title: Osmotically induced natriuresis and blood pressure response involves angiotensin AT1 receptors in the subfornical organ.
abstract: OBJECTIVE
  In the present study we tested the hypothesis of whether the centrally induced natriuresis and blood pressure increase after intracerebroventricular injection of hypertonic saline involves the subfornical organ, as suggested by the occurrence of osmosensitive cells as well as a high concentration of angiotensin II receptors in this brain area.
  
  
  METHODS
  All experiments were performed in conscious Wistar rats. A chronic cannula was inserted into the lateral brain ventricle for intracerebroventricular injection and a chronic indwelling intracranial guide cannula for microinjection was placed in the subfornical organ. In addition, the rats were provided with ureter catheters for urine collection.
  
  
  RESULTS
  Intracerebroventricular injections of hypertonic saline (0.3 mol/l; n = 7) increased renal sodium excretion from 180.0 +/- 30.0 to 279.0 +/- 34.0 mol/l/60 min (P < 0.001) accompanied by an increase in mean arterial pressure of 8.3 +/- 1.2 mmHg (P < 0.01). No change in urinary volume was observed. After injection of the specific AT1 receptor antagonist, losartan, into the subfornical organ (5 micrograms/200 nl; n = 8) the natriuresis and blood pressure response to intracerebroventricular hypertonic saline was completely abolished. Control injections of losartan into areas adjacent to the subfornical organ had no effect on the responses to hypertonic saline.
  
  
  CONCLUSIONS
  Our results suggest that the centrally induced natriuresis and blood pressure responses to hypertonic saline are mediated by an angiotensinergic mechanism involving the subfornical organ.
authors.affiliation: V Medical Department, University of Heidelberg, Mannheim, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Rohmeiss
authors.forename: C
authors.initials: C
authors.lastname: Beyer
authors.forename: B
authors.initials: B
authors.lastname: Hocher
authors.forename: F
authors.initials: F
authors.lastname: Qadri
authors.forename: N
authors.initials: N
authors.lastname: Gretz
authors.forename: M
authors.initials: M
authors.lastname: Strauch
authors.forename: T
authors.initials: T
authors.lastname: Unger
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D007093:Imidazoles / Q000494:pharmacology; D007276:Injections, Intraventricular; D019808:Losartan; D008297:Male; D008845:Microinjections; D009318:Natriuresis / Q000187:drug effects; D009997:Osmotic Pressure; D051381:Rats; D017208:Rats, Wistar; D011945:Receptors, Angiotensin / Q000502:physiology*; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D013356:Subfornical Organ / Q000378:metabolism*; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D007093:Imidazoles; D011945:Receptors, Angiotensin; D012462:Saline Solution, Hypertonic; D013777:Tetrazoles; D019808:Losartan