Document Detail

Alpha-2 adrenergic transmission and human baroreflex regulation.
MedLine Citation:
PMID:  15037555     Owner:  NLM     Status:  MEDLINE    
We observed earlier that central alpha-2 adrenoceptor stimulation in mice greatly augments parasympathetic tone. To test the effects in humans, we assessed autonomic vasomotor tone and baroreflex regulation in 9 normal young adults on 2 occasions, once with and once without clonidine. We determined heart rate (HR), beat-by-beat blood pressure (BP), and muscle sympathetic nerve activity. HR variability was analyzed in the time and frequency domain. Pharmacological baroreflex slopes were determined using incremental phenylephrine and nitroprusside infusions. Clonidine lowered resting BP (122+/-4/73+/-3 versus 100+/-7/55+/-3 mm Hg, P<0.01), muscle sympathetic nerve activity (18+/-3 versus 4+/-2 bursts/min, P<0.01), and HR (62+/-3 versus 56+/-3 bpm, P<0.05). The baroreflex heart rate curve was reset to much lower HR values and showed no saturation at low HR. HR variability profoundly increased during clonidine plus phenylephrine (total power: 3224+/-843 versus 8943+/-2329 ms2, P<0.05). High-frequency power was 1451+/-520 at baseline and 6720+/-2475 ms2 during baroreceptor loading (P<0.05). The low-frequency/high-frequency ratio decreased (1.94+/-0.41 versus 0.69+/-0.10, P<0.05). In contrast, clonidine reduced resting sympathetic vasomotor tone and shifted the operating point of the sympathetic baroreflex to a flat part of the sympathetic baroreflex curve. The shift decreased the ability of the baroreflex to withdraw sympathetic vasomotor tone during baroreflex loading. These baroreflex changes were associated with a moderate increase in phenylephrine responsiveness. We conclude that alpha-2 adrenoceptor stimulation has a differential effect on baroreflex HR and vasomotor regulation. alpha-2 Adrenoceptor stimulation greatly augments baroreflex-mediated bradycardia, most likely by parasympathetic activation.
Jens Tank; Andre Diedrich; Elke Szczech; Friedrich C Luft; Jens Jordan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-03-22
Journal Detail:
Title:  Hypertension     Volume:  43     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-05-06     Completed Date:  2004-10-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1035-41     Citation Subset:  IM    
Department of Nephrology and Hypertension, Franz-Volhard-Clinic, Medical Faculty of the Charité and HELIOS Klinikum, Berlin, Germany.
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MeSH Terms
Action Potentials / drug effects
Adrenergic alpha-Agonists / pharmacology*
Adrenergic beta-Antagonists / pharmacology
Antihypertensive Agents / pharmacology*
Baroreflex / drug effects*,  physiology
Blood Pressure / drug effects
Bradycardia / chemically induced
Cardiotonic Agents / pharmacology
Clonidine / pharmacology*
Cold Temperature / diagnostic use
Drug Interactions
Heart Rate / drug effects
Middle Aged
Nitroprusside / pharmacology
Parasympathetic Nervous System / drug effects*,  physiology
Peroneal Nerve / drug effects,  physiology
Phenylephrine / pharmacology
Pressoreceptors / drug effects*,  physiology
Propranolol / pharmacology
Receptors, Adrenergic, alpha-2 / agonists*,  physiology
Stroke Volume / drug effects
Sympathetic Nervous System / drug effects,  physiology
Vasomotor System / drug effects,  physiology
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Adrenergic beta-Antagonists; 0/Antihypertensive Agents; 0/Cardiotonic Agents; 0/Receptors, Adrenergic, alpha-2; 15078-28-1/Nitroprusside; 4205-90-7/Clonidine; 525-66-6/Propranolol; 59-42-7/Phenylephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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