Linked Life Data

2833134

Source:http://linkedlifedata.com/resource/pubmed/id/2833134

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1988-5-2
pubmed:abstractText
The aim of this study was to examine the effects of adenosine (AD)-induced hypotension on preganglionic adrenal (aSNA) and postganglionic renal (rSNA) sympathetic nerve activity. rSNA (n = 10) and aSNA (n = 6) were recorded together with mean arterial pressure (MAP) and heart rate (HR) in chloralose-anesthetized, artificially ventilated rats. In each experiment, hypotension was induced by equihypotensive doses of AD (0.03-2.0 mg.kg-1.min-1) and sodium nitroprusside (SNP) (1-10 micrograms.kg-1.min-1). SNP induced a progressive reflex tachycardia and a reflex increase in rSNA to levels 159 +/- 35% above control at a MAP reduction of 55% of the normotensive control value. Equipotent doses of AD induced a decrease in HR and significantly less pronounced reflex increase in rSNA. The maximal increase in rSNA with AD was 55 +/- 19% at a MAP reduction of 30%. At higher infusions rates of AD, rSNA progressively declined toward the normotensive control values. However, AD elicited a progressive increase in preganglionic aSNA that was not significantly different from the increase seen during SNP infusion. It is concluded that AD-induced hypotension is associated with a suppression of postganglionic sympathetic nerve activity caused by an inhibition of ganglionic neurotransmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0003-2999
pubmed:author
pubmed:issnType
Print
pubmed:volume
67
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
307-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Pre- and postganglionic sympathetic nerve activity during induced hypotension with adenosine or sodium nitroprusside in the anesthetized rat.
pubmed:affiliation
Department of Physiology and Anesthesia, Sahlgren's Hospital, University of Göteborg, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't