Linked Life Data

18079268

Source:http://linkedlifedata.com/resource/pubmed/id/18079268

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-3-10
pubmed:abstractText
Exercise training (EX) has become an important modality capable of enhancing the quality of life and survival of patients with chronic heart failure (CHF). Although 4 wk of EX in animals with CHF evoked a reduction in renal sympathetic nerve activity and ANG II plasma levels and an enhancement in baroreflex sensitivity at rest (Liu JL, Irvine S, Reid IA, Patel KP, Zucker IH, Circulation 102: 1854-1862, 2000; Liu JL, Kulakofsky J, Zucker IH, J Appl Physiol 92: 2403-2408, 2002), it is unclear whether these phenomena are causally related. CHF was induced in rabbits by ventricular pacing (360-380 beats/min) for 3 wk. CHF rabbits were EX for 4 wk at 15-18 m/min, 6 days/wk, 30-40 min/day. Three groups of rabbits were studied: CHF (with no EX), CHF-EX, and CHF-EX + ANG II infusion [in which ANG II levels were kept at or near levels observed in CHF (non-EX) rabbits by subcutaneous osmotic minipump infusion]. EX prevented the increase in plasma ANG II levels shown in CHF rabbits. CHF and CHF-EX + ANG II infusion rabbits had significantly depressed baroreflex sensitivity slopes (P < 0.01 for sodium nitroprusside and P < 0.001 for phenylephrine) and higher baseline renal sympathetic nerve activities than CHF-EX animals. EX downregulated mRNA and protein expression of ANG II type 1 receptors in the rostral ventrolateral medulla in CHF rabbits. This was prevented by ANG II infusion. These data are consistent with the view that the reduction in sympathetic nerve activity and the improvement in baroreflex function in CHF after EX are due to the concomitant reduction in ANG II and angiotensin receptors in the central nervous system.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
104
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
616-24
pubmed:meshHeading
pubmed-meshheading:18079268-Angiotensin II, pubmed-meshheading:18079268-Animals, pubmed-meshheading:18079268-Baroreflex, pubmed-meshheading:18079268-Chronic Disease, pubmed-meshheading:18079268-Disease Models, Animal, pubmed-meshheading:18079268-Down-Regulation, pubmed-meshheading:18079268-Exercise Therapy, pubmed-meshheading:18079268-Heart Failure, pubmed-meshheading:18079268-Hemodynamics, pubmed-meshheading:18079268-Infusion Pumps, Implantable, pubmed-meshheading:18079268-Kidney, pubmed-meshheading:18079268-Male, pubmed-meshheading:18079268-Medulla Oblongata, pubmed-meshheading:18079268-Nitroprusside, pubmed-meshheading:18079268-Phenylephrine, pubmed-meshheading:18079268-Physical Conditioning, Animal, pubmed-meshheading:18079268-RNA, Messenger, pubmed-meshheading:18079268-Rabbits, pubmed-meshheading:18079268-Receptor, Angiotensin, Type 1, pubmed-meshheading:18079268-Sympathetic Nervous System, pubmed-meshheading:18079268-Time Factors, pubmed-meshheading:18079268-Vasoconstrictor Agents, pubmed-meshheading:18079268-Vasodilator Agents
pubmed:year
2008
pubmed:articleTitle
Exercise training enhances baroreflex sensitivity by an angiotensin II-dependent mechanism in chronic heart failure.
pubmed:affiliation
Dept. of Cellular and Integrative Physiology, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural