title: Carotid baroreceptor stimulation, sympathetic activity, baroreflex function, and blood pressure in hypertensive patients.
abstract: In animals, electric field stimulation of carotid baroreceptors elicits a depressor response through sympathetic inhibition. We tested the hypothesis that the stimulation acutely reduces sympathetic vasomotor tone and blood pressure in patients with drug treatment-resistant arterial hypertension. Furthermore, we tested whether the stimulation impairs the physiological baroreflex regulation. We studied 7 men and 5 women (ages 43 to 69 years) with treatment-resistant arterial hypertension. A bilateral electric baroreflex stimulator at the level of the carotid sinus (Rheos) was implanted > or =1 month before the study. We measured intra-arterial blood pressure, heart rate, muscle sympathetic nerve activity (microneurography), cardiac baroreflex sensitivity (cross-spectral analysis and sequence method), sympathetic baroreflex sensitivity (threshold technique), plasma renin, and norepinephrine concentrations. Measurements were performed under resting conditions, with and without electric baroreflex stimulation, for > or =6 minutes during the same experiment. Intra-arterial blood pressure was 193+/-9/94+/-5 mm Hg on medications. Acute electric baroreflex stimulation decreased systolic blood pressure by 32+/-10 mm Hg (range: +7 to -108 mm Hg; P=0.01). The depressor response was correlated with a muscle sympathetic nerve activity reduction (r(2)=0.42; P<0.05). In responders, muscle sympathetic nerve activity decreased sharply when electric stimulation started. Then, muscle sympathetic nerve activity increased but remained below the baseline level throughout the stimulation period. Heart rate decreased 4.5+/-1.5 bpm with stimulation (P<0.05). Plasma renin concentration decreased 20+/-8% (P<0.05). Electric field stimulation of carotid sinus baroreflex afferents acutely decreased arterial blood pressure in hypertensive patients, without negative effects on physiological baroreflex regulation. The depressor response was mediated through sympathetic inhibition.
authors.affiliation: Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany.
authors.forename: Karsten
authors.initials: K
authors.lastname: Heusser
authors.forename: Jens
authors.initials: J
authors.lastname: Tank
authors.forename: Stefan
authors.initials: S
authors.lastname: Engeli
authors.forename: André
authors.initials: A
authors.lastname: Diedrich
authors.forename: Jan
authors.initials: J
authors.lastname: Menne
authors.forename: Siegfried
authors.initials: S
authors.lastname: Eckert
authors.forename: Tim
authors.initials: T
authors.lastname: Peters
authors.forename: Fred C G J
authors.initials: FC
authors.lastname: Sweep
authors.forename: Hermann
authors.initials: H
authors.lastname: Haller
authors.forename: Andreas M
authors.initials: AM
authors.lastname: Pichlmaier
authors.forename: Friedrich C
authors.initials: FC
authors.lastname: Luft
authors.forename: Jens
authors.initials: J
authors.lastname: Jordan
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002346:Carotid Sinus / Q000294:innervation*; D004351:Drug Resistance / Q000502:physiology; D004599:Electric Stimulation Therapy / Q000379:methods*; D005240:Feasibility Studies; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D009433:Neural Inhibition / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology*; D011446:Prospective Studies; D012083:Renin / Q000097:blood; D013318:Stroke Volume / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents; D012083:Renin