title: Influence of prolonged baroreflex activation on arterial pressure in angiotensin hypertension.
abstract: Despite recent evidence indicating sustained activation of the baroreflex during chronic infusion of angiotensin II (Ang II), sinoaortic denervation does not exacerbate the severity of the hypertension. Therefore, to determine whether Ang II hypertension is relatively resistant to the blood pressure-lowering effects of the baroreflex, the carotid baroreflex was electrically activated bilaterally for 7 days in 5 dogs both in the presence and absence of a continuous infusion of Ang II (5 ng/kg per minute) producing high physiological plasma levels of the peptide. Under control conditions, basal values for mean arterial pressure (MAP) and plasma norepinephrine concentration (NE) were 93+/-1 mm Hg and 99+/-25 pg/mL, respectively. By day 7 of baroreflex activation, MAP and NE were reduced to 72+/-4 mm Hg (-21+/-3 mm Hg) and 56+/-15 pg/mL, respectively, but PRA was unchanged (control=0.41+/-0.06 ng ANG I/mL per hour). All values returned to basal levels by the end of a 7-day recovery period. After 7 days of Ang II infusion, MAP increased from 93+/-3 to 129+/-3 mm Hg, whereas NE fell from 117+/-15 to 86+/-23 pg/mL. During the next 7 days of baroreflex activation/Ang II infusion, further reductions in NE were not statistically significant, and on the final day of baroreflex activation, the reduction in MAP was only 5+/-1 mm Hg, compared with 21+/-3 mm Hg in the control normotensive state. These findings indicate that long-term baroreflex-mediated reductions in arterial pressure are markedly diminished, but not totally eliminated, in the presence of hypertension produced by chronic infusion of Ang II.
authors.affiliation: Department of Physiology, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA. tlohmeier@physiology.umsmed.edu
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Lohmeier
authors.forename: Terry M
authors.initials: TM
authors.lastname: Dwyer
authors.forename: Drew A
authors.initials: DA
authors.lastname: Hildebrandt
authors.forename: Eric D
authors.initials: ED
authors.lastname: Irwin
authors.forename: Martin A
authors.initials: MA
authors.lastname: Rossing
authors.forename: David J
authors.initials: DJ
authors.lastname: Serdar
authors.forename: Robert S
authors.initials: RS
authors.lastname: Kieval
mesh_terms: D000804:Angiotensin II / Q000008:administration & dosage; D000818:Animals; D017704:Baroreflex; D001794:Blood Pressure; D001798:Blood Proteins / Q000378:metabolism; D004285:Dogs; D004334:Drug Administration Schedule; D004573:Electrolytes / Q000097:blood / Q000652:urine; D006339:Heart Rate; D006400:Hematocrit; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D018377:Neurotransmitter Agents / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000008:administration & dosage
chemical_list: D001798:Blood Proteins; D004573:Electrolytes; D018377:Neurotransmitter Agents; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009638:Norepinephrine