Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-5-6
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1035-41
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15037555-Action Potentials, pubmed-meshheading:15037555-Adrenergic alpha-2 Receptor Agonists, pubmed-meshheading:15037555-Adrenergic alpha-Agonists, pubmed-meshheading:15037555-Adrenergic beta-Antagonists, pubmed-meshheading:15037555-Adult, pubmed-meshheading:15037555-Antihypertensive Agents, pubmed-meshheading:15037555-Baroreflex, pubmed-meshheading:15037555-Blood Pressure, pubmed-meshheading:15037555-Bradycardia, pubmed-meshheading:15037555-Cardiotonic Agents, pubmed-meshheading:15037555-Clonidine, pubmed-meshheading:15037555-Cold Temperature, pubmed-meshheading:15037555-Drug Interactions, pubmed-meshheading:15037555-Heart Rate, pubmed-meshheading:15037555-Humans, pubmed-meshheading:15037555-Male, pubmed-meshheading:15037555-Middle Aged, pubmed-meshheading:15037555-Nitroprusside, pubmed-meshheading:15037555-Parasympathetic Nervous System, pubmed-meshheading:15037555-Peroneal Nerve, pubmed-meshheading:15037555-Phenylephrine, pubmed-meshheading:15037555-Pressoreceptors, pubmed-meshheading:15037555-Propranolol, pubmed-meshheading:15037555-Receptors, Adrenergic, alpha-2, pubmed-meshheading:15037555-Stroke Volume, pubmed-meshheading:15037555-Sympathetic Nervous System, pubmed-meshheading:15037555-Vasomotor System
pubmed:year
2004
pubmed:articleTitle
Alpha-2 adrenergic transmission and human baroreflex regulation.
pubmed:affiliation
Department of Nephrology and Hypertension, Franz-Volhard-Clinic, Medical Faculty of the Charité and HELIOS Klinikum, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't