title: Sympathetic nerve activity in conscious renal hypertensive rats treated with an angiotensin converting enzyme inhibitor or an angiotensin II antagonist.
abstract: OBJECTIVE
  To assess in conscious two-kidney, one clip renal hypertensive rats whether angiotensin converting enzyme (ACE) inhibition with lisinopril, angiotensin II receptor blockade with losartan or vasodilation with sodium nitroprusside have similar effects on intra-arterial mean blood pressure, heart rate and splanchnic nerve activity.
  
  
  RESULTS
  A bolus dose of lisinopril or losartan (both 10 mg/kg, intravenously) induced within 2 h an equal reduction in mean blood pressure, whereas sodium nitroprusside infused during the same period (at 10 micrograms/min) lowered mean blood pressure, but less strongly. The heart rate was accelerated significantly more during sodium nitroprusside infusion than during lisinopril or losartan treatment. Splanchnic nerve activity increased significantly only in those rats given sodium nitroprusside. No change in the parameters studied was observed in vehicle-treated rats. The doses of lisinopril and losartan were repeated after 12 and 24 h. Before administration of the last dose, the mean blood pressure was still low. Administration of lisinopril or losartan again 24 h after the initial dose had no further effect on the mean blood pressure, heart rate or splanchnic nerve activity.
  
  
  CONCLUSIONS
  These results obtained in rats with a renin-dependent form of hypertension show that blockade of the renin-angiotensin system for 24 h produces an equivalent blood pressure reduction irrespective of whether it is due to ACE inhibition or angiotensin II antagonism. The results also indicate that there is less reflex activation of sympathetic nerve activity when blood pressure is lowered with a blocker of the renin-angiotensin system rather than with a direct vasodilator such as sodium nitroprusside.
authors.affiliation: Division of Hypertension, University Hospital, Lausanne, Switzerland.
authors.forename: M
authors.initials: M
authors.lastname: Niederberger
authors.forename: J F
authors.initials: JF
authors.lastname: Aubert
authors.forename: J
authors.initials: J
authors.lastname: Nussberger
authors.forename: H R
authors.initials: HR
authors.lastname: Brunner
authors.forename: B
authors.initials: B
authors.lastname: Waeber
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D006339:Heart Rate / Q000187:drug effects; D006977:Hypertension, Renal / Q000188:drug therapy / Q000503:physiopathology*; D007093:Imidazoles / Q000627:therapeutic use*; D017706:Lisinopril / Q000627:therapeutic use*; D019808:Losartan; D008297:Male; D009599:Nitroprusside / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000187:drug effects; D013153:Splanchnic Nerves / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects*; D013777:Tetrazoles / Q000627:therapeutic use*
chemical_list: D057911:Angiotensin Receptor Antagonists; D001713:Biphenyl Compounds; D007093:Imidazoles; D013777:Tetrazoles; D000804:Angiotensin II; D009599:Nitroprusside; D000803:Angiotensin I; D017706:Lisinopril; D019808:Losartan