  Renin release was studied in kidneys from LH rats, either controls or chronically (aged 3-7 weeks) treated with hydralazine or deprived of sodium. The influence of L-type calcium channels was studied acutely using a specific activator (BAY K8644) or modulator (verapamil). Lyon low blood pressure (LL) rats served as controls.
  
  
  METHODS
  Kidneys were isolated from LH or LL rats aged 7 weeks and single-pass perfused at three pressure levels: 70, 85 and 160 mmHg.
  
  
  RESULTS
  LH rat kidneys differed from LL rat kidneys in having elevated vascular resistances, decreased glomerular filtration rate, pressure natriuresis and pressure-dependent renin release. Hydralazine treatment and sodium deprivation did not significantly modify the pressure-independence of renin release by LH rat kidneys. BAY K8644 (1 x 10(-8) and 5 x 10(-8) mol/l) induced significantly greater vasoconstrictor effects in LH than in LL rat kidneys but did not affect the renin release already stimulated by low perfusion pressure. Verapamil (5 x 10(-6) mol/l) dilated LH more than LL rat kidneys. It did not change the renin release observed at low, but enhanced it at high, perfusion pressure. This effect was more marked in LL than in LH rat kidneys.
  
  
  CONCLUSIONS
  The poor stimulation of renin release by low perfusion pressure in LH rat kidneys does not appear to be a consequence of high blood pressure level, sodium retention and alteration in L-type calcium channels. However, results demonstrate that these channels participate in the increased vascular resistances exhibited by LH rat kidneys.
authors.affiliation: Département de Physiologie et Pharmacologie Clinique, URA CNRS 1483, Faculté de Pharmacie, Lyon, France.
authors.forename: I A
authors.initials: IA
authors.lastname: Medeiros
authors.forename: B L
authors.initials: BL
authors.lastname: Zhang
authors.forename: S
authors.initials: S
authors.lastname: Bertolino
authors.forename: J
authors.initials: J
authors.lastname: Sassard
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D004039:Diet, Sodium-Restricted; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D066298:In Vitro Techniques; D007668:Kidney / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D012083:Renin / Q000378:metabolism*; D013997:Time Factors; D014700:Verapamil / Q000494:pharmacology
chemical_list: D006830:Hydralazine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D014700:Verapamil; D012083:Renin