title: Renal denervation does not abolish sustained baroreflex-mediated reductions in arterial pressure.
abstract: Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean arterial pressure and plasma norepinephrine concentration were 95+/-2 mm Hg and 96+/-12 pg/mL, respectively. During day 1 of baroreflex activation, mean arterial pressure decreased 13+/-1 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean arterial pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with sustained decreases in plasma norepinephrine concentration ( approximately 50%) and plasma renin activity (30% to 40%). All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean arterial pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were comparable to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were similar to those observed before renal denervation. These findings demonstrate that the presence of the renal nerves is not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex.
authors.affiliation: Department of Physiology, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216-4505, USA. tlohmeier@physiology.umsmed.edu
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Lohmeier
authors.forename: Drew A
authors.initials: DA
authors.lastname: Hildebrandt
authors.forename: Terry M
authors.initials: TM
authors.lastname: Dwyer
authors.forename: Austin M
authors.initials: AM
authors.lastname: Barrett
authors.forename: Eric D
authors.initials: ED
authors.lastname: Irwin
authors.forename: Martin A
authors.initials: MA
authors.lastname: Rossing
authors.forename: Robert S
authors.initials: RS
authors.lastname: Kieval
mesh_terms: D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D001798:Blood Proteins / Q000378:metabolism; D002339:Carotid Arteries / Q000502:physiology; D003714:Denervation; D004285:Dogs; D004558:Electric Stimulation; D006339:Heart Rate / Q000502:physiology; D006400:Hematocrit; D007668:Kidney / Q000294:innervation* / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism; D009994:Osmolar Concentration; D011188:Potassium / Q000097:blood / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood / Q000652:urine; D013564:Sympathetic Nervous System / Q000502:physiology*; D013997:Time Factors
chemical_list: D001798:Blood Proteins; D012964:Sodium; D012083:Renin; D011188:Potassium; D009638:Norepinephrine