title: Chronic angiotensin II infusion causes differential responses in regional sympathetic nerve activity in rats.
abstract: Angiotensin II (AngII)-induced hypertension in experimental animals has been proposed to be attributed in part to activation of the sympathetic nervous system. This sympathetic activation appears to be accentuated in animals consuming a high-salt diet (AngII-salt hypertension). However, accurate quantification of sympathetic activity is difficult, and controversy remains. It is particularly important to ask which are the critical vascular beds targeted by increased sympathetic nerve activity (SNA) in AngII-salt hypertension. To address this issue, mean arterial pressure and renal SNA or lumbar SNA were continuously recorded during a 5-day control period, 11 days of AngII (150 ng/kg per minute, SC), and a 5-day recovery period in conscious rats on a high-salt (2% NaCl) diet. Although mean arterial pressure reached a new steady-state level of 30 to 35 mm Hg above control levels by the end of the AngII period, renal SNA decreased by 40% during the first 7 days of AngII and then returned toward control levels by day 10 of AngII. In contrast, lumbar SNA remained at control levels throughout the AngII period. In another experiment we measured hindlimb norepinephrine spillover in conscious rats on normal (0.4%) or high- (2.0%) salt diets before and during 14 days of AngII administration. AngII had no significant affect on hindlimb norepinephrine spillover in either group. We conclude that chronic AngII modulates renal and lumbar SNAs differentially in rats consuming a high-salt diet and that AngII-salt hypertension in the rat is not caused by increased SNA to the renal or hindlimb vascular beds.
authors.affiliation: Department of Integrative Biology and Physiology, University of Minnesota, Room 6-125 Jackson Hall, Minneapolis, MN 55455, USA.
authors.forename: Misa
authors.initials: M
authors.lastname: Yoshimoto
authors.forename: Kenju
authors.initials: K
authors.lastname: Miki
authors.forename: Gregory D
authors.initials: GD
authors.lastname: Fink
authors.forename: Andrew
authors.initials: A
authors.lastname: King
authors.forename: John W
authors.initials: JW
authors.lastname: Osborn
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002319:Cardiovascular System / Q000294:innervation; D002908:Chronic Disease; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006614:Hindlimb / Q000098:blood supply / Q000294:innervation; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000294:innervation; D008161:Lumbosacral Region / Q000098:blood supply / Q000294:innervation; D008297:Male; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D017673:Sodium Chloride, Dietary; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009638:Norepinephrine